[16, 17] Both anti-gp41 mAbs used in one study[17] were active in

[16, 17] Both anti-gp41 mAbs used in one study[17] were active in ADCC and Fc-dependent inhibition of viral replication in macrophages, though they were non-neutralizing in conventional neutralization assays. Taken together, these two studies strongly support a role of Fc-mediated effector function in the post-infection control of viraemia. They also suggest that the protective effect check details is at a very early step in infection as postulated above. Future studies of a role for Fc-mediated effector function in blocking acquisition and post-infection control would benefit greatly from a better understanding of the effector cells extant at the local site of virus entry, the innate epithelial cell

response to virus, and the impact of non-neutralizing mAbs with potent Fc-mediated effector function on early viral dynamics and escape. Characterization of these variables using the approaches reviewed in references [6, 36, 37] for post-infection control of viraemia mediated by non-neutralizing mAbs, should inform the design of more definitive passive immunization studies

to resolve the controversy of whether Fc-mediated effector function plays a role in the blocking of acquisition. The author thanks Drs Yongjun Guan, Mohammed Sajadi, Roberta Kamin-Lewis, Marzena Pazgier, Robert C. Gallo and Tony DeVico for their support and fruitful discussions leading to the ideas discussed Alectinib in vivo in this review. They are not responsible for errors on the part of the author. The exemplary efforts of the laboratory technical staff

and postdoctoral fellows are greatly appreciated. This manuscript is supported by Grant #OPP1033109 from The Bill and Melinda Gates Foundation and by R01AI087181 from National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD. The author owns stock in Profectus Biosciences, Baltimore, MD. “
“Vibrio vulnificus causes fatal septicemia in susceptible subjects Edoxaban after the ingestion of raw seafood. In the present study, the roles of cyclic adenosine monophosphate (cAMP) receptor protein (CRP) in V. vulnificus pathogenesis were investigated. A mutation in the V. vulnificus crp gene resulted in a significant down-regulation of various virulence phenotypes, except for RtxA1-mediated cytoskeletal rearrangement. Bacterial growth was impeded by the crp mutation. In addition, colony morphology was converted from opaque to translucent type by this mutation, which implies a decrease in capsule production. The crp mutant also showed significant decrease in motility and adhesion to host cells. V. vulnificus CRP positively regulated production of hemolysin and protease at transcriptional level. All these changes in the crp mutant were fully complemented in trans by a plasmid harboring the wild-type gene. In contrast, CRP negatively regulated the expression of RtxA1. The crp mutant caused the cytoskeletal rearrangement in HeLa cells, which is a hallmark activity of RtxA1 toxin.

Subsequent analysis of autoantibody binding to the RLDNRYQPMEPN p

Subsequent analysis of autoantibody binding to the RLDNRYQPMEPN peptide was assessed using a confirmatory enzyme-linked immunosorbent assay format, with six patients displaying significant binding using this method. Antibodies against this epitope, along with four others (aa 393–402, aa 437–446, aa 479–488 and aa 717–726), were reactive to the heavy chain structure of the MPO protein. One epitope, GSASPMELLS (aa 91–100), was within the pro-peptide structure of MPO. B cell epitope prediction algorithms identified all or part of the seven epitopes

defined. These results provide major common human anti-MPO immunodominant antigenic targets which can be used to examine further the potential pathogenic mechanisms for these autoantibodies. PD0332991 order The use of indirect immunofluorescence has identified two major types of anti-neutrophil cytoplasmic antibodies: cytoplasmic ANCA (c-ANCA) and perinuclear ANCA (p-ANCA). The ANCA-associated vasculitides (AAV) vary in clinical presentation, yet all

of them share the same central pathology: inflammation of Mitomycin C vessel walls. AAV are serious diseases with an extremely high mortality rate when left untreated. Since the discovery of ANCAs more than two decades ago, the definite claim of their pathogenic role in the disease process of systemic vasculitis has been confounded by variations not only in the distribution of ANCA-positive individuals in relation to actual disease but also in the inconsistencies they present in terms of disease severity, activity and progression. The primary antigenic target of p-ANCA is the lysosomal enzyme myeloperoxidase

(MPO). Anti-MPO antibodies can be found in a variety of immune-mediated disorders, Teicoplanin including Churg–Strauss syndrome (40–60%), crescentic glomerulonephritis (64%), Wegener’s granulomatosis (24%) and most commonly in microscopic polyangiitis (MPA), wherein these antibodies are detected among 80% of affected individuals [1–3]. Strong evidence also exists from animal experiments showing that p-ANCA directed against MPO can cause vasculitis that resembles human vasculitic disease [4]. Direct pathogenic roles of MPO-ANCA have been demonstrated by their binding to target antigens expressed on the surface of primed neutrophils and monocytes, leading to the induction and release of oxygen metabolites, which trigger vascular injury [5–7]. Knowledge about the target epitopes of autoantibodies can provide valuable insight into the mechanisms that initiate and regulate the autoimmune response. Epitope mapping can identify molecular mimics and elucidate the relationship between an alloantigen and autoimmune disease.

Mechanistically, this could be traced back to Lcn2-mediated chang

Mechanistically, this could be traced back to Lcn2-mediated changes of Erk1/2 signaling. Accordingly, the i.p. injection of Lcn2 into C57BL/6 mice stimulated the mobilization of neutrophils while we found a significantly reduced neutrophil chemotactic activity of cells obtained from Lcn2 KO mice. This observation transmitted to a reduced accumulation of neutrophils in

intra-dermal lesions infected with Salmonella typhimurium in Lcn2 KO mice as compared to WT mice. This was not only due to a reduced chemotaxis but also to an impaired cellular adhesion of neutrophils in the absence of Lcn2. We herein describe a novel role of Lcn2 as an important paracrine chemoattractant and an indispensable factor for neutrophil function JQ1 mouse in inflammation. Tissue infiltration of leukocytes in response to inflammatory or infectious

stimuli BGB324 research buy warrants previous adhesion of leukocytes to endothelial cells and subsequent migration across subendothelial basement membranes. Following cellular damage, epithelial cells produce IL-8 or its murine ortholog keratinocyte chemokine (KC), respectively, which in turn attracts neutrophil granulocytes (PMNs, polymorphonuclear neutrophils) to cross the epithelial barrier to the affected site [1]. As part of their anti-infective armory, PMNs produce and release several antimicrobial peptides and proteolytic enzymes. One of these peptides is the 21 kDa protein neutrophil gelatinase associated lipocalin also called lipocalin-2 (Lcn2) [2]. Lcn2 is stored in so-called secondary granules together with lactoferrin, calprotectin (S100A8/A9), or Mac-1 (CD11b/CD18), which play essential roles for neutrophil effector functions

and migration [3, 4]. Lipocalins are a family of structurally related proteins characterized by eight β-strands that form a β-barrel defining a calyx [3, 5]. Lcn2 is expressed and secreted by immune cells, hepatocytes and renal tubular cells, in which it is involved in different biological functions [3, 6-11]. On the one hand Lcn2 this website acts as an antimicrobial protein, and this function is based on its ability to capture and deplete bacterial siderophores, which are released by certain bacteria as means of iron acquisition [8]. Accordingly, Lcn2 expression is linked to resistance toward infections with gram-negative, siderophore-producing bacteria such as Escherichia coli or Salmonella typhimurium [7, 12-15]. On the other hand Lcn2 can affect iron traffic in cells, which may be partly referred to its interaction with recently identified mammalian siderophores [16, 17]. Additionally, Lcn2 promotes differentiation and structural organization of renal epithelial cells and its expression is induced upon renal cell injury. Accordingly, the administration of Lcn2 positively affected the outcome of mice suffering from experimental renal ischemia [14, 18].

In addition, RNAi of either enzyme induced transient, abnormal ph

In addition, RNAi of either enzyme induced transient, abnormal phenotypes associated with altered movement. The data also suggested that both cathepsin B and L proteases are essential for host (rat) gut penetration and that interference with the function of either of the two enzymes has a severe impact on worm virulence (80). The metacestode Selumetinib clinical trial larval stage of the fox tapeworm Echinococcus multilocularis is the causative agent of alveolar echinococcosis, a serious zoonosis in rodents and

humans (81). Because of its accessibility to in vitro cultivation (82), E. multilocularis has been established as a laboratory model for studying the molecular basis of larval taeniid cestode development and host–parasite interactions.

In this context, it is highly desirable to be able to perform functional genomics studies to investigate the role of defined parasite genes in these processes. The first attempts to establish transfection in Echinococcus were reported by Spiliotis and colleagues (Table 1). A plasmid containing the cyano-fluorescent protein (CFP) under the control of the promoter of the ezrin–radixin–moesin (ERM)-like protein gene (83) was transfected into primary cells using cationic lipid vesicles. Because of the strong autofluorescence of the E. multilocularis cells, the authors were unable to visualize the expression of the reporter gene CFP, but Selleckchem KPT330 the reporter protein could be detected by Western blot several days after transfection (84). In this publication, the use of Listeria monocytogenes as a transfection vehicle was also explored as suicide strains of this facultative intracellular bacterium have already DNA ligase been used to deliver foreign DNA into host cells (85). Here, E. multilocularis metacestode tissue was incubated with L. monocytogenes carrying a plasmid for the expression of GFP after which primary cells were isolated and cultured for several days. The authors were able to detect fluorescent bacteria

close to the nuclei of primary cells, indicating an intracellular location of L. monocytogenes, but have not yet been able to achieve transfer of foreign DNA into Echinococcus cells using this method. Recently, RNAi (Table 2) was also applied successfully in E. multilocularis (86). To establish whether a functioning RNAi pathway is present in Echinococcus, the authors scanned the available E. multilocularis genomic sequences for the presence of dicer and argonaute orthologs. RT-PCR analysis established that both genes were expressed in E. multilocularis primary cell cultures. Subsequent exposure to siRNA facilitated by electroporation, targeting emgapdh, em14-3-3 and ERM-like protein resulted in efficient knock-down to 10–30% of the original transcript levels which remained down-regulated for at least two weeks. This was confirmed by Western blot analysis where levels of the respective proteins were shown to be down-regulated between 70% and 90%.

43 RFM also enhances the production of NO, which might be respons

43 RFM also enhances the production of NO, which might be responsible for parasite killing.44 This was a comprehensive study carried out to investigate the abundance of localized and circulating cytokines in patients with CL caused by L. tropica. Furthermore, the study carried out a comparative assessment of different treatment regimens on the

host immune response, which will help to explore the action of chemotherapy. The higher production of IL-8 in CL patients, leading to excessive inflammatory cell activation, predominantly PMNs that provide shelter to parasites, may allow the parasite to survive and multiply, leading to the development of disease. The observation of high levels of NO and MCP-1 following treatment suggests that MCP-1 orchestrates the induction of leishmanicidal activities in human macrophages Cabozantinib via the generation

of NO. Financial assistance by the Indian Council of Medical Research is gratefully acknowledged. None of the authors of this paper have conflict of interest to disclose. “
“Natural killer (NK) cells are important components of the innate immune system that mediate effector and regulatory functions. As effector cells, NK cells help control virus-infected cells through cell-mediated antibody-dependent mechanisms such as antibody-dependent cellular cytotoxicity (ADCC). Although macaques are an important and reliable

animal model for the study of retrovirus-induced human diseases, and despite the crucial role played by NK cells in innate MK-2206 cell line and adaptive immune responses against simian immunodeficiency virus (SIV), only a few studies have attempted to characterize different macaque NK cell subpopulations. In the present study, we identified a subpopulation of circulatory CD8α− macaque NK cells that express NK lineage markers and exhibit cytotoxic potential. CD8α− NK cells were phenotypically characterized as CD3− CD14− CD20− CD8α− cells ID-8 that express NK cell markers including CD16, CD56, granzyme B, perforin, NKG2D and KIR2D. Based on their CD56/CD16 expression patterns, cells within the CD8α− gate can be divided into four subpopulations: CD56dim CD16bright, CD56dim CD16−, CD56bright CD16−, and CD56− CD16− cells. In contrast, CD8α+ NK cells are 95% CD56dim CD16bright, which correlates with their high cytotoxic potential. Upon interleukin-15 activation, CD8α− cells up-regulated CD69 expression and produced low levels of interferon-γ and tumour necrosis factor-α. Sorted CD8α− NK cells were capable of killing MHC-I-devoid target cells and mediated ADCC responses against SIV gp120-coated target cells in the presence of macaque anti-gp120 antibodies.

Mechanisms by which signals from outside the CNS can alter microg

Mechanisms by which signals from outside the CNS can alter microglial activation are also discussed. The authors describe animal studies indicating click here that age-related changes in microglia cause impairment of neurogenesis and neuronal plasticity together with associated

cognitive deficits. Importantly, when considering extrapolation towards therapy in humans, reversing the neuroinflammation has functional benefits. The information in this review provides an important basis with which to understand how the ageing brain reacts to superimposed neurodegenerative pathology, the effects of systemic inflammation and reactions to brain injury. Since the observations of Corsellis and Bruton in the 1970s documenting neurodegenerative pathology in the brains of boxers suffering from dementia pugilistica, there have been intriguing hints linking traumatic brain

injury and subsequent long-term progressive neurodegeneration. There has recently been a resurgence of interest in this field, which has come in particular from North America, concerning repeated head injuries sustained as a result of sporting activities such as ice hockey and football and their associated long-term effects (chronic traumatic encephalopathy). The review by Bioactive Compound Library cost Colin Smith of the effects of traumatic brain injury, both single and repetitive, on microglial activation and neurodegeneration, is therefore particularly timely. He develops the argument that microglial activation as a response to

injury in the short tem is beneficial, removing cell debris and promoting tissue repair. However, if the activated state of microglia is not subsequently down-regulated, it may become self-perpetuating and lead to chronic neurodegeneration associated with accumulation of neurodegeneration-related proteins such as tau, amyloid-β and TDP-43. Stephen Gentleman considers in detail the relationship between accumulation of different neurodegeneration-associated proteins in the CNS and microglial activation: are they simply reacting to the pathology, mafosfamide are they instrumental in the pathogenesis of neurodegenerative disease, or both? He compares and contrasts our current knowledge of the contribution of microglia in a disorder with extracellular aggregation of protein (AD) and those with intracellular protein aggregations (amyotrophic lateral sclerosis and Parkinson’s disease). Clive Holmes considers the evidence that inflammation in the CNS cannot be considered in isolation from inflammation occurring elsewhere in the body (that is, systemic or peripheral inflammation). Information from clinical and preclinical studies shows that peripheral inflammation due to infection or other causes including rheumatoid arthritis, diabetes and atherosclerosis, has an effect on cognitive function both acutely and in the long term.

V S), and

the Netherlands Organization for Scientific Res

V.S), and

the Netherlands Organization for Scientific Research (NWO-ALW to A.V.S). The authors thank: Carmel Daunt and Mariam Sofi for technical assistance; Errin Johnson (Sir William Dunn School of Pathology, University of Oxford) for scanning EM, Josh Lorimer, Aaron Moldrich, and Gabriela Panoschi for animal care; David Vremec and Ken Shortman for the gift of antibodies, staff of Monash Micro Imaging for assistance with in vivo DC imaging experiments, Gabrielle Belz for the gift of OT-I Ly5.1 mice, and Drs Michel Nussenzweig and Wolfgang Weninger for the gift of CD11c-YFP mice. The authors declare no financial or commercial conflict of interest. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such Selleckchem Acalabrutinib materials are peer reviewed and may be re-organized for online delivery, but are not copy-edited or typeset. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors. Figure S1. Splenocyte distribution is normal in both naïve and immunized CD37−/−mice. FACS analyses of the major splenocyte and T lymphocyte populations in WT and CD37−/− mice that were (A) naïve, (B) 10 days post-immunization and (C) 14 days post-immunization with B16-OVA. The frequencies of NK cells (CD3−NK1.1+),

T-cells (CD3+), B cells (CD19+), DC (CD11c+MHC-II+), Granulocytes (F4/80−Gr1+) and Macrophages learn more (F4/80+CD11c−) are expressed as a percentage relative Amino acid to the total

number of viable cells (left axis). The frequencies of T-cell subpopulations including NKT (CD3+NK1.1+), Th (CD3+CD4+), Tc (CD3+CD8+) and T regulatory (CD3+Foxp3+) cells are expressed as a percentage relative to the total number of viable CD3+ T-cells (right axis). Histogram bars represent the mean frequency of the given population +/-SD and significance tested via ANOVA (n = 3–4 mice/group). Figure S2. The Th1-polarizing cytokine IL-12p70 is secreted at normal levels by CD37−/-DC. Purified naïve splenic DC were pooled from four mice/group and cultured with either media alone, 10 ng/mL CpG peptide or 1 ng/mL LPS. All conditions were supplemented with GM-CSF, IL-4 and IFNy. After 24 hours, IL-6, TNFa, IL-10 and IL-12p70 secretion was quantified in supernatants via flow cytometric bead array. Histogram bars represent the average cytokine concentration from three independent experiments + SEM and significance tested via ANOVA (n = 3 experiments/group). (B) BMDC maturation was assessed by flow cytometric analysis of surface CD80, CD86 and MHC Class II upregulation post LPS activation (1 ng/mL). “
“The establishment of immune tolerance and prevention of chronic rejection remain major goals in clinical transplantation. In bone marrow (BM) transplantation, T cells and NK cells play important roles for graft rejection. In addition, graft-versus-host-disease (GVHD) remains a major obstacle for BM transplantation.

However, the statistically significant difference in mean virus l

However, the statistically significant difference in mean virus loads between the PBS- and ChAdV68.GagB-immunized mice was not maintained following the Bonferroni adjustment for multiple comparisons (Fig. 2D); this was Hydroxychloroquine nmr mainly due to the PBS-treated mouse variation in virus loads. In particular, rChAdV-68 showed a superior trend as a stand-alone vector relative to the other two tested vectors. Although a single immunization with ChAdV68.GagB protected against EcoHIV/NDK challenge, it is likely that in a more rigorous and relevant human system, a heterologous prime-boost regimen will be required for achieving protective efficacy against HIV-1. Therefore,

immunogenic and protective synergies among the ChAdV68.GagB Palbociclib ic50 (C), MVA.GagB (M), and pTH.GagB DNA (D) vaccines

were explored. BALB/c mice were vaccinated using DDM, DDC, CM, or MC regimens and approximately 2 weeks later, the animals were bled and challenged with EcoHIV/NDK as depicted in Figure 3A. In the pooled blood prior to challenge, the dual regimens elicited polyfunctional, AMQ-specific CD8+ T cells, of which total IFN-γ-producing cells reached 20.1, 15.9, 19.2, and 17.9% of the total CD8+ cells (Fig. 3B). Responses detected in the spleen collected 5 days after the challenge were decreased compared with the prechallenge PBMCs (Fig. 3C), which may be a reflection of the inability of the challenge virus to replicate vigorously in mouse cells. Quantification of the EcoHIV/NDK DNA in the splenocytes showed respective 5.0-, 6.3-, 7.0-, and 6.0-fold decreases in the virus load mean for the DDM, DDC, CM, or MC regimens, however, again statistical significance of any pairwise comparison was annulled by Bonferroni adjustment (Fig. 3C). Thus, dual heterologous regimens elicited higher frequencies of AMQ-specific T cells over a single ChAdV68.GagB vaccine administration and resulted

in a trend of increased fold reduction in virus load by ChAdV68.GagB aided by heterologous prime or boost compared with ChAdV68.GagB vaccination alone with the caveat that Cediranib (AZD2171) it may have been easier to control lower viremia in Figure 3D compared with Figure 2D. We are currently evaluating in phase I/IIa clinic trial triple regimens of DDDCM and DDDMC using recombinant ChAdV-63 [38] as the simian adenovirus vector. Therefore here, we also tested triple regimens of DCM and DMC in the mouse EcoHIV/NDK challenge model. Thus, larger groups of BALB/c mice were vaccinated using the two schedules depicted in Figure 4A. The first set of animals from each group was bled and challenged at peak responses 17 days after the vaccinations. Polyfunctional, AMQ-specific cells were induced in the PBMCs, of which the IFN-γ+-cell frequencies reached 29.6 and 30.1% of total CD8+ cells for the DCM and DMC regimens, respectively (Fig. 4B), and decreased at least in the spleen after challenge (Fig. 4C). In both groups of mice after challenge, lower than 0.

Furthermore, LCMV infection in vivo or LCMV-infected DCs in vitro

Furthermore, LCMV infection in vivo or LCMV-infected DCs in vitro rendered, via TLR2, CD4+CD25+ Tregs capable of diminishing T1D. We identify novel mechanisms by which TLR2 promotes immunoregulation and controls autoimmune diabetes in naïve or infected hosts. This work should help understand T1D etiology and develop novel immune-based therapeutic

interventions. Type 1 diabetes (T1D) is a genetic disease resulting in the destruction of insulin-producing β cells by autoreactive T cells in the pancreatic islets of Langerhans IBET762 1. The importance of additional environmental factors such as infections in the development of this disease has long been reported, but to date whether and how these might trigger or prevent T1D is not understood 2. It has been proposed that the inflammatory events induced upon anti-infectious immunity enable enhanced presentation of β-cell antigens to autoreactive T cells. Pro-inflammatory https://www.selleckchem.com/products/pirfenidone.html cytokines cause the up-regulation of class I MHC molecules on β cells, and may thereby “unmask” them for recognition by CD8+ T cells 3. In addition, concomitant damage to β cells and activation of APCs by the infection may promote the presentation of β-cell antigens to CD8+ T cells. This has notably been demonstrated in NOD mice using Coxsackievirus B4 4, or in RIP-LCMV mice, which transgenically

express lymphocytic choriomeningitis virus (LCMV) antigens on their β cells and develop autoimmune diabetes following LCMV infection 5–7. Inflammatory signals not only promote DC and T-cell activation but might also directly cause β-cell destruction 8–10, therefore strongly contributing to T1D development. On the other hand, studies in humans and mice suggest that infections and inflammation might play a protective role in T1D; notably, disease can be prevented in

NOD mice by infection with a number of viruses 2. Antiviral immunity may increase resistance to diabetogenic infections or “distract” the immune system from their detrimental effect 11. In addition, Nitroxoline as we reported recently 12, viral infections may shape the immune system such that diabetogenic T cells are impaired or kept under control by immunoregulatory mechanisms. We found that viral infection triggered the expansion of invigorated CD4+CD25+ Tregs that produced TGF-β and protected from autoimmune diabetes by synergizing with programmed death-ligand 1 (PD-L1). These findings indicated a beneficial role of virally induced inflammation in T1D. A number of studies in mice have underscored the capacity of pro-inflammatory agents to prevent rather than induce T1D when intervening in the absence of β-cell damage and autoantigen 13. TLRs are usually referred to as “danger-sensing” molecules that play a central part in triggering inflammation and immunity in response to infection 14.

We took the patient back to the operating room on postoperative d

We took the patient back to the operating room on postoperative day number 5 for successful reconstruction with simultaneous fibula and ALF flaps. The microvascular surgeon must always be poised to rapidly

address intraoperative complications that may critically compromise the success of the free flap or, more seriously, jeopardize the patient’s life. © 2012 Wiley Periodicals, Inc. Microsurgery, 2013. “
“Vascularized composite allotransplantation (VCA) has become a clinical reality, prompting research aimed at improving the risk-benefit ratio of such transplants. Here, we report our experience with a gracilis myocutaneous RG-7388 free flap in Massachusetts General Hospital miniature swine as a preclinical VCA model. Fourteen animals underwent free transfer of a gracilis myocutaneous flap comprised of the gracilis muscle and overlying

skin, www.selleckchem.com/products/pifithrin-alpha.html each tissue supplied by independent branches of the femoral vessels. End-to-end anastomoses were performed to the common carotid artery and internal jugular vein, or to the femoral vessels of the recipients. Thirteen of fourteen flaps were successful. A single flap was lost due to compromise of venous outflow. This model allows transplantation of a substantial volume of skin, subcutaneous tissue, and muscle. The anatomy is reliable and easily identified and harvest incurs minimal donor morbidity. We find this gracilis myocutaneous flap an excellent pre-clinical model for the study of vascularized composite allotransplantation. © 2012 Wiley Periodicals, Inc. Microsurgery 2013. “
“The purpose was to investigate the effects of local tetanus toxin (TeTx) application on sciatic nerve regeneration following a rat model of transection injury. After both sciatic nerves were transected and repaired with three epineural sutures, 12 male

Wistar albino rats were divided into two groups. 0.25 ml (2.5 flocculation units) TeTx was injected into Clomifene a piece of absorbable gelatin sponge in TeTx group. In controls, 0.25 ml saline injected. Assessments were performed by using climbing degrees, compound muscle action potentials (CMAPs) and histological parameters (axon number and axonal diameter) 12th week. CMAPs amplitudes were 11.6 ± 4.7 mV and 1.4 ± 1.3 mV in gastrocnemius and interdigital muscles in TeTx group (5.8 ± 2.4 mV and 0.2 ± 0.1 mV, P < 0.05). Climbing degrees were significantly different (61.6 ± 1.7 vs. 38.3 ± 2.6, P < 0.05). Total axon numbers were higher (1341.1 ± 57.3 vs. 877.5 ± 34.9, P < 0.05) and the mean axon diameter was smaller (4.2 ± 2.1 vs. 2.5 ± 1.9, P < 0.05) in the TeTx group. This preliminary study firstly demonstrated the effectiveness of TeTx on nerve repair in experimental sciatic rat model based on functional, electromyographic and histological parameters. © 2014 Wiley Periodicals, Inc. Microsurgery 34:384–389, 2014. "
“Background: Microvascular anastomotic coupling devices have been available to microsurgeons for over 20 years.