The culture was diluted 1:100 into fresh broth and then shaken at 37°C until the late logarithmic growth phase. To produce agar medium, LB broth was solidified by adding 1.5% (wt/vol) agar (Nacalai Tesque, Kyoto, Japan). Specific pathogen-free female C57BL/6 mice were purchased from Japan SLC (Shizuoka, Japan). All experimental mice were 8–10 weeks old. The animals were housed under specific pathogen-free conditions in a small level two animal containment facility and given Hydroxychloroquine purchase free access to sterile water and certified mouse chow. All experiments were carried out in accordance with the guidelines for the care and use of laboratory animals

of Osaka University of Pharmaceutical Sciences. Acinetobacter baumannii was grown until the late logarithmic growth phase, centrifuged at 3,500 ×g for 10 min, resuspended and diluted appropriately in PBS, and used immediately. Mice were anesthetized and i.n. inoculated with approximately

107 or 108 CFU A. baumannii in 50 μL PBS. The actual Selleckchem NVP-BKM120 inoculum concentrations were determined by plating 10-fold serial dilutions onto LB ager plates. Clinical signs were monitored and scored as follows: 0, no abnormal clinical signs; 1, ruffled fur and moving slowly; 2, ruffled fur, hunched posture, and moving very slowly; 3, hunched posture, moving very slowly, and squeezed eyes; 4, dead. Pulmonary lobes were harvested at the indicated time points and fixed in 10% neutral buffered formalin, which was then replaced by a sucrose solution. The lungs were then embedded in OTC (Tissue-Tec; Miles Inc., Elkhart, IN, USA) and frozen at −80°C. The tissue segments were sectioned (6 μm) on a cryostat and stained with hematoxylin and eosin (H & E). Acinetobacter baumannii-inoculated mice were killed and lungs and spleen were removed. Each tissue was homogenized with PBS in a loose glass homogenizer. Cell suspensions were plated on LB agar plates and cultured at 37°C for

12 hrs. Anti-M-CSFR (AFS98) was a gift from Dr S. I. Nishikawa (RIKEN, Kobe, Japan) (21). Anti-Gr1 (RB6–8C5) and anti-NK1.1 (PK136) were provided by the Cell Resource Center for Biomedical Research Institute of Development, MTMR9 Aging and Cancer Tohoku University. Anti-CD11b (M1/70), CD45 (30-F11), CD3 (145–2C11) and CD49 (DX5) were purchased from BD Pharmingen (San Jose, CA, USA). To deplete neutrophils, NK/NKT cells, and macrophages, mice were injected i.p. with 250 μg anti-mouse monoclonal antibodies, RB6–8C5, PK136, and AFS98 (23–25), respectively, on Days 5, 3, and 1 before and Days 1 and 3 post-inoculation with A. baumannii. Pulmonary lobes were removed, minced in Hanks’ Balanced Salt Solution (HBSS; Invitrogen, Carlsbad, CA, USA) and incubated with 150 U/mL collagenase (Sigma, St Louis, MO, USA) and 0.1 mg/mL DNase I (Wako Pure Chemicals, Osaka, Japan) for 30 min at 37°C. Spleens were homogenized in PBS using a loose glass homogenizer, centrifuged for 5 min, resuspended in PBS, and passed through nylon mesh (70 μm).

In INCB024360 chemical structure the urinary continence system, urethral closure pressure for prohibiting the release of urine is produced by the urethral sphincter,

which is composed of both striated and smooth muscle cells. Recently, transurethral transplantation of stem cells derived from muscle satellite cells29–33 or adipose-derived mesenchymal cells34–36 have been widely investigated for the potential to regenerate urethral sphincters. These novel therapies have been performed in some hospitals, and the results have been similar to those with bulking agents alone. However, there is little evidence to indicate that the transplanted cells actually reconstruct muscle tissue necessary for the recovery of functional urethral sphincters. Our strategy to regenerate urethral sphincters that will inhibit urine leakage depends upon the use of autologous bone marrow-derived cells. These cells are capable of differentiating

both in vitro and in vivo along multiple pathways that include striated and smooth muscle37 as well as bone, cartilage, adipose, neural cells, tendon, and connective tissue.38–40 As secondary effects, bone marrow-derived cells can produce cytokines and growth factors that accelerate healing in damaged tissues and inhibit apoptosis and the development of fibrosis.41–46 Previously, we showed that bone marrow-derived cells of wild type mice, when implanted into freeze-injured urinary bladders of nude mice where most of the smooth muscle is lost, differentiate into smooth muscle cells.1 Contributing to the success of these experiments that used allogenically transplanted cells was the absence of an immune response in the nude Pexidartinib cell line mice. In the translation of these developing technologies to clinical therapy, the use of autologous cells are superior to allogenic cells because the autologous cells are not burdened with immunological rejection or ethics problems. In this review, we show that the implantation of autologous bone marrow-derived cells can regenerate Inositol monophosphatase 1 functional urethral sphincters

in a rabbit post-surgical ISD-related urinary incontinence-like model. We have considered many sources of cells from which to derive adult somatic stem cells that could regenerate urethral sphincters. Based on the literature, three sources seem to offer the greatest likelihood of success: muscle-derive satellite cells, adipose-derived mesenchymal cells, and bone marrow-derived cells. Among these, bone marrow-derived cells are the easiest to culture in terms of growth, capacity of differentiation, and production of cytokines and growth factors. These characteristics of bone marrow-derived cells have been demonstrated by many laboratory and clinical studies. However, an important consideration is the operation to harvest the bone marrow cells. This procedure is generally considered to have higher patient risks compared to harvesting muscle- and adipose-derived cells.

Intracranial localization is very rare and only a few cases have been reported. This report intends to present the clinical, radiological and pathological pictures of a primary central nervous system angiosarcoma along with a review of the literature. A 35-year-old woman presented at our institution with weakness and sensory disturbances of her

right hand. Neuroimaging revealed a roughly round, hemorrhagic and moderately enhancing lesion in the left frontal posterior region. The tumor was totally removed under awake anesthesia and continuous monitoring of motor and language functions. Histopathology revealed selleck chemical an epithelioid angiosarcoma. Radical removal, followed by adjuvant radiotherapy and chemotherapy, is able to completely control the disease for a relatively long period. “
“We studied one frontal lobe tumor and multiple spinal cord tumors (one in an extramedullary location) that had been resected from a 24-year-old man. The frontal lobe tumor was well demarcated and non-infiltrating, and consisted of eosinophilic, elongated fibrillary cells arranged in a fascicular pattern. A similar histology was reproduced

in the spinal cord tumors, with additional areas showing standard features of ependymoma. Immunohistochemical and ultrastructural observations revealed that all the tumors were ependymal in nature with positivity for GFAP and epithelial membrane antigen and negativity for oligodendrocyte transcription factor 2, showing intra- and intercellular microrosettes, leading us to a diagnosis of tanycytic ependymoma for the frontal lobe tumor and tanycytic ependymoma Rapamycin mw with ordinary ependymomatous component for the spinal cord tumors. The spinal extramedullary tumor was a schwannoma. Importantly, selleck chemicals llc a heterozygous truncating mutation in the NF2 gene was identified in the blood lymphocytes from the patient. It is known that multiple nervous system tumors can occur in neurofibromatosis type 2 (NF2), which is caused by mutation in the NF2 gene, and that

occurrence of ependymoma, including the tanycytic variant, can be associated with this genetic condition. The present case provides further information about the clinicopathology of tanycytic ependymoma with details of the immunohistochemical, ultrastructural and genetic features. “
“Chordoid glioma is a rare, slowly growing tumor of the CNS, which is always located in the third ventricle of adults. Chordoid glioma has classic histological features consisting of clusters and cords of epithelioid tumor cells embedded within a mucinous stroma with rich lymphoplasmacytic infiltrate. The important distinctive immunohistochemical feature of this neoplasm is strong and diffuse reactivity for GFAP. Here, we report four cases of chordoid glioma that occupied the anterior portion of the third ventricle or suprasellar region. These four cases were all adult females with almost typical clinical, radiological, histologic and immunohistochemical characteristics of chordoid glioma.

In NOD mice, establishment of tolerance to insulin can lead to CAL 101 prevention of diabetes [95,100,101] as well as remission of established disease [93]. Importantly, CD8+ and CD4+ T cell responses to insulin have also been reported in type 1 diabetes patients [91,94,96,99,102]. Furthermore, in humans, the non-MHC locus that confers

the strongest susceptibility to type 1 diabetes is the insulin gene variable number of tandem repeats (VNTR) regulatory region [104], and disease-associated alleles are correlated with reduced thymic expression of the insulin gene [105]. We are exploring the feasibility of DEC-205-mediated delivery of the entire preproinsulin molecule, rather than only the known epitopes targeted by effector T cells. This strategy

should facilitate translation to patients expressing diverse MHC molecules. In addition, the epitopes recognized by insulin-specific regulatory T cells are largely uncharacterized and could differ from those targeted by pathogenic effector T cells [106]. The finding that DC-expanded Tregs of a single specificity can both prevent and reverse type 1 diabetes in NOD mice [23,90] provides critical support for this approach. We found that peptide-linked anti-DEC-205 could induce tolerance even in NOD mice with ongoing islet inflammation [69]. However, when contemplating the translation of such a strategy to humans, there is a concern that antigen delivery to DCs in the context of an inflammatory environment could lead to exacerbation of a pathogenic autoimmune response rather than tolerance induction. One potential remedy to

Y-27632 supplier be considered is the simultaneous use of siRNA specific for co-stimulatory molecules which could be targeted to the DCs in vivo through either DEC-205 or another DC receptor. In vivo siRNA delivery, although difficult to achieve, has been conducted through cell surface receptors by other groups [107–110]. Another possible strategy would be to use microsphere carriers of anti-sense oligonucleotides that can down-modulate co-stimulatory molecules on DCs in vivo[111]. DC-based therapeutics for type 1 diabetes should be considered at all stages Selleck Baf-A1 of the disease, including prediabetes, new-onset diabetes and the setting of islet transplantation. In general, it has been easier to prevent diabetes in the NOD mouse model than it has been to reverse it [112]. For this and other reasons, it has been argued that prevention should be the goal [106]. However, given the more favourable risk to benefit ratio represented by new-onset diabetes patients, it may be easier to conduct clinical trials in such individuals, and there are examples of successful reversal of type 1 diabetes in NOD mice (e.g. by transfer of DC-expanded Tregs[90] or in vivo delivery of anti-sense oligonucleotides for CD80, CD86 and CD40 [111]).

The primary end-point was Hb change between baseline and the evaluation period (weeks 29–33), with a non-inferiority margin of −0.5 g/dL.

Three hundred and fifty-five subjects received ≥1 dose of DA. Mean (95% confidence interval [CI]) change in Hb between baseline and the evaluation period was 2.16 (1.98–2.33) g/dL for the Q2W group and 1.97 (1.80–2.14) g/dL for the QM group, the mean (95% CI) difference in Hb change being −0.19 (−0.43 to 0.05) g/dL. Most subjects (97.9% Q2W; 98.1% QM) achieved a Hb level ≥10.0 g/dL and ≥1.0 g/dL increase in Hb from baseline. Mean DA (SD) weekly equivalent doses over the evaluation period were 0.20 (0.23) and 0.27 (0.31) μg/kg per week for the Q2W and QM groups, respectively. Safety profiles were similar between groups. In subjects INCB024360 price with CKD-ND, QM dosing was non-inferior to Q2W dosing for anaemia correction and had a similar safety profile. “
“Horseshoe kidney is the most common congenital renal fusion anomaly.

Immunoglobulin A nephropathy is a common glomerulonephritis worldwide. However, the co-occurrence of these diseases had not been reported in the literature. We report the first two cases with the occurrence of immunoglobulin A nephropathy in horseshoe kidney. The first case was a 26-year-old male with hypertension and proteinuria (1.4 g/24 h), his pathological finding was primary immunoglobulin A nephropathy. The second case was a 15-year-old female who presented with recurrent peliosis on bilateral lower extremities, haematuria and proteinuria (1.7 g/24 h). Her renal biopsy finding was Henoch–Schonlein purpura nephritis (secondary immunoglobulin A nephropathy). In both cases, STA-9090 renal biopsy was performed by experienced doctors under ultrasonic guidance at the renal upper pole and no postoperative complications were observed. After they were treated based on the renal pathological findings for 6 months, urine eltoprazine protein

excretion decreased significantly and blood pressure and serum creatinine stabilized. It is possible that immunoglobulin A nephropathy occurs in a horseshoe kidney patient. Renal biopsy may be valuable and viable for horseshoe kidney patients with heavy proteinuria to identify pathologic type of glomerulopathy and to guide treatment, if renal biopsy is performed by experienced doctors at the renal upper pole under renal ultrasonic guidance. Horseshoe kidney (HSK) is the most common congenital renal fusion anomaly.[1] Immunoglobulin A (IgA) nephropathy is the most common glomerulonephritis worldwide.[2] However, the co-occurrence of HSK and IgA nephropathy had not been reported in the literature. Patients with HSK are predisposed to many complications, including urinary infection, renal calculus, ureteropelvic junction obstruction and a variety of benign and malignant tumors;[3] moreover, it is also common that HSK is combined with heavy proteinuria. Blood supply is aberrant in approximately two-thirds of patients with HSK, including accessory renal arteries.

Three pools were made to avoid excessive relative dilution of individual peptides. Pool #1 additionally included the matrix protein epitope GILGFVFTL (a human but not a murine epitope). A single large pool of listeriolysin peptides (15-mers overlapping by 11) was the kind gift Selleck AZD2014 of Cerus Corporation (Concord, CA, USA). The study was reviewed and supervised by a local institutional review board (Massachusetts General

Hospital) and Biosafety Committee (Harvard Medical School Committee on Microbiological Safety). The study was also reviewed and approved by the NIH/NIAID Prevention Science Review Committee, an independent Data Safety Monitoring Board (DSMB) (three physicians with expertise in listeriosis, clinical trials and enteric infections), an NIH physician medical monitor, and the US Food and Drug Administration (FDA, BB IND #12760). All of these groups appreciated the goals of the study to be the further evaluation of safety and physiological and immunological responses to listerial vectors, and Y-27632 cost not as a prelude to the development of a new influenza vaccine, and found it ethically acceptable. All subjects provided written informed consent to participate. Healthy men and women, aged 18–45 years old, were recruited by advertising and

underwent a complete screening physical exam and standard laboratory procedures, as described previously (9). Potential volunteers must have previously tolerated a course

of therapy with penicillin or ampicillin. In addition to standard clinical screening laboratories, volunteers were required to have normal iron studies, normal liver function tests, and a pre-study stool sample that was negative BCKDHA for routine enteric pathogens, ova and parasites, as well as L. monocytogenes. Subjects were not HLA haplotyped, as this would have been prohibitively limiting and expensive. Subjects were also not screened in any way for previous exposure to L. monocytogenes or for previous influenza exposure, expecting that most would have been previously exposed, especially to influenza. L. monocytogenes are ubiquitous organisms, despite best food safety efforts. It was hypothesized that existing immunity to influenza or listerial antigens might be “boosted” by this oral vaccination. Frozen inocula (0.9% w/v saline with 20% glycerol, 1.3 mL/vial) were produced utilizing good manufacturing practices by contract with the Walter Reed Army Institute of Research Pilot Bioproduction Facility (Silver Spring, MD, USA), a requirement of the funder. Vials were thawed at 4°C for 15 min and diluted with 0.9% saline for administration to volunteers in 30 mL. Based on spread plate cultures prior to freezing and multiple assessments of thawed vials, each inoculation of a given number of live colony forming units (CFU) also contained approximately two-fold greater dead organisms, or residual thereof.

Chaplains were well used in some services. Participants had received no pre and little in-service training or education in spiritual care. Suggestions for improvements included in-service

training, better utilization of chaplaincy services and training in advance care Enzalutamide mouse planning. Most participants indicated they would attempt to provide some form of spiritual care, either directly or by referring the patient to appropriate services. However, participants generally demonstrated a lack of confidence in addressing a patient’s spiritual needs. “
“Rodent models of renal physiology and pathology are crucial to our understanding of the molecular, histological and functional sequelae that contribute to kidney diseases. One of the most important measures of renal function is glomerular filtration rate (GFR). Whilst the accurate determination of GFR is pivotal to understanding the progression of disease and/or the benefits of treatment strategies, LY294002 clinical trial in rodents the conventional methods for assessment of GFR are inconvenient and cumbersome, not the least because they involve stress and often, anaesthesia.

The legitimacy of assay-based assessment of plasma and urine markers of GFR in mice has also been heavily scrutinized for their insensitivity to minor declines in GFR and inaccurate detection of renal biomarkers. Whilst infusion-based clearance methods of GFR assessment are thus the gold standard in terms of accuracy, they are limited by the fact that they are primarily non-recovery procedures. This presents Tolmetin a dilemma when trying to document the progression

of renal disease, as these measures cannot be taken in the same experimental subject. Here we review a technique of transcutaneous measurement of FITC-sinistrin to calculate GFR in small rodents, using a Non-Invasive Clearance Device (NIC-Kidney Device). This is a recently validated non-invasive technique for measuring GFR in small rodents that allows for the real time measurement of GFR in conscious animals, without the need for plasma and urine assays. “
“Background:  Vascular calcification (VC) contributes to cardiovascular disease in haemodialysis (HD) patients. Few controlled studies have addressed interventions to reduce VC but non-calcium-based phosphate binders may be beneficial. No published randomized study to date has assessed the effect of lanthanum carbonate (LC) on VC progression. Methods:  We conducted a pilot randomized controlled trial to determine the effect of LC on VC. Forty-five HD patients were randomized to either LC or calcium carbonate (CC). Primary outcome was change in aortic VC after 18 months. Secondary outcomes included superficial femoral artery (SFA) VC, bone mineral density (BMD) of lumbar spine and serum markers of mineral metabolism. At baseline, 6 and 18 month computed tomography was performed to measure VC and BMD. A random effect linear regression model was performed to assess differences.

For Western blots 3 × 106 B cells were lysed in RIPA buffer. Nitrocellulose membranes were blocked in Tris-buffered saline/5% dry milk, and incubated with anti-RAG-1 1 : 200, anti-Ku70 1 : 1000, Fluorouracil anti-RAG-2 1 : 200, anti-GAPDH (Millipore, Schwalbach, Germany) or anti-β-actin (Cell Signaling Technologies, Danvers, MA). Real-time RT-PCR was performed using a High Pure RNA Isolation Kit (Roche), First Strand cDNA Kit with oligo(dT) primers (Fermentas, St Leon-Rot, Germany), Absolute QPCR SYBR GREEN Low ROX Mix (ABgene House, Epsom, UK), primers

(Table 1, MWG Biotech) and a 7900 HT Fast Real Time PCR System (Applied Biosystems, Darmstadt, Germany). Relative expression to β-actin was calculated as rE = 1/(2Ct(target) − Ct(β-actin)). Interleukin-6 (72 hr) was EGFR inhibitors cancer measured using the OptEIA ELISA kit (BD Biosciences); IgM (13 days) was quantified using the IgM ELISA (Bethyl Laboratories, Montgomery, AL). For polyreactivity ELISA, plates were coated with 10 μg/ml lipopolysaccharide (Sigma), pneumovax (Aventis Pasteur, Lyon, France), tetanus toxoid (Statens Serum Institute, Copenhagen, Denmark) or 100 μg/ml salmon

sperm DNA [Sigma; double-stranded DNA (untreated), single-stranded DNA (boiled)], rehydrated, blocked with PBS/3% FCS and incubated with B-cell supernatant and anti-human immunoglobulin-horseradish peroxidase (1 : 5000). Statistical significance was determined using the paired two-tailed Student’s t-test; significant differences are indicated with *P ≤ 0·05 and **P ≤ 0·005. In the present study we asked whether TLR9 could participate in receptor revision. As IL-6

was previously found to be essential for the expression of RAG proteins in B-cell progenitors[20] and in mature B cells,[5, 6] we first determined the preconditions for induction of B-cell-derived IL-6: CpGPTO represented potent inducers of IL-6 (Fig. 1a), but IL-6 was also stimulated by combination of CD40L and rhIL-4, used as a surrogate for T-cell help (Fig. 1a), and combination of CpGPTO with Staurosporine chemical structure CD40L synergistically enhanced IL-6 production (Fig. 1a). By comparison, CpGPTO triggered proliferation in all conditions but the combination of CD40L and rhIL-4 (Fig. 1b). Having confirmed this prerequisite for re-expression of RAG, we approached the analysis of RAG expression. RNA and protein lysates from freshly isolated peripheral blood B cells were compared with those from B cells stimulated with CpGPTO, CD40L ± rhIL-4 or a combination of these stimuli. As expected, RAG-1 mRNA was not found in freshly isolated B cells but – paralleling IL-6 induction – became detectable in B cells stimulated for 24 hr or longer with either CD40L/rhIL-4 or CpGPTO, or combinations of CpGPTO with CD40L ± rhIL-4 ± BCR stimulation with anti-human immunoglobulin F(ab′)2 (Fig. 2a).

The authors declare no financial or commercial conflicts of interest. “
“Opisthorchis viverrini infection causes opisthorchiasis and is a risk factor

for cholangiocarcinoma via chronic inflammation. To investigate the mechanism of O. viverrini -induced liver disease, we applied a proteomic approach to examine alterations in hepatic protein levels in O. viverrini -infected hamsters. Two-dimensional gel electrophoresis (2DE) revealed that O. viverrini infection induced upregulation (1·5- to 4·3-fold) of 25 proteins and downregulation (1·5 to 2·5-fold) of 24 proteins compared with uninfected animals. Expression of proteins related to stress response, DNA replication and repair, and cell structure was significantly increased, whereas that of proteins ABT-263 associated with normal liver function, such as metabolism, blood volume maintenance and find more fatty acid cycle was decreased. Among the upregulated proteins, a 2·7-fold increase in peroxiredoxin 6

(Prdx6), an antioxidant protein, was confirmed by 2DE and immunoblot analysis, Western blot and quantitative PCR. Immunohistochemical analysis showed that Prdx6 expression was observed mainly in the cytoplasm of inflammatory cells. These results suggest that Prdx6 is important for host defence against O. viverrini infection. This study provides basic information for Prdx6 as a potential biomarker and therapeutic target for opisthorchiasis. Infection with human liver fluke, Opisthorchis viverrini, causes opisthorchiasis, a major public health problem affecting the poorest regions of South-East Asia, including Thailand, Lao People’s Democratic Republic, Cambodia and central Vietnam (1). In Thailand, eight million people are estimated to be infected with O. viverrini, representing about 9·6% of the population (2). Humans become infected with O. viverrini by consuming raw or undercooked fish, which contains the infective metacercaria stage of the parasite. The parasite migrates to intrahepatic bile Protein kinase N1 ducts via the common bile duct, and produces eggs that are excreted in the faeces after approximately 30 days (3). The disease is usually persistent

for many years with chronic infection and remains clinically silent unless detected by ultrasonography (4). Chronic O. viverrini infection induces various hepatobiliary diseases, including cholangitis, cholecystitis, gallstones, hepatomegaly and intrahepatic cholangiocarcinoma (CCA) (1). The highest incidence of CCA occurs in the north-eastern region of Thailand, especially Khon Kaen Province, where O. viverrini infection is endemic (5,6). A cellular response to parasite antigens released from mature worm stimulates a local inflammatory response (7). Host immune responses to mechanical and immunological irritation caused by parasites lead to release of free radicals, growth factors, proteolytic enzymes and fibrogenic cytokines from inflammatory and epithelial cells, which contribute to a variety of pathologies including CCA (6,8,9).

© 2010 Wiley-Liss, Inc. Microsurgery 30:509–516, 2010. “
“Multiple soft tissue finger defects in different shapes and locations are usually difficult to manage. Such defects commonly involve tendons and bones. Palmar soft tissue defects may also lead to vascular compromise. In this retrospective report,

we report the results of seven patients with multiple soft tissue finger defects that were covered by syndactylizing arterialized venous flaps. Six of the patients suffered hot-pressing JAK activation machine and crushing injuries, one patient had a rolling belt injury. All patients presented with soft tissue defects on palmar or dorsal sides involving at least two digits. The palmar forearm was donor site for all patients. At least one afferent artery and two efferent veins were selected for the anastomosis. Lengths of afferent and efferent veins were long enough to perform healthy anastomosis outside the injury zone. The afferent vessels were anastamosed to the digital arteries with the largest possible diameter or to the common digital arteries to maximize flow. The efferent veins were anastamosed to dorsal veins. Separations of the digits were performed

after three weeks by longitudinal incisions. The mean follow-up period was 12 months. None of our patients suffered RAD001 clinical trial a flap loss. Syndactylizing arterialized venous flaps may be used for composite or single

tissue reconstruction for multiple finger defects with satisfactory cosmetic and functional outcomes. © 2014 Wiley Periodicals, Inc. Microsurgery 34:527–534, 2014. “
“This article aims to investigate the critical role of Non-specific serine/threonine protein kinase the venous-perforator in the decision-making process of choosing the best suitable perforator-complex in a deep inferior epigastric perforator (DIEP) flap. Forty consecutive DIEP breast reconstructions were pre-operatively evaluated by CT-Angiography to identify the dominant and centrally located abdominal wall perforators. The CTA results were used as a guide to conduct a Color-Duplex-Ultrasound examination that was mainly focused on investigating the accompanying venous-perforator. In group-A (n = 20) perforator-complex selection was based on the size of the arterial-perforator, whilst in group-B (n = 20) it was based on the size of the venous-perforator. All single perforator-complex DIEP flaps survived. No significant differences were recorded concerning the size of arterial-perforator between the two groups; however the size of venous-perforator was significantly larger in group-B (P < 0.05). In group-A, four flaps showed vascular compromise intraoperative that was salvaged by flap supercharge with the superficial inferior epigastric system. In contrast, in group-B, all flaps were re-vascularized uneventfully (P < 0.05).