Between the moderate LCL and the low-responsive ADCL, there is a weak, definite cellular hypersensitivity form known as borderline disseminated cutaneous leishmaniasis (BDCL), which has been shown to be lesser immunosuppressed than ADCL. On the other hand, L. (V.) braziliensis infection can cause not only LCL and BDCL but also the mucocutaneous leishmaniasis (MCL), the cellular hypersensitivity pole

of infection with a prominent Th1-type immune response (3). In this way, the ACL caused by these two Leishmania species presents a clinical–immunological spectrum where L. (L.) amazonensis shows selleck chemicals llc a tendency to lead infection to the anergic pole of cellular immune response, whereas L. (V.) braziliensis leads infection to the hypersensitivity pole of host cellular immune response (4). The diversity of clinical manifestations has mainly been associated www.selleckchem.com/products/ABT-888.html with antigenic differences of the different species of parasites (5), but also with the host immune-genetic background (6,7). The dendritic cells (DCs), both Langerhans cell (LC) and dermal dendritic cell (dDC), have been recognized as the main antigen-presenting cells in the skin with a capacity to capture antigen and migrate to the draining

lymph node for activation of a T-cell immune response (8). In this way, DCs seem to play a pivotal role in ACL immunopathogenesis once they represent the vehicle that promotes the first contact of Leishmania with the host immune response. PFKL Some studies have shown that in mice experimentally infected with L. (L.) major, the dDC and not LC as was previously postulated, were able to stimulate antigen-specific T-cell proliferation, suggesting that dDCs are crucial for initiating an appropriate and effective cellular immune response (9–11). In this way, Brewig et al (12). showed that proliferation of L.major-specific CD8+ T cells was reduced during the early

phase of the immune response in the absence of Langerin+ dDC and the impaired CD8+ T-cell response was because of the absence of Langerin+ dDC and not LCs, proposing a novel concept for the role of DCs in the immunopathogenesis of murine cutaneous leishmaniasis by L. major, where the priming of CD4+ T cells is mediated by Langerin-negative dDCs, while Langerin-positive dDCs are involved in the early priming of CD8+ T cells, leading to parasite elimination. Recently, using low-dose infection with L. major, Kautz-Neu et al (13). showed smaller lesions with decreased parasite loads, reduced number of CD4+ Foxp3+ T cells accompanied by increased IFN-γ production in mice depleted in Langerin+ DC; moreover, selective depletion of LC demonstrated that the absence of LC and not Langerin+ dDC was responsible for the reduction T reg cells and the enhanced Th1 response resulting in attenuated disease.

Leukocytes (106) were stained RG7204 manufacturer with the appropriate concentration of the following antibodies: CCR6 (29-2L17; Biolegend, Inc.), CCR9 (polyclonal; Santa Cruz), CD3 (145-2C11), TCR δ chain (GL3), PE TCR β chain (H57-597),

α4 integrin chain (R1-2), α4β7 integrin (DATK32), CD25 (7D4), CD2 (RM2-5), CD45RB (16A), CD69 (H1.2F3), CD122 (TM-Beta1) (BD Pharmingen). For intracellular cytokine staining, cells were preincubated for 4 h with PMA (20 ng/mL), ionomycin (500 ng/mL), and brefeldin A (10 μg/mL) at 37°C at 5% CO2. After surface marker staining, cells were fixed, permeabilized, and stained with anti-IL-17, anti-IFN-γ, and anti-IL-4 antibodies (BD Pharmingen). IgG isotypes were used as irrelevant antibodies. Analysis was performed by using Cell Quest program in FACScalibur flow cytometer (Becton Dickinson, San Jose, CA, USA). Counts are reported as numbers of cells after the multiplication www.selleckchem.com/products/MG132.html of the percentage of T lymphocyte population by the total number of leukocytes. Gating strategy is shown in Supporting Information Fig. 5. Levels of CCL25, IL-17, IFN-γ, and IL-4 in cell-free pleural washes, recovered 24 h after challenge, were evaluated by sandwich enzyme-linked immunosorbent assay (ELISA) by using matched antibody pairs from R&D , according to manufacturer’s instructions. Mesothelial cells were recovered from C57BL/6 mice

pleura 14 days after s.c. sensitization as previously described [[11]] and yielded at least 90% of cytokeratin 7+ cells (data not shown), a cell surface marker that characterizes mesothelial cells [[66]]. Cells (4 × 105/well) were stimulated with rmIL-4 (40 ng/mL; R&D Systems) and supernatants were recovered after 12 Sulfite dehydrogenase h, for CCL25 evaluation. Murine thymic endothelioma cells (tEnd.1) were cultured in trans-well polycarbonate culture inserts placed in 24-well culture plates (8.0-μm pore diameter, BD Falcon) and allowed to grow to confluence. tEnd.1 cell monolayers were prestimulated with rmIL-4 (40 ng/mL; R&D Systems), SPW or OPW for 30 min, washed and added to 24-well culture plates containing PBS, rmCCL25 (100 ng/mL; R&D Systems),

SPW, or OPW. Spleen T lymphocytes (85% purity) were pretreated for 30 min with mAb anti-α4 integrin chain and anti-α4β7 integrin at saturating concentration (25 μg/mL; BD Pharmingen) and added (106 cells/well) to the tEnd.1 monolayers and allowed to migrate for 3 h (37°C, 5% CO2). IgG isotypes were used as irrelevant antibodies. Transmigrated cells were counted and stained for flow cytometry, as described above. Results are expressed as transmigration index, generated by using the number of cells that migrated toward buffer as comparison. Donor and recipient C57BL/6 mice were i.pl. injected with OVA 14 days post immunization. T lymphocytes were recovered from donor mice 24 h after challenge, labeled with CFSE (1 μM/4 × 107 cells), and treated or not with anti-α4 integrin chain (25 μg/mL).

S2e). Gal-1, gal-3 and gal-9 were also explored by their effect on anti-CD3/anti-CD28-induced cytokines in peripheral T lymphocytes. Lymphocytes were stimulated during 24 h

with anti-CD3 and anti-CD28 in the presence or not of gal-1, gal-3 and gal-9 as indicated in Material and methods. Cytokine production was determined using a bead-based immunoassay. Our results showed that the presence of gal-1 during T cell receptor (TCR) stimulation induces a high production of IL-10, P = 0·02 (Fig. 4c). An augmented IL-4 production was also observed in those lymphocytes co-incubated with gal-3 and anti-CD3/anti-CD28; however, this difference was not statistically significant (data not shown). Most published studies on the immunopathogenesis of asthma and other inflammatory diseases focus on proinflammatory mediators. However, in recent years the study of cells and Palbociclib solubility dmso molecules with immunoregulatory activity has Kinase Inhibitor Library chemical structure begun to gain importance. The data presented here show that airway cells obtained from induced sputum samples of asthma patients express lower levels of gal-1 and gal-9 and higher levels of IL-5 and IL-13 compared with cells from healthy subjects. In addition, we have identified macrophages as the cells from sputum expressing gal-1 and gal-9. A recent study analysed

the presence of galectin-bound proteins in broncoalveolar lavage (BAL) from patients with mild asthma, and a different profile of galectin-bound proteins was observed between patients and healthy subjects. In parallel, authors describe that BAL contains galectins at low concentrations, suggesting that functional interactions with galectins occur at sites where airway cells are present [24]. Numerous studies have highlighted the immunomodulatory

properties of galectins [7]. Sodium butyrate The anti-inflammatory properties of gal-1 have been evaluated in animal models of chronic inflammation [13, 25-27]. However, the role of gal-1 in asthma has not been explored previously. Published data highlight the ability of gal-1 to counteract Th1 and Th17-mediated responses through a number of anti-inflammatory mechanisms. One reported mechanism is a skewing of the balance from Th1 towards Th2 polarized immune responses, mainly through the induction of Th1 cell apoptosis. The numerous anti-inflammatory effects of gal-1 include induction of IL-10 release [28, 29], down-regulation of the secretion of TNF-α and IFN-γ [30, 31] and inhibition of transendothelial migration as well as chemotaxis of neutrophils [32]. Disruption of all these processes could contribute to exacerbated inflammatory responses in an environment with defective expression of this lectin. In the context of asthma, IL-10 plays a key role in the control of inflammatory process, able to down-modulate the Th2 response [33-35]. Decreased IL-10 expression has been linked recently to the impaired ability of natural regulatory T cells from allergic asthma patients to induce a tolerogenic phenotype in dendritic cells [36].

However, this relationship changed dependent

upon the amount of periodontal disease and the amount of antibody to pathogens. Somewhat counterintuitively, in patients with more generalized periodontitis or having the highest level of antibody to the pathogens, the correlation in antibody levels to the pathogens and commensals were minimal. This finding supports the hypothesis that with chronic infection leading to oral tissue destruction, the host immune response selleckchem is dysregulated and selectively recognizes and responds to the pathogens, while not responding as robustly to the multitude of commensal bacteria within the context of the large polymicrobial ecology [7,30,37]. We did, however, observe a significant correlation between antibody levels to P. gingivalis and periodontal Wnt inhibitor status. These relationships were noted in blacks and males within this population of smoking patients and correlated specifically with the frequency of disease sites, linking the antibody more directly to the infectious challenge. In summary, the data show an elevated immune response to pathogens compared to commensals within this smoking population and suggesting that the host immune system has the ability to discriminate between potential pathogenic versus commensal species in the complex biofilms. Response to the pathogens was also shown to be greatest in the subjects with the greatest extent

of disease, comparable to previous findings in other populations and was most notable with antibody to P. gingivalis[21,38]. mTOR inhibitor The observation that black males demonstrated the most severe periodontal disease, which was not commensurate with their level of smoking, supports the need for additional studies to identify the factor(s) that could be contributing to disease susceptibility/expression. While we acknowledge that this was not an exhaustive study of antibody specificities to oral bacterial, the findings highlight processes by which the immune system

recognizes pathogens such as P. gingivalis, and this response would be predicted to help to manage the periodontal disease immunopathology in adult populations. As importantly, it must be considered that antibodies are effector molecules in the host immune response and principal protective factors against extracellular bacterial pathogens. In that regard, previous studies have described antibody subclass distribution to oral pathogens [25,39,40] and suggested variations in the profiles related to the particular bacterial species. These findings were extended to potential success or failure of the antibodies to protect the host effectively. A range of studies have suggested that the immune response to oral pathogens does not mature effectively, as estimated via antibody avidity [41–46], and could contribute to lowered protective capacity. Furthermore, examination of the effector functions of antibodies to the oral pathogens has provided some challenge due to, for example, the gingipains from P.

This result suggests that iNKT cell activation by microbes can lead to severe inflammation

in some cases. Recent studies have indicated that the iNKT cell response to Sphingomonas spp. is important in the pathogenesis of PBC, an autoimmune disease characterized by the destruction of small bile ducts in the liver. PBC patients express antibodies against mitochondrial PDC-E2 in serum (45). Interestingly, N. aromaticivorans, a member of the Sphingomonodaceae family found in human intestines, also expresses PDC-E2 (45). Serum from PBC patients reacts with N. aromaticivorans, but not with E. coli (45). Mice infected with N. aromaticivorans express antibodies against PDC-E2 and develop chronic inflammation in the small bile duct mediated by autoreactive T cells, iNKT cells being required in ABT-263 ic50 this process (59). These

results indicate that iNKT cells play an important Cilomilast role in PBC pathogenesis. When iNKT cells are activated by αGalCer or its analogues, they stimulate many other cells, including APCs, NK cells, B cells and conventional T cells (1–4). Glycolipid mediated iNKT cell activation induces protective responses against various microbial pathogens including bacteria, fungi, parasites and viruses (1–4). For example, αGalCer treatment has a positive effect during certain microbial infections. In mouse pneumonia models with P. aeruginosa and S. pneumoniae,αGalCer treatment induces rapid clearance of bacteria from the lungs by activating alveolar macrophages and increasing neutrophil recruitment to the lungs, respectively (11, 60). In a urinary tract infection model with E. coli, P. aeruginosa, and methicillin resistant Staphylococcus aureus, αGalCer treatment enhances antibacterial effects (61). α−galactosylceramide treatment has also been shown to be protective in mice infected with intracellular fungi and bacteria. During C. neoformans infection, αGalCer treatment enhances clearance of fungi from the lungs and spleen through an enhanced Th1 response (62).

When mice infected with L. monocytogenes, an intracellular Gram-positive bacterium, are treated with αGalCer, bacterial numbers in the liver, Buspirone HCl spleen and peritoneal cavity decrease compared to control mice (63). iNKT cells stimulated by αGalCer enhance the killing of L. monocytogenes in macrophages with an increased respiratory burst (63). Similarly, in M. tuberculosis infected mice, αGalCer treatment prolongs survival and decreases the bacterial burden and tissue injury in the lungs (64). Furthermore, a combination of αGalCer and isoniazid, a first line antibiotic for tuberculosis, reduces bacterial numbers in the spleen and lungs in mice significantly more than does isoniazid alone (65). Human iNKT cells have also been shown to have lytic activity involving granulysin (an antimicrobial peptide) against M. tuberculosis infected APCs, and this is greatly enhanced by αGalCer (22).

Homogenous and inverted face control conditions indicated that infants’ preference was not driven by the majority of faces in arrays or by low-level features. Thus, 3.5-month-olds found the presence of an other-race face among own-race faces to be more salient than the reverse configuration. selleck products This asymmetry suggests sensitivity to an ORF at 3.5 months. Thus, a key mechanism of race-based processing in adults has an early onset, indicating rapid development of specialization early in life. “
“How do infants use their knowledge of native language sound patterns when learning words? There is ample

evidence of infants’ precocious acquisition of native language sound structure during the first year of life, but much less evidence concerning how they apply this knowledge to the task of associating sounds with meanings in word learning. To address this question, 18-month-olds were presented with two phonotactically legal object labels (containing sound sequences that occur frequently in English) or two phonotactically illegal object labels (containing sound sequences that never occur in English), paired with novel objects. Infants were then

HDAC inhibitor tested using a looking-while-listening measure. The results revealed that infants looked at the correct objects after hearing the legal labels, but not the illegal labels. Furthermore, vocabulary size was related to performance. Infants with larger receptive vocabularies displayed greater differences between learning of legal and illegal labels Interleukin-2 receptor than infants with smaller vocabularies. These findings provide evidence that infants’ knowledge of

native language sound patterns influences their word learning. “
“The primary purpose of this study was to examine the association between prenatal cigarette exposure and physiological regulation at 9 months of age. Specifically, we explored the possibility that any association between prenatal cigarette exposure and infant physiological regulation was moderated by postnatal environmental tobacco smoke (ETS) exposure or infant gender. We evaluated whether male infants with prenatal cigarette exposure or infants who were also exposed to ETS after birth had the highest levels of physiological dysregulation. Respiratory sinus arrhythmia (RSA) was obtained from 206 (142 exposed and 64 nonexposed) infants during a baseline period and during procedures designed to elicit both positive and negative affect. There was a significant suppression of RSA during the negative affect task for nonexposed infants, but not for exposed infants. Postnatal ETS exposure did not moderate this association; however, gender did moderate this association such that boys with prenatal cigarette exposure had a significant increase in RSA rather than the suppression seen among both nonexposed boys and girls. These results provide additional support for the idea that boys are particularly vulnerable to the effects of prenatal cigarette exposure.

On the other hand, for those mice surviving until day 40, the cytokine response reflects protective immunization plus a controlled infection. With i.p. vaccinated mice, the expression levels of cytokine transcripts clearly indicated a mixed Th1/Th2 response.

Thus, the presence of recNcPDI in the nanogel formulations led to IL-4 expression levels similar to what was found in spleens of mice vaccinated with recNcPDI and SAPs alone. With the exception of the group vaccinated with chitosan/alginate-mannose nanogels carrying recNcPDI, the levels of IL-10 and IL-12 transcripts were increased in all vaccinated groups compared with the saponin control group. While the bias for IL-12 would suggest click here a Th1 bias, this may be reflecting an influence of the nanogels in promoting immune effector defence development.

Ratios favouring IL-12 over IL-10 are seen with developing effector immunity, while ratios favouring IL-10 tend towards more regulatory and tolerogenic pathways. In i.n. vaccinated mice, the diminished cerebral infection intensity is also associated with a mixed Th1/Th2 cytokine response. However, in contrast to the i.p. vaccination, i.n. vaccination with vaccine antigen free of nanogels induced an immune response favouring a higher IL-10 to IL-12 ratio. The ratio was not so biased towards Tyrosine Kinase Inhibitor Library IL-10 to suggest a regulatory pathway, but more being suggestive of a Th2-biased immune response. Certainly, this may be seen as relating to the protection against disease and relates to the conclusion of Debache et al. (19) of a Th2-biased response based on antibody isotype profile. However, the cholera toxin control group (CT) displays a similar cytokine profile, and no significant protection is achieved in this group. Moreover, vaccinations with the chitosan/alginate nanogels reduced the IL-10

levels to be on a par with those of IL-12. As for the mannosylated nanogels, these induced an IL-10 to IL-12 ratio clearly in favour of IL-12. While IFN-γ was similar in all groups, IL-4 was reduced with mice given the nanogels, particularly the mannosylated nanogels. Overall, it is possible that particular delivery vehicles may bias the immune response Celecoxib towards a more active rather than regulatory response with respect to IL-12 levels compared with IL-10. There may even appear to be a more Th1 or Th2 or mixed profile. However, it seems clear that these are not the sole factors determining protection. Other factors, such as the innate responses, are likely to be important for determining the protective effects of nanogel-delivered vaccines. In conclusion, this paper reports on the use of chitosan-based nanogels (with or without mannosylated surfaces) as a delivery system for the vaccine candidate recNcPDI in a nonpregnant mouse model for neosporosis, employing i.p. and i.n. antigen delivery. We showed that i.p.

Developing B cells in the bone marrow express CD25 during the pre-B-cell stage [8, 9] but the function of CD25 on these immature B cells is largely unknown as they do not proliferate in response to IL-2 MK-1775 ic50 [9]. CD25+ B cells in the periphery are today believed to be activated B cells; however, most of these studies are performed in vitro [10] and very little is known about the expression of CD25

on B cells after activation in vivo. The CD25+ B-cell population consists of about 1% of the whole B-cell population in a naïve mouse spleen and previous studies have revealed considerable phenotypical difference between the CD25+ B cells in bone marrow and those present in secondary lymphoid organs [2]. While CD25+ B cells isolated from bone marrow displayed an immature phenotype, CD25+ B cells isolated from secondary lymphoid organs display a more mature and activated phenotype when compared with XL765 cell line CD25− B cells characterized by higher expression

of surface IgA and IgG as well as a higher expression of the costimulatory molecules CD80 and CD86 [2]. In addition, we have shown that human circulating CD25+ B cells display different phenotypic and functional properties when compared with the CD25− B cells. CD25+ B cells performed significantly better as antigen-presenting cells in allogeneic mixed lymphocyte reaction (MLR) and B cell–specific blocking of the CD25 expression led to abrogation of the

MLR. CD25+ B cells also expressed significantly higher levels of surface immunoglobulin but lacked the ability to secrete them [3]. Overall, the human CD25+ B cells display a more mature phenotype and seem belong to the pentoxifylline memory B-cell population [4]. The aim of this study has been to analyse the functional properties of CD25+ B cells in mice with respect to immunoglobulin and cytokine production, antigen presentation, migration and homing. Our results clearly show that CD25+ B cells are highly differentiated and might belong to the memory B-cell subset. Mouse strains.  Naval Medical Research Institute (NMRI) and C57BL/6 female mice were used. C57Bl/6 mice were used only in the mixed lymphocyte reaction experiments. Permission from the local animal research ethics committee, in accordance with national animal welfare legislation, was obtained for all the mice experiments. B-cell isolation.  Spleens were passed through a 70-μm nylon mesh (BD Bioscience, Erembodegem, Belgium) into a Petri dish containing 10 ml phosphate-buffered saline (PBS). Cell suspension was centrifuged; the pellet resuspended in NH4Cl solution (0,83%, pH 7.29) and kept on ice for 7 min to lyse erythrocytes, followed by two washing steps in cold PBS. The cells were counted and incubated with optimal concentration of Fc-block (2.4G2; BD Bioscience) for 8 min at room temperature to avoid unspecific binding via Fc-receptor interaction.

14% vs. 89.27%) with a statistical significant (P < 0.005).

The device was most effective in ENT (94.6% vs. 84%), breast reconstructive surgeries (97.3% vs. 82.36%), and orthopedic oncology (97.37% vs. AZD6244 mw 83.72%), whereas with reanimation operations and trauma/orthopedics subspecialties, it showed no necessity. In neurosurgery and in other/esthetic surgeries, the study was too small to draw definite deductions. We recommend the usage of the implantable Doppler probe as an effective monitoring system for free-flap surgeries, with emphasis on subspecialties where the device demonstrated better results than traditional monitoring methods. © 2010 Wiley-Liss, Inc. Microsurgery, 2011. “
“In this study, we introduced scalp reconstruction using free anterolateral thigh (ALT) flaps and evaluated postoperative outcomes in nine patients between March 2000 and April 2012. Five patients had problems of exposed prosthesis, three required reconstruction after resection of scalp tumor and one patient presented with third degree flame burns of the scalp. All flaps survived without re-exploration, except three flaps with tip necrosis requiring secondary procedures of debridement and small Z-plasty reconstructions. The superficial temporal artery and its concomitant vein were used as recipient vessels, apart from two cases where previous

surgery and flame burns excluded these choices, for which facial arteries and veins were used instead. Forskolin Primary closure of the donor-site was possible in six cases; with skin grafting

performed for the other three patients. All donor sites healed without complications. Ergoloid The ALT flap offers the advantage of customizable size, option of fascia lata as vascularized dural replacement, and minimal flap atrophy typical of muscle flaps. Indications include very large defects, defects with exposed prosthesis, or defects with bone or dural loss. Our experience lends credible support to the use of customized free ALT flaps to achieve functional and cosmetically superior result for the reconstruction of large scalp defects, especially with bone exposure. © 2013 Wiley Periodicals, Inc. Microsurgery 34:14–19, 2014. Free tissue transfer is often required for large complex defects of the scalp including those with infection, radiation damage, bone loss or prosthesis exposure.[1-4] Although the latissimus dorsi (LD) muscle or musculocutaneous free flaps are acceptable alternative,[2, 5-10] the main disadvantage is of the limited skin paddle, need for skin grafts and significant atrophy of muscle, which lead to palpable or exposed hardware. Alternatives such as the scapular flap, rectus abdominis flap and radial forearm flaps have been described but is limited to smaller sized defects.[11-14] Song et al.[15] first described the anterolateral thigh (ALT) flap in 1984, based on the descending or transverse branch of the circumflex femoral artery.

2b). Immunohistochemistry also shows that the sham-injured urethral sphincters are composed of distinct muscle tissues containing numerous myoglobin- (Fig. 2c) and SMA-positive cells (Fig. 2d). In contrast, the

7-day-old freeze-injured internal urethral orifices appear to be relaxed, creating a larger orifice (Fig. 2e). The injured urethral sphincters show reactive changes, including loss of muscle mass and relative disorganization of the remaining muscle tissues (Fig. 2e). Accompanying these changes is the loss of the majority of the striated and smooth muscle cells (Fig. 2f) and the absence of most myoglobin- (Fig. 2g) and SMA- positive cells (Fig. 2h). These findings of induced ISD-related urinary incontinence are similar to other models of urinary incontinence4,48–50 with respect to loss of striated and smooth muscle and reduced leak point

pressures. The Epacadostat urinary sphincters of patients with post-surgical urinary incontinence are irreversibly damaged. However, this appears not to be the case in our model system. The cell-free injected control rabbits show a weak but natural Z-VAD-FMK molecular weight recovery of striated and smooth muscle cells that is accompanied by a slight increase in leak point pressure. These results are not entirely surprising. Rabbits may have inherently different regenerative powers than humans. Additionally, and of possibly greater importance, the rabbits are young and in good health, in contrast to patients with ISD-related urinary incontinence, who are typically elderly and not in

good general health. In our rabbit model, we intentionally avoided more severe and serious sphincter damage that would have produced irreversible incontinence because of the potential for urethral stricture or perforation, followed by death. Thus, our model is considered to be an Thiamine-diphosphate kinase acute incontinence of relatively short duration. Ten days after harvesting the bone marrow cells and placing them in culture, and 7 days after freeze-injury operation, we divide the rabbits into cell implantation and cell-free injection control groups.3 For the cell implantation group, we implant the 0.5 × 106 autologous bone marrow-derived cells suspended in 100 µL culture medium. A total of 2.0 × 106 cells are injected through a 29-gauge syringe needle into the injured regions at the 3-, 6-, 9-, and 12-o’clock positions. For the cell-free injection control group, we similarly inject 100 µL of cell-free culture medium. The number and volume of the implantation cells are chosen to avoid further damaging the host tissues or the implanted cells due to shear stress. At each operation, the retention of small swellings containing the implanted cells or control media is visually confirmed. At 7 days after cell implantation, the leak point pressure of the cell-implantation group, 13.15 ± 2.