The authors further showed that type I interferons, produced by nonmonocytic cells, induced CCR2 ligand expression on monocytes leading to recruitment of monocytes to the infected tissues. Collectively, the observations described in this section ind-icate that monocytes

are recruited from the bone marrow to selleck chemicals llc the blood during infection and that they differentiate into cells displaying properties shared by cells of the dendritic family. These “inflammatory dendritic cells,” through NO and TNF-α production, have a major role in the clearance of infectious agents. Notably, NO, which is generated by the actions of iNOS, has remarkable microbicidal properties, altering pathogen metabolism: NO can interact with oxygen species to form oxidant derivatives causing DNA deamination, strand breaks, and other alterations Alvelestat price [14]; and it can inhibit the metabolic activity and function of some trypanosomal proteins by chemically modifying their cysteine residues and/or by binding to metalloproteins that mediate crucial metabolic processes [15]. TNF-α, on the other hand, presents a lectin-like domain that binds specific glycoproteins in the flagellar pocket of T. brucei disturbing the osmoregulatory

capacity of the pathogen and leading to its lysis [16, 17]. TNF-α has also been shown to bind gram-negative bacteria through specific TNF-α receptors expressed on the bacteria that differ from TNFR1 and TNFR2 Nintedanib (BIBF 1120) expressed by eukaryotic cells. In the case of TNF-α/Shigella flexneri complexes, their phagocytic uptake by human and mouse macrophage cell lines has been shown to be increased two- to five-fold as compared with untreated bacteria [18]. In 2007, two reports clearly suggested that these monocyte-derived DCs may also be involved in the next phase of the immune response, that is, adaptive immunity. Leon et al. [19] reported that, during Leishmania major infection, two de novo formed DC subsets

were found in popliteal LNs. One population derived from monocytes that had been recruited to the dermis and had subsequently migrated to the LNs, whereas the other population developed from monocytes directly recruited to the LNs. Among the DC subsets present in the popliteal LNs, only these two monocyte-derived subsets were infected by Leishmania major, suggesting a role in T-cell immunity. Although both identified DC subsets were able to promote IFN-γ production by T cells and expressed I-Ad-LACK complexes, only the DC subset derived from the monocytes that were first recruited to the infection site (the skin) before migration to the LNs appeared to be essential for the induction of pathogen-specific T-cell responses. At the same time, Tezuka et al. [20] highlighted the role of inflammatory DCs in IgA production in the mucosa-associated lymphoid tissues.

After 48 h, cultures were pulsed with 0.4 μCi [3H]thymidine (Amersham Biosciences, Braunschweig, Germany),

and incubated for another 24 h. After harvesting, incorporated DNA was measured in a β-counter (Perkin Elmer, Rodgau, Germany). Cytotoxicity of freshly sorted splenic CXCR3− and CXCR3+ NK cells Epigenetics Compound Library cell assay (5×105/mL) against YAC-1 target cells was assessed by standard 4 h chromium release assay. Target cells were labeled with 3 MBq Na51CrO4 (Hartmann Analytic, Braunschweig, Germany), incubated for 1 h at 37°C, washed two times and used for the assay within 1 h. Cells were plated in V-bottom 96-well plates. Background values were determined by incubating target cells without effector cells. Maximal values were obtained by lysing target cells with 1% Triton X-100 (Sigma-Aldrich).

After 4 h, cells were pelleted and 100 μL supernatant of each well was used for measurement of 51Cr release in a γ counter (MicroBeta/PerkinElmer, Waltham, MA, USA) in triplicates with E:T ratios of 10:1, 5:1, 2.5:1 and 1.25:1. Specific lysis was calculated by: [(experimental release–spontaneous release)/(maximum release–spontaneous release)] ×100. Lysosomal granule exocytosis was determined by CD107a expression. For this experiment, lymphocytes (E:T ratio 10:1) or sorted CXCR3− and CXCR3+ NK cells (E:T ratio 2:1) were incubated at 37°C in 5% CO2 together selleck compound with YAC-1 cells for 4 h. Anti-CD107a mAb was added directly oxyclozanide to the cell suspensions at a final concentration of 0.01 mg/mL. After 1 h of incubation, Monensin (BD Biosciences) was added as a golgi block at a final concentration of 5 μg/mL and incubation was continued for additional 3 h. In case of subsequent intracellular cytokine staining, brefeldin A (Sigma-Aldrich) was added at a final concentration of 2 μg/mL for the last 3 h of incubation time. Samples were finally surface-stained and analyzed via multicolor flow cytometry. In order to determine the IFN-γ production, sorted

CXCR3− and CXCR3+ NK cells were cultured in 96-well round-bottom culture plates (Greiner, Frickenhausen, Germany) in the presence of rIL-2 (100 U/mL), rIL-12 (10 ng/mL) and rIL-18 (5 ng/mL) for 15–17 h. Optimal cytokine concentrations were determined by earlier dose titrations. Brefeldin A (Sigma-Aldrich) was added at a final concentration of 2 μg/mL for the last 2 h of incubation time. Analysis of intracellular IFN-γ was preceded by surface staining at 4°C. After 30 min, cells were washed twice and resuspended in PBS containing 3% FCS. After fixation with 4% paraformaldehyde (Merck) for 10 min, cells were perforated with 0.1% saponin buffer (PBS supplemented with 0.1% saponin (Riedel-de Haën, Seelze, Germany) and 0.01 M HEPES (Roth, Karlsruhe, Germany)) and anti-IFN-γ mAb was added. After 30 min of incubation and three washes, cells were analyzed as described above.

Such an interaction has been shown to promote the activation of microglia in vitro[65] and its genetically engineered or pharmaceutical abrogation results in amelioration of EAE expression.[66] Ponomarev et al. described a two-step process for microglia activation in EAE. They proposed that the CD40-independent first step occurring just before EAE onset is mediated by pro-inflammatory cytokines released by encephalitogenic T cells, such as IFN-γ, and results in www.selleckchem.com/products/emd-1214063.html microglial cell proliferation and up-regulation of MHC class II, CD40 and CD86; the second step of activation, which is CD40-dependent, occurs at the peak of disease and is characterized by a further

increase in expression of activation markers and a reduced proliferation.[64] Upon full activation, microglia can act as antigen-presenting cells to present phagocytosed myelin antigen to encephalitogenic T cells leading to their expansion in the CNS and severe disease expression.[64] However, antigen presentation

is unlikely to be the main mechanism of damage mediated by microglia in EAE; rather, release of inflammatory cytokines and reactive oxygen species may be more relevant. A recent study identified Peli1, a family member of E3 ubiquitin ligases implicated in TLR and IL-1 receptor signalling in innate immune cells, as an essential regulator of microglia activation during EAE pathogenesis that is required for mitogen-activated protein kinase (MAPK)-dependent production of pro-inflammatory cytokines and chemokines.[67] Peli1 knockout mice selleck chemical were refractory to EAE APO866 induction and showed reduced numbers of CNS-infiltrating cells and activated resident microglia. Peli1 was abundantly expressed in microglia and absolutely required for microglial activation during EAE, as shown by studies in Peli1-knockout GFP-expressing chimeric mice.[67] In vitro studies showed that Peli1 affects MAPK activation through MyD88-dependent TLR regulation, and acts by promoting

degradation of TNF receptor-associated factor 3, a potent inhibitor of MAPK activation and gene induction.[67] Another molecule that plays an important role in microglia activation leading to neurotoxicity is macrophage migration inhibitory factor (MIF), a pro-inflammatory cytokine identified as a marker of clinical worsening in MS patients.[68] A recent study has shown that MIF can drive the activation of microglia both in vitro in primary microglia cell cultures, and in vivo in EAE-affected mice or in the focal EAE model in MIF-deficient mice.[69] Increasing concentrations of MIF induced dose-dependent changes in expression of inflammatory molecules, such as TNF-α, IL-1β, IL-6 and inducible nitric oxide synthase, in primary microglia in vitro, that were accompanied by morphological changes from resting to activated and/or phagocytic phenotype.

[252] In addition, these data have contributed to the idea that the fetus generates a significant inflammatory

response under these conditions[253] and that this response may subject the fetal brain to processes leading to cerebral palsy.[254] Several animal models have been used to examine fetal neurologic insult in the context of maternal systemic infection or inflammation and the resulting preterm labor. These studies have included systemic injection of LPS in pregnant sheep[255] and intrauterine injection in rabbits[256] and in mice.[257-259] The mouse model of preterm birth initiated with injection of LPS revealed the important role of the cytokine interleukin 10.[260, 261] In addition, human studies have suggested the potential role of this cytokine in modifying preterm birth-related brain injury.[262] The study of inflammation-related preterm birth and brain Tanespimycin mw injury offers another opportunity for productive iterative study in humans and animals. Programming’ is said to occur during ‘a critical period when the system is plastic

and sensitive to the environment followed by loss of plasticity and a fixed functional capacity’.[263] ‘Fetal programming’ in humans is said to occur as a result of adaptation to undernutrition in an adverse intrauterine environment contributes significantly to obesity, metabolic syndrome, and cardiovascular disease.[264] Increasingly, animal models are being used to delineate these mechanisms, and several models utilizing rats, mice, rabbits sheep, and MS-275 manufacturer non-human primates have been utilized (see Fischer et al.,[16] Seki et al.,[265]

and Vuguin[158] for reviews)]. Some of these models proceed through well-recognized defects in fetal development, such GPX6 as IUGR. This issue is one that is ripe for an iterative process involving studies in animals and humans. An area that would be particularly amenable to animal experimentation would be the examination of multigenerational effects of exposure during pregnancy.[266] Although the relevant tissue in humans is sometime hard to access, genetic variability found from sampling peripheral blood can be informative in conjunction with specific gene manipulation in rodents. For example, technology exists to manipulate embryos by using viral constructs to target genes to trophoblast.[11, 267] It is therefore not difficult to imagine an experimental paradigm whereby candidate genes from human genetic studies would be considered for overexpression or ‘knock down’ in trophoblast using this technology. Pregnancies using these manipulated embryos could then be observed or further challenged and observed for preterm birth. In this way, and perhaps many others, bioinformatics, systems biology, and the use of animal models could be woven into and increasingly efficient iterative method to understand the complex biology of abnormal pregnancy.

Nuclear factor-erythroid 2-related factor 2 (Nrf2) is one check details of the most important cellular defense mechanisms against oxidative stress. NAD(P)H quinine oxidoreductase (NQO1), was the well-studied Nrf2 target genes that are up-regulated through the antioxidant response element regulatory element in response to oxidative stress. The aims of the research was investigated

the effects of Zn deficiency on diabetes-induced renal oxidative damage, inflammation and fibrosis, and the relation with Nrf2 and NQO1. Methods: Type 1 diabetes was induced in FVB mice with multiple low doses of streptozotocin. Once hyperglycemia was established, diabetic and age matched control mice were treated with and without Zn chelator, N, N, N′, N′-tetrakis (2-pyridylemethyl) ethylenediamine (TPEN) at 5 mg/kg daily for 4 months. Renal oxidative damage, inflammation

and fibrosis mice were examined by histopathological observation, Naphthol AS-D Chloroacetate esterase assay, immunofluorescent staining, and Western blotting assay. Human renal tubular HK 11 cells were treated by TPEN and Zn, the expression of Nrf2 and NQO1 were examined by immunofluorescent and Western bloting assay. Results: Chronic treatment with TPEN significantly click here oxyclozanide decreased renal Zn levels in both diabetic and control mice. Compared to group with diabetes or TPEN alone, Diabetes/TPEN group showed a significant decrease in Nrf2 expression along with significant increases of renal oxidative damage (protein nitration and lipid oxidation), renal inflammation [infiltrated inflammatory cells and expression of plasminogen activator inhibitor-1(PAI-1) ], and renal fibrosis [PAS staining and expression of profibrotic mediator connective tissue growth factor (CTGF)]. Mechanistic study with human renal tubular HK 11 cells showed that TPEN removal of intracellular Zn decreased

Nrf2 and NQO1 expression, which could be significantly attenuated by Zn supplementation. Conclusion: These results indicated that Zn deficiency significantly enhanced diabetes-induced renal oxidative damage, inflammation and structural remodeling through downregulation of Nrf2 expression and function. CHOI SOO Y1, LIM SUN W2, YOO EUN J1, SANADA SATORU3, LEE HWAN H1, KWON MI J1, LEE-KWON WHASEON1, KWON HYUG M1,3 1UNIST; 2Catholic University of Korea; 3University of Maryland Introduction: We reported previously that, in patients with ∼30 years of type 1 diabetes, proteinuria was associated with ∼50% higher activity of the TonEBP transcription factor in monocytes (1).

4 gradually increased after 1 and 5 h of incubation (not shown). In contrast, no BCG was ingested

after 15 min, and only small amounts of BCG were ingested after 1 h, where partial uptake of BCG by THP-1 cells was visible (Fig. 6A, yellow arrow). Some TB10.4 co-localized with Lamp-1 at 15 min of incubation, and increasing amounts of TB10.4 was found in Lamp-1-positive compartments after 1 and 5 h (Fig. 5). BCG was not observed inside Lamp-1 positive vesicles after 1 h, but after 5 h some of the internalized BCG was clearly found to co-localize with Lamp-1, although significant BCG-derived fluorescence was also present in Lamp-1- compartments (Fig. 6). Selleck GS-1101 Interestingly, when the macrophages were incubated with both vaccines (TB10.4-AF546 and BCG-eGFP) simultaneously, we found that although both vaccines were taken up by the same cell, we did not observe any co-localization inside the macrophages.

This suggested that the vaccines were transported to distinct subcellular compartments for subsequent processing (Fig. 7). In summary, both TB10.4 and BCG were transported to Lamp-1+ compartments inside macrophages. However, the vaccines were taken up with different Ferrostatin-1 kinetics, and a larger part of BCG than TB10.4 was also present in Lamp-1− compartments. TB10.4 and BCG were never found to co-localize, which indicated that they localized to different pools of Lamp+ as well as Lamp− compartments. This difference in intracellular location could possibly explain the different TB10.4 epitope patterns

following immunization with TB10.4/CAF01 and BCG. In this article, we examined the TB10.4 epitope recognition pattern after immunization with recombinant TB10.4 in CAF01, vaccination with BCG or following infection with M.tb and found that different epitopes were recognized in these three scenarios. Although epitopes have been identified in M.tb proteins other than TB10.4 12, 14, 23, a detailed comparison between post immunization however and post infection epitopes has not been described. As previously shown, we found that infection with virulent M.tb induced a significant CD8 response against TB10.4 P1 and P2, whereas immunization with TB10.4 or BCG did not (in contrast to i.v. administration of BCG at high doses (∼1×106 CFU/mouse), which does give a significant CD8 response specific for TB10.4) (Fig. 2) 15, 24, 25. The recombinant BCG::RD1-strain expressing the ESAT-6 secretion system showed similar TB10.4 epitope recognition patterns as virulent M.tb, both recognizing the MHC-I restricted epitopes in P1 and P2 and the MHC-II restricted epitope in P8 (data not shown), corresponding to earlier described epitopes 24, 26, 27. As it has been suggested that the RD1 region enables M.tb to escape the phagosome 28, it could be speculated that altered intracellular trafficking of BCG might lead to a different epitope pattern and/or to new protective epitopes.

The results are expressed as the difference in the percentage of apoptotic K562 cells at a particular effector to target cell ratio minus the percentage of apoptotic K562 cells cultured in the medium alone. Statistical analysis.  Statistical find more analyses were performed using Statistica 8.0 data analysis software (StatSoft, Inc., Tulsa,

OK, USA). The difference between groups was calculated by the Kruskal–Wallis non-parametric test, and a P value of <0.05 was considered statistically significant. The Mann–Whitney U test was used to determine the difference among groups with the level of significance adjusted to the number of mutual comparisons. Flow cytometry analysis of GNLY expression within gated peripheral blood lymphocytes shows that 4.7% of lymphocytes in healthy person express GNLY with a MFI of 7 (Fig. 1A). The histogram indicates fluctuation in the percentage and MFI of GNLY with respect to isotype-matched controls in patients with NSTEMI (Fig. 1B) on days 1, 7, 14, 21 and 28 after the acute coronary event that matched the summary data shown in the charts (Fig. 1C). The percentage of GNLY-positive lymphocytes was significantly higher (median, 28.67) on day 7 after the acute coronary event

compared with healthy examinees (median, 2.6) or with Angiogenesis inhibitor values on day 14 (median 0.28). On day 1, GNLY was slightly increased compared to healthy examinees, but it was significantly higher when compared to that of patients with NSTEMI on day 14 (Fig. 1C). MFI of GNLY in lymphocytes decreased significantly from day 7 to day 28 compared to healthy examinees or to day 1 (Fig. 1C). Using immunocytochemistry,

GNLY protein was visualized Cytidine deaminase as red-labelled granules beneath the cell membrane of lymphocytes in healthy examines and patients with NSTEMI. The highest expression of GNLY was on day 7, and the lowest expression of GNLY was on day 14 (Fig. 1D). Labelling with irrelevant isotype-matched mouse immunoglobulin G1 (IgG1) was negative (upper left microphotographs in Fig. 1D). In the dot plots of PBL from healthy examinees shown in Fig. 2A, CD3+ CD56− T cells are located within the solid line rectangle and CD3+ CD56+ NKT cells are presented within the dashed line rectangle with respect to isotype-matched control. In patients with NSTEMI, the frequency of GNLY-positive NKT cells (Fig. 2B) and T cells (Fig. 2D) was increased on day 7 compared to the percentage observed in healthy examinees and in patients with NSTEMI on day 14 after an acute coronary event. On day 1, the percentage of GNLY+NKT cells was higher than in healthy examinees (Fig. 2B). The MFI of GNLY essentially did not change in NKT (Fig. 2C) and T cells (Fig. 2E) during the investigation period. The dot plots in Fig. 3A show a sample flow cytometry with the gates set up for the analysis of GNLY expression in total NK cells and their subsets.

Microsurgery 30:397–400, 2010. “
“Autologous breast reconstruction is safe in advanced age, yet no study has examined its effects on the aging abdomen. We, therefore, studied 145 women who participated in a prospective study of abdominal strength following abdominal free flap breast reconstruction, comparing preoperative and late follow-up scores find more in patients ≥60 years old (11 unilateral, 13 bilateral) compared with patients <60 (58 unilateral, 63 bilateral). Simple in-office tests were utilized to test abdominal strength. No differences were noted in unilateral absolute scores at either time point, however, a decrease in upper abdominal strength was noted in the younger cohort over time (P = 0.01). Bilateral

analyses revealed absolute score decreases

in upper abdominal strength for both cohorts but no major differences between the two. We conclude that autologous breast reconstruction with abdominal tissue in older patients result in little to no difference in abdominal function as compared with younger patients. © 2012 Wiley Periodicals, Inc. Microsurgery, mTOR inhibitor 2013. “
“Background: Large or extensive gouty tophi on the feet can cause functional impairment, drainage sinus, and infected necrosis, finally resulting in complex soft-tissue defects with tendon, joint, bone, nerve, and vessel exposure. Reconstruction of complex soft-tissue defects of the foot is still challenging. The purpose of this report was to review the outcomes of free-flap reconstructive surgery for treating the metatarsal joint defects of the feet caused by chronic tophaceous gout. Methods: Ten patients who had large tophus masses (>5 cm) and ulceration on the feet were admitted to our hospital between September 2006 and September 2010. Six patients underwent free-flap reconstruction after debridement to resurface the circumferential wound, protect the underlying structures, and provide a gliding surface for exposed tendons. The patients’ age, sex, comorbidities, location and size of the defects, reconstructive procedures,

surgical outcomes, complications, Montelukast Sodium follow-ups, and recurrence of tophaceous gout were reviewed and recorded. Results: The mean patient age was 49.8 years (range, 36–72 years). The average skin defect size was 92.2 cm2. Five patients were treated using free anterolateral thigh flaps, and 1, using a free medial sural flap. These free flaps were safely raised and showed excellent functional and cosmetic results, with a mean follow-up of 31.7 months (range, 7–50 months). Conclusion: Chronic tophaceous gout can cause severe skin infection and necrosis, even resulting in deformity or sepsis if left untreated. Surgical debridement is inevitable in patients with extensive wounds. We reconstructed the large, ulcerative skin and soft-tissue defects on the dorsum of the foot by performing free-flap reconstruction after adequate debridement and achieved good functional and cosmetic results. © C 2011 Wiley Periodicals, Inc. Microsurgery, 2011.

pullorum. This organism was first described in 1994 selleck chemical after clinically derived CLO isolates were examined by various methods, and within 387 samples, six strains of H. pullorum were identified (including NCTC 12826, NCTC 12827, UB3166, UB3659) all associated with gastrointestinal

illness (Burnens et al., 1994; Stanley et al., 1994). One of the patients was a 27-year-old man with diarrhoea, 30 kg weight loss and deranged liver enzymes. No gastrointestinal histology or clinical progress was reported on this case; hence, the similarity of his disease to IBD cannot be commented upon further. One patient was HIV-positive. Helicobacter pullorum (NCTC 13155) has also been associated with diarrhoeal illness in humans in a German study describing two cases with diarrhoea (without blood), one of whom also had common variable immunodeficiency (Steinbrueckner et al., 1997). Both cases apparently resolved spontaneously. The first (immunosuppressed) case was treated once asymptomatic with roxythromycin after which stools were negative for H.

pullorum; however, the second case continued to have positive stools and went on to have a second episode of diarrhoeal illness during which the organism was again cultured. This suggests the possibility of chronic carrier status. Interestingly, in one case, the organism was first identified as C. jejuni/coli based on its BMN 673 in vitro appearance, growth conditions and oxidase/catalase tests. As we shall see, standard laboratory methods of identification may underestimate the burden of lower gastrointestinal Helicobacter (and indeed novel Campylobacter) disease. One study has potentially contradicted the possibility of H. pullorum being a pathogenic agent resulting in diarrhoeal disease in humans. The work of Ceelen

et al. (2005) examined 531 stool samples from patients with gastroenteritis alongside stool from 100 healthy individuals by H. pullorum-specific PCR. This study demonstrated a strikingly similar prevalence within the two cohorts. The gastroenteritis group were PCR-positive for H. pullorum in 4.3% of cases and the controls in 4.0%. The authors rightly state that DNA positivity may come from ingested foodstuffs and that it does not necessarily infer replication of the organisms within the gastrointestinal tract. Other possibilities explored included a Tobramycin variable pathogenicity within the organisms themselves or variable host factors (which may include immunodeficiency or genetic susceptibility). The PCR primers designed by Stanley et al. (1994), which were apparently utilized in this study, have since been revised (Fox et al., 2000). It is not clear what effect, if any, this may have had on the prevalence data provided by the work of Ceelen. The pathogenicity of H. pullorum was recently studied in vitro by Varon et al. (2009) utilizing human gastric (AGS) and intestinal (CaCo-2 and HT-29) epithelial cell lines.

We report a progressive lower extremity lymphedema (LEL) case successfully treated with a ladder-shaped LVA. A 67-year-old female with secondary LEL refractory to conservative treatments underwent LVA. A ladder-shaped

LVA was performed at the left ankle. In the selleck inhibitor ladder-shaped LVA, 3 lymphatic vessels and 1 vein were anastomosed in a side-to-side fashion; 2 lymphatic vessels next to the vein were anastomosed to the vein, and the other lymphatic vessel was anastomosed to the nearby lymphatic vessel. Using ladder-shaped LVA, 6 lymph flows of 3 lymphatic vessels could be bypassed into a vein. Six months after the LVA operation, her left LEL index decreased from 212 to 195, indicating edematous volume reduction. Ladder-shaped Selumetinib chemical structure LVA may be a useful option when there are 3 lymphatic vessels and 1 vein in a surgical field. © 2013 Wiley Periodicals, Inc. Microsurgery 34:404–408, 2014. “
“This study evaluated the results of repair of the radius defect with a vascularized tissue

engineered bone graft composed by implanting mesenchymal stem cells (MSCs) and a vascular bundle into the xenogeneic deproteinized cancellous bone (XDCB) scaffold in a rabbit model. Sixty-four rabbits were used in the study. Among them, four rabbits were used as the MSCs donor. Other 57 rabbits were divided into five groups. In group one (n = 9), a 1.5 cm bone defect was created with no repair. In group two (n = 12), the bone defect was repaired by a XDCB graft alone. In group three (n = 12), the defect was repaired by a XDCB graft that included a vascular bundle. In group four (n = 12), the defect was repaired by a XDCB graft seeded with MSCs. In group Sodium butyrate five (n = 12), the defect was repaired by a XDCB graft including a vascular bundle and MSCs implantation. The rest three rabbits were used as the normal control for the biomechanical test. The results of X-ray and histology at postoperative intervals (4, 8, and 12 weeks) and biomechanical examinations at 12 weeks showed that combining MSCs and a vascular bundle implantation

resulted in promoting vascularization and osteogenesis in the XDCB graft, and improving new bone formation and mechanical property in repair of radius defect with this tissue engineered bone graft. These findings suggested that the vascularized tissue engineered bone graft may be a valuable alternative for repair of large bone defect and deserves further investigations. © 2011 Wiley-Liss, Inc. Microsurgery, 2011. “
“The comparisons of two different methods of donor nephrectomy were performed in this study. Fisher inbred rats were used as donors and recipients of kidneys. In method A (the conventional technique), meticulous blunt dissection of the abdominal aorta, inferior vena cava, and renal arteries/veins, was followed by ligating and cutting the superior mesenteric artery and small vessels entering the above vessels. Both donor kidneys were irrigated after the suprarenal aorta and inferior vena cava were cross-clamped (n = 10).