However, we found that SIRPα was rapidly induced on Kupffer cells

However, we found that SIRPα was rapidly induced on Kupffer cells following L. donovani infection, via a mechanism

involving G-protein-coupled receptors. Thus, we describe a novel amplification pathway affecting cytokine production by hepatic iNKT cells, which may facilitate the breakdown of hepatic tolerance after infection. “
“The transfer of alloreactive regulatory T (aTreg) cells into transplant recipients represents an attractive treatment option to improve long-term graft acceptance. We recently described a protocol for the generation of aTreg cells in mice using a nondepleting anti-CD4 antibody (aCD4). Here, we investigated whether adding TGF-β and retinoic acid (RA) or rapamycin (Rapa) can further improve aTreg-cell generation and function. Murine CD4+ T cells were cultured with allogeneic B cells in the

presence of aCD4 alone, aCD4+TGF-β+RA or aCD4+Rapa. GPCR Compound Library cell assay Addition of TGF-β+RA or Rapa resulted in an increase of CD25+Foxp3+-expressing T cells. Expression of CD40L and production of IFN-γ and IL-17 was abolished in aCD4+TGF-β+RA aTreg cells. Additionally, aCD4+TGF-β+RA aTreg cells showed the highest level of Helios and Neuropilin-1 co-expression. Although CD25+Foxp3+ cells from AG-014699 in vivo all culture conditions displayed complete demethylation of the Treg-specific demethylated region, aCD4+TGF-β+RA Treg cells showed the most stable Foxp3 expression upon restimulation. Consequently, aCD4+TGF-β+RA aTreg Methane monooxygenase cells suppressed effector T-cell differentiation more effectively in comparison to aTreg cells

harvested from all other cultures, and furthermore inhibited acute graft versus host disease and especially skin transplant rejection. Thus, addition of TGF-β+RA seems to be superior over Rapa in stabilising the phenotype and functional capacity of aTreg cells. Regulatory T (Treg) cells play an important role in the suppression of unwanted immune responses after transplantation [1] or after allogeneic stem cell transplantation [2]. Treg cells are essential for maintaining peripheral tolerance and for preventing autoimmune diseases such as systemic lupus erythematosus [3], rheumatoid arthritis [4] or diabetes [5]. Treg cells can be categorised into two groups, natural Treg (nTreg) cells, which develop in the thymus [6], and adaptive Treg cells or so-called induced (iTreg) Treg cells, which develop from CD4+CD25− cells in the periphery. Treg cells are mainly characterised by their expression of CD4 and CD25 [7]. Although both subsets express the fork head transcription factor Foxp3, nTreg cells and iTreg cells differ in DNA methylation pattern of the Foxp3 gene [8]. Furthermore, nTreg cells have been shown to express the Ikaros transcription family member Helios [9], although the selectivity of Helios expression in thymus-derived Treg cells was recently challenged [10].

Lu et al have suggested that recipient-derived MCs are crucial f

Lu et al. have suggested that recipient-derived MCs are crucial for Treg-mediated peripheral tolerance [11], indicating that the function of mast cells in suppressing immune responses was related to Tregs. Our study showed that CD4+CD25+ FoxP3+ cells could be induced by BMMCs. This finding may supply a new mechanism suggesting that MCs are crucial for Treg-mediated transplant tolerance [11]. This method may also become a new method for the induction of Tregsin vitro. Our results showed that the highest percentage of Tregs was found in the highest ratio (2:1) of BMMCs to T cells. TGF-β1 expression in BMMCs was determined in our experimental

groups. Jahanyar et al. concluded that mast cell-derived TGF-β may serve as important mediators for Treg activation in allografts [21], and other studies reported that the percentage of Tregs increased with the higher level of added TGF-β1 [22]. Therefore, it seems that the increase of Tregs with a higher ratio of BMMCs HM781-36B price may be related to more BMMCs-derived TGF-β1. Consistent with previous studies, and in order to test whether BMMC-derived TGF-β1 is involved in Carfilzomib chemical structure the generation of Tregs, TGF-β1

neutralizing antibody was added to the co-culture system [4]. The conversion of Tregs was reduced significantly by the TGF-β1 neutralizing antibody, but the TGF-β1 neutralizing antibody could not reverse Treg induction completely. The percentages of Tregs were still higher than control, even with the application of TGF-β1 neutralizing antibody. Whether there were some other mediators derived from BMMCs which also had the potential to induce Tregs is debatable. Metz considered that IL-4 may be related to the suppression function of MC in the immune response [6]. Therefore, IL-4 neutralizing antibody was applied to block the function of IL-4, but there were no significant differences after the application of IL-4 neutralizing antibody.

Although this study did not provide direct evidence for BMMCs as the main source of TGF-β1, it suggests that BMMC-derived TGF-β1 is involved in the regulation of Treg cell generation in vitro. Our experiment concerned mainly the relationship between mast cells and Tregsin vitro. Huang et al. showed that tumour-infiltrating mast cells may promote tumour growth through one way of increasing Treg cells in vivo[23]. Demeclocycline This leads us to conclude that perhaps Tregs can be induced by mast cells in vivo. More studies will be conducted to clarify this phenomenon. In conclusion, our experiments demonstrate that Tregs can be induced by BMMCs in vitro, and secreting TGF-β1 by BMMCs is one of the principal factors for the effect. This finding may provide new evidence that mast cells have the ability to suppress immune responses by way of Treg induction. Furthermore, the study may supply new data for identifying clearly the role of mast cells in immune systems. This work was funded by National Natural Science Foundation of China (no.

Neither the withholding of nor withdrawing from dialysis is eutha

Neither the withholding of nor withdrawing from dialysis is euthanasia. No physician-assisted suicide (PAS) is entirely different to the ceasing of a treatment.

PAS is a positive act done by a patient to cease life and where a physician has assisted in its execution (usually by prescribing medications used in the suicide). The KPT-330 supplier withdrawing of treatment, including dialysis, is an entirely different act where the death, when it results is due to the underlying disease and not due to the action taken by the patient. Lisa Phipps and Robert Walker With variable availability of renal supportive care (RSC) programmes available throughout Australia and New Zealand, there is a need for provision of training in this area to be available to all medical and paramedical staff Online resources may be a potential source of training material for staff and information for patients and families. The possibility of exchange programmes between renal medicine and palliative care should be explored as a way of enhancing education in both fields. The ANZSN and the ANZ Society of Palliative Cobimetinib chemical structure Care both have special interest groups in RSC. The potential for

bringing these two groups together to facilitate cross-specialty training should be explored. The incidence of end-stage kidney disease (ESKD) in Australia and New Zealand is increasing (ANZDATA 2011). Patients with ESKD both on dialysis and conservative care pathways are sicker and more debilitated than in the past.[1] Patients with chronic kidney disease (CKD) and ESKD are amongst the most Tau-protein kinase symptomatic of any chronic disease group.[2, 3] With increasing evidence that patients with multiple co-morbidities may not benefit from dialysis,[4-6] it is essential that nephrologists are trained in the conservative management of ESKD. The current curricula for Australian and New Zealand Nephrology advanced

trainees ( recognizes this under learning objective 2.3.8 ‘plan and manage the non-dialysis pathway’. Manage common ESKD problems – pruritus, fatigue, xerostomia, depression, constipation, insomnia, nausea, vomiting, dyspnoea and pain Adjust drug doses according to reduced GFR Liaise with allied health staff Describe reduced life expectancy to a patient with respect, empathy and dignity. However with only a small number of conservative care clinics in Australia and New Zealand, trainees and nephrologists may receive very limited exposure to symptom control and conservative management. This has been the experience overseas, with a survey of nephrology trainees in the US revealing their training resulted in them feeling least prepared to manage a patient at the end of life.

parvum antigens on dendritic cells, we generated an enriched popu

parvum antigens on dendritic cells, we generated an enriched population of immature DCs by culturing whole BM cells in GM-CSF. We assessed the differentiation status of the loosely adherent cells by day 14. On the day of the BM harvest, <5% of whole BM cells were expressing the myeloid DC markers. By the time the cells were harvested

from the plates, at day 14, >90% of the cells were expressing CD11c and CD11b and a subset expressed other DC markers, such as CD86, CD80, CD40 and MHCII (Figure 1). These unstimulated DCs were then used for subsequent in vitro studies. The same time frame and format was used for the DCs generated from the whole BM Opaganib datasheet of the MyD88 KO mice (data not shown). In order to identify the differentiation/maturation status of the BMDC, we examined the expression levels of DC-SIGN (CD209) as well as CD86, CD80, CD40, MHCI and MHCII as shown in Figure 1. CD86 and CD80 were already high in the unstimulated cells, whereas marked increases were observed with CD40, MHCII and CD209 when DCs were treated with either sporozoites

or cryptosporidial antigen-treated cultures. In order to investigate the role DCs play in eliciting responses to different C. parvum antigen presentation/maturation, we incubated DCs with either freshly excysted intact sporozoites or solubilized sporozoite lysate. We also looked at the responses to several recombinant antigens, such as Cp23, Cp40, Cp17 and P2 (18,22,24). All antigen preparations as well as conditioned media preparations were tested for endotoxin and were below 0·03 EU. Lipopolysaccharide was used as a positive Epigenetics Compound Library molecular weight control and was also tested at different concentrations and yielded consistent results, indicating that MoDCs were biologically active. As shown in Figure 2(a), solubilized sporozoite antigen was able to induce significant increases in the expression of IL-12p70

from DCs as compared to Thymidylate synthase media alone (>200-fold increase), whereas freshly excysted sporozoites induced much lower-level IL-12 responses. In contrast, expression levels of IL-12p70 from DCs isolated from MyD88 KO mice were at or below background levels (Figure 2a, b). Recombinant antigens Cp40 and Cp23 were also able to significantly increase IL-12p70 expression, as observed in Figure 2(b). This finding indicates that the solubilized as well as recombinant antigens can induce the maturation of the DCs and subsequently initiate an innate immune response. Treatment of dendritic cells with cryptosporidial antigens induced increased expression levels of the Th1 cytokine, IL-2 (Figure 3 a, b). Again, significantly reduced expression levels of IL-2 were observed in the BMDCs of MyD88 KO mice in responses to C. parvum antigen, with the exception of LPS that has been shown to induce the maturation of MyD88-deficient dendritic cells (25).

9,15–18 Further studies are needed to increase our understanding

9,15–18 Further studies are needed to increase our understanding of the roles of eosinophils and IL-5 in inflammatory responses and other diseases in which hypereosinophilia occurs. The differential migration of eosinophils versus neutrophils to thyroids of IFN-γ−/− and WT mice during the development of G-EAT offers a unique opportunity to examine the role of eosinophil trafficking to sites of inflammation and to investigate the potential role of these

cells in the induction and resolution of inflammation. Neutralization of IL-5 markedly inhibited migration of eosinophils to thyroids of IFN-γ−/− mice during development of G-EAT. However, IL-5 neutralization had no effect on the severity or rate of resolution of inflammation in G-EAT, suggesting that eosinophil migration has no apparent pathogenic role in G-EAT. WT and IFN-γ−/− DBA/1 mice were produced Everolimus in our animal facilities at the University of Missouri as previously described.6–8 Both male and female mice (6–10 weeks old) were used. G-EAT was induced as previously described.1,5 Briefly, mice were injected intravenously

(i.v.) twice at 10-day intervals with 150 μg of MTg3 and 15 μg of lipopolysaccharide (LPS) (Escherichia coli 011:B4; Sigma Chemical Co., St Louis, MO). Seven days later, donor spleen cells were re-stimulated in vitro selleck products with 25 μg/ml MTg and 5 ng/ml IL-12.1 Cells were harvested after 72 hr and washed twice, and 3·5 × 107 cells were transferred i.v. to 500-Rad irradiated

syngeneic recipients. Anti-IL-5 was purified from culture supernatants of the anti-IL-5-producing hybridoma TRFK-5 (provided by Dr Robert Coffman, DNAX Research Institute, Palo Alto, CA, USA) using protein G. IFN-γ−/− recipients of IFN-γ−/− donor cells were given 300 μg of anti-IL-5 intraperitoneally (i.p.) or rat immunoglobulin G (control IgG) every 4 days beginning on the Rebamipide day of cell transfer until euthanasia. WT recipients of WT donor cells were used for comparison. Thyroids were removed from groups of five or six recipient mice 20 days (peak of disease) or 40–50 days (fibrosis versus resolution) after cell transfer.1–6 Thyroids were fixed in formalin, sectioned and stained with haematoxylin and eosin (H&E), and scored quantitatively for G-EAT severity (the extent of inflammatory cell infiltration and thyroid follicle destruction) using a scale of 1+ to 5+, as described previously.6 1+ thyroiditis is defined as an infiltrate of at least 125 cells in one or several foci; 2+ is 10–20 foci of cellular infiltration involving up to 25% of the gland; 3+ indicates that 25–50% of the gland is infiltrated; 4+ indicates that > 50% of the gland is destroyed by infiltrating inflammatory cells; and 5+ indicates virtually complete destruction of the thyroid with few or no remaining follicles. Thyroid lesions were also evaluated qualitatively.

No serum miRNA was regulated exclusively in aUC compared with iUC

No serum miRNA was regulated exclusively in aUC compared with iUC patients. Four miRNAs were higher and three miRNAs

were lower in the mucosa of aCD than iCD. Two miRNAs were higher and three miRNAs were lower in the mucosa of aUC than iUC. No serum miRNAs coincided with tissue miRNAs in aCD and aUC patients. Our results suggest Decitabine in vivo the existence of specific miRNA expression patterns associated with IBD and their different stages and support the utility of miRNA as possible biomarkers. This pilot study needs to be validated in a large prospective cohort. Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory gastrointestinal disorder, the pathophysiology of which remains unclear. The theory accepted most commonly is that IBD

and the associated gastrointestinal inflammation are likely to be the result of the interaction between a defective immune response to a luminal factor (probably intestinal flora), epigenetic and environmental factors (e.g. smoking) and its influence in genetically predisposed subjects [1-3]. Genetic factors involved in inflammation and immune functions are known to play a very important role in IBD physiopathology. Micro-RNAs (miRNAs) are a class of small non-coding RNAs, involved in the control of gene expression at the post-transcriptional level [4]. Following the discovery of miRNAs, the number of publications regarding their biogenesis and functions has been increasing exponentially and the miRNA sequence database, miRBase, is growing continuously [5, 6].

BVD-523 mouse MiRNAs are involved in the regulation of many biological processes such as the cell cycle, differentiation, Exoribonuclease proliferation, apoptosis, fibrosis and immune function [7]. Emerging evidence has demonstrated that miRNAs can also play an important role in the development of cancer as well as in the induction of chronic inflammatory and autoimmune diseases [8, 9]. miRNAs have been found in tissues, serum, plasma and other body fluids. It has been demonstrated that the levels of miRNAs in serum are stable, reproducible and consistent among individuals of the same species [10]; for this reason, such levels are now being used as a non-invasive biomarker for different pathologies (i.e. cancer, autoimmune disease, inflammation) [10, 11]. Previous studies, focused particularly on cancer, have discovered that circulating miRNA profiles can be correlated with tissue miRNA profiles [12, 13]. In most cases, those changes in circulating miRNA profiles can precede the standard blood biomarkers and possess prognostic value [12, 14, 15]. These properties mean that miRNAs are attractive, blood-based, non-invasive biomarkers. Recently, several papers have focused investigation on the altered expression of miRNAs in IBD and their important role as regulators and possible diagnostic biomarkers in IBD [8, 16-18].

© 2012 Wiley Periodicals, Inc Microsurgery, 2012 “

© 2012 Wiley Periodicals, Inc. Microsurgery, 2012. “
“Pulsed acoustic cellular expression (PACE) is a treatment that applies focused acoustic shock waves to promote tissue healing. The aim of this study was to assess the effect of PACE treatment on inflammatory responses in a cremaster muscle ischemia/reperfusion injury model. Seventeen cremaster muscle flaps were evaluated

in four groups: nonischemic controls (n = 5), 5-hour ischemia controls (n = 4), preischemic (5-hour) PACE conditioning (n = 4), and postischemic (5-hour) PACE conditioning (n = 4). The expression of proinflammatory cytokines (TNFα, IL-6, IL-1α, IL-1β, GM-CSF) and chemokines (CCL3, CCL4, CXCL4) was assessed using TaqMan® real-time PCR. Expression of ELAM-1, VCAM-1, and ICAM-1 was assessed by immunostaining. Preischemic PACE conditioning upregulated expression of IL-6, CCL3, CCL4, and CXCL4, and downregulated expression of TNFα, GM-CSF, and IL-1α. Postischemic PACE conditioning significantly decreased expression of all evaluated genes. Pre- and postischemic PACE conditioning decreased expression of ELAM-1 and ICAM-1. Results of the study indicate

that application Ruxolitinib clinical trial of PACE conditioning may have a beneficial effect on the recovery of tissues subjected to the ischemia/reperfusion injury. Postischemic PACE conditioning revealed anti-inflammatory effect as confirmed by decreased expression of inflammatory cytokines, chemokines, and cell adhesion molecules (ELAM-1 and Rho ICAM-1) that are responsible for leukocyte

recruitment into ischemic tissues. Hence, PACE therapy may be used effectively in clinical practice as a convenient therapeutic strategy to protect tissues against ischemia/reperfusion related injury after microsurgical procedures of free tissue transfers. © 2012 Wiley Periodicals, Inc. Microsurgery, 2013. “
“The reconstruction of complex hand injury such as multifinger soft tissue defect remains a challenging problem. Two cases of repair of multifinger injury with exposed bones using the free chimeric flaps based on the dorsalis pedis vessels are presented. Two male patients, 46 years old and 36 years old, suffered from a thermocompression injury to the dorsum of fingers resulting in soft tissue defects of multiple fingers. The chimeric free flap was designed and applied to cover the defects. The donor sites were covered by skin grafts. The postoperative courses were uneventful. Both patients were followed up for 10–12 months. The maximal flexion angle of the distal interphalangeal, proximal interphalangeal, and metacarpophalangeal joints were 40°–85° at the end of the follow-up. The protective sensation was achieved on the dorsal fingers. The report suggests that the free chimeric flaps based on the dorsalis pedis artery may be an alternative for the reconstruction of the multifinger dorsal soft tissue defects. © 2013 Wiley Periodicals, Inc. Microsurgery 33:660–666, 2013.

For intracellular staining

For intracellular staining LY294002 of GM-CSF, isolated leukocytes were incubated with 50 ng/mL PMA, 500 ng/mL ionomycin, Golgi-Plug (1 μL/mL) containing brefeldin A in RPMI-1640 at 37°C for 4 h. Thereafter,

cells were stained with rat antimouse CD4-FITC, rat antimouse CD45-V450, fixed and permeabilized with Cytofix/Cytoperm (BD), and stained with rat antimouse GM-CSF-PE (BD). Apoptotic and dead CD4+ T cells were detected by staining with 7-AAD and CD4-allophycocyanin. Fas expression on CD4+ T cells was analyzed by staining with hamster antimouse Fas-PE and CD4-FITC. Controls were stained with isotype-matched control antibodies. All antibodies and reagents were obtained from BD Biosciences (Heidelberg, Germany) unless otherwise mentioned. Flow cytometry was performed on a FACScan (BD Biosciences), and the data were analyzed with WinMDI or Cell Quest software. Primary astrocytes Poziotinib clinical trial were isolated from 1- to 2-day-old newborn mice and cultured as published before [43]. To obtain pure astrocytes, cells were harvested from astrocyte cultures and stained with rat antimouse CD11b-PE. Pure astrocytes (CD11b−) were then separated from CD11b+ microglia with a FACSVantage cell sorter (BD). Neuronal cultures were obtained according to Lenz et al. [44]

with slight modifications. Briefly, pregnant female mice were sacrificed by cervical dislocation at gestational day 18.5, and dissociated cells of each embryonic brain were cultivated in flasks coated with poly-L-lysine in Neurobasal medium supplemented with B27 (Invitrogen) and 500 μM L-glutamine (Gibco). The purity of cultures for neurons was ≥98%, as determined by immunofluorescence

staining for Janus kinase (JAK) neuron-specific class III β-tubulin. DNA was isolated from sorted astrocytes and microglia, respectively, as well as from cultured neurons using a DNA isolation kit (Qiagen, Germany). For the detection of FasL expressed on the surface of astrocytes, mixed astrocyte/microglia cultures were stained with mouse antimouse FasL-PE and CD11b-FITC. Controls were stained with isotype-matched control antibodies. For histology on paraffin sections, mice anesthetized with methoxyflurane were perfused with 0.1 M PBS followed by 4% paraformaldehyde in PBS, spinal cords were processed and stained with hemalum and eosin, cresyl violet, and luxol fast blue. In addition, paraffin sections were used for immunohistochemical demonstration of GFAP, neurofilament, Mac3, and CD3 (Serotec, Düsseldorf, Germany) by an ABC protocol as described [45]. Total mRNA was isolated from the spinal cords of nonimmunized and MOG35–55- immunized mice (RNeasy kit, Qiagen, Germany) at day 15 and day 22 p.i., respectively. SuperScript reverse transcriptase kit with oligo (dT) primers (Invitrogen, Germany) was used to generate cDNA from total mRNA.

64±10 87×106 and WT: 31 54±15 52×106 for B220+; Hax1−/−: 3 71±0 7

64±10.87×106 and WT: 31.54±15.52×106 for B220+; Hax1−/−: 3.71±0.77×106 and WT: 2.55±1.05×106 for T1; Hax1−/−: 6.91±3.61×106 and WT: 4.73±2.23×106 for T2; Hax1−/−: 5.89±2.89×106 and WT: 4.53±2.39×106 for mature B cells; Hax1−/−: 2.92±1.84×106 and WT: 2.34±1.16×106 for MZ B cells). Our data clearly demonstrate that Hax1−/− LSK cells in a Hax1+/+ environment were able to fully reconstitute the lethally irradiated hosts. To further investigate the reason for the massive B lymphocyte deficiency, we investigated the expression of CXCR4 and BAFFR on splenic B cells. CXCR4 is expressed on hematopoietic precursors 22 as well as on centroblasts within the germinal centre

18. CXCR4-expressing cells migrate towards CXCL12, expressed by stromal cells and germinal center dark zone compartments. Thus, an impaired CXCR4 expression would severely impede normal B-cell development. Alternatively, signals through the BAFFR have a significant role in promoting B-cell survival and homeostatic proliferation 23. For real time analysis, we isolated total splenocytes of four 10-wk-old WT and Hax1−/− mice and enriched for B lymphocytes using magnetic cell sorting. Both the CXCR4 and the BAFFR DNA Damage inhibitor amplification showed prominent amplification products. Most interestingly, CXCR4 expression

in HAX1-deficient B cells was decreased by around 70% compared to WT cells. BAFFR expression was slightly, but not significantly, decreased in HAX1-deficient B cells (Fig. 7A). However, the decreased expression had no effect on the formation of follicular structures. No differences in the distribution of B- Teicoplanin and T-cell areas, as stained by CD3 and B220, were detectable (Fig. 7B). Because of the fact that the transfer of Hax1−/− bone marrow cells into a HAX1+ environment gave rise to normal levels of B220+ cells and functional B-cell subsets, we conclude that the severely decreased

CXCR4 expression on HAX1-deficient B cells is not solely responsible for the described B-cell loss in Hax−/− mice. Previously, we described HAX1 as interaction partner of membrane bound IgE (mIgE) 24. From that point of view, it would have been of most interest to analyse IgE responses on a Hax1-deficient background. However, the short lifespan of Hax1−/− mice impeded a direct analysis. Therefore, we focused on the detailed investigation of the biological function of HAX1 during lymphocyte development. Hax1−/− mice are characterized by a severely diminished cellularity of lymphoid tissues accompanied by a significant reduction of B and Tlymphocytes. Recently, Chao et al. 25 reported on the role of HAX1 with a similar approach. Our results demonstrate that the developmental impairment is not restricted to specific developmental stages. We observed reduced numbers of B cells from the pro-pre B-cell stage in the bone marrow to mature stages in the spleen. The analysis of splenic subpopulations clearly demonstrated a continuation of the developmental defects for T1 and T2 B cells 26, 27.

044) Group one showed two good, two satisfactory, six moderate,

044). Group one showed two good, two satisfactory, six moderate, and one bad results while the second group showed five good, six satisfactory, one bad and no moderate results (P = 0.026). The first time to show clinical response in group one was the third month while in the second group it was at 1.5 month (P < 0.001). In addition, the first time to show electromyographic response in group one was at the sixth month while in group two it was at the third month Vein wrapping is a simple technique that could be used reliably to augment primary neurorrhaphy particularly in cases with associated vascular or tendon injuries GSK126 to prevent scarring and enhance functional and electrophysiological

recovery. © 2013 Wiley Periodicals, Inc. Microsurgery 34:361–366, 2014. “
“A 19-year-old male patient with type 1 von Willebrand’s disease underwent two separate superficial inferior epigastric artery free flap tissue transfers and three revision procedures for reconstruction of a postextirpative mid-facial

defect. Intravenous 1-desamino-8-D-arginine vasopressin (DDAVP) was administered as bleeding prophylaxis prior to incision for free tissue transfer. For each debulking procedure, DDAVP was administered by intranasal sprays in minutes prior to incision and redosed 12 and 24 hours postoperatively. There were no incidents of either thrombosis or bleeding. This outcome indicates that 0.3 μg/kg intravenous DDAVP may be effective as bleeding prophylaxis for patients with mild and quantitative defects in von Willebrand factor undergoing microvascular reconstruction. © 2011 Wiley-Liss, Inc.

Microsurgery, 2011. “
“Postoperative Selleckchem APO866 vascular compromise is a common but critical complication requiring emergent re-exploration, and remains a chief cause of free flap failure. This study investigated the relationship between postanesthetic shivering (PAS) and the development of postoperative complications associated with free flap reconstruction. One hundred thirty-six patients who underwent head and neck cancer resection selleck and free flap reconstruction were retrospectively enrolled. Fifteen patients were assigned to the PAS group, while the others were assigned to the non-PAS (NPAS) group. The odds ratios of acute re-exploration or total failure of the free flap in the PAS group was 3.5 and 14.9, respectively. The dose of meperidine was positively correlated with PAS prevention in our statistical ROC curve analysis. The minimum effective dose of meperidine for PAS prevention was 0.35 mg/kg with 75% sensitivity and 60% specificity. These findings indicate that an optimal dose of meperidine could prevent PAS, which is shown to be associated with a decrease in the incidence of the early post-surgical re-exploration rate of these free flaps related to circulatory compromise. © 2013 Wiley Periodicals, Inc. Microsurgery 34:106–111, 2014. “
“Several authors have reported the usefulness and benefits of lymphoscintigraphy.