The electron micrographs are numerous and high in quality, with clear and concise figure Selleck HIF inhibitor legends which are well referenced within the main body of the text. It is easy to dip in and out of and find the particular area of interest. The editors of this book state that they have not attempted to reproduce previous encyclopaedic texts of TEM in diagnostic

pathology. However for a relatively small book a lot of ground is covered. Chapters cover the ultrastructural pathology of renal disease, transplant renal biopsies, skeletal muscle, nerve, tumours, microbial ultrastructure, ciliary disorders and sperm centriolar abnormalities, lysosomal storage diseases, CADASIL, platelet disorders, congenital dyserythropoietic anaemia types I and II, Ehlers-Danlos Syndrome, and occupational and environmental lung disease. I like the fact that where appropriate many of the chapters start by describing and illustrating ‘normal’ tissue, something you never normally see in diagnostic electron microscopy. The book also covers the practical aspects of electron microscopy, including how to cut up and process samples in order to gain the maximum amount of information from them. Detailed protocols are included and, having had to do TEM on a histological section on a slide for

the first time recently, I can speak from experience and say that the protocols are clear, easy to follow and really do work. There is also a section on trouble shooting problems with sectioning of blocks which is useful, and a discussion of hot topics in modern diagnostic electron microscopy. This includes chapters covering digital imaging LY2606368 research buy in diagnostic EM, the uncertainly of measurement and the impact of microwave technology and telemicroscopy. From a neuropathological point of view the CADASIL chapter provides a logical and practical approach for how to screen the sample for the presence of the classical GOM deposits that confirm a positive diagnosis of CADASIL. The electron micrographs in this chapter show clear examples of the GOM deposits and also show that they should not be confused with other non-specific electron dense deposits often see in samples that are submitted

as possible CADASIL. The chapters on skeletal muscle and nerve Cyclin-dependent kinase 3 cover 64 pages in total and give a good but brief overview of these tissues. The chapters cover practical aspects of how to handle and process these tissues, the ultrastructure of normal tissue, possible artefacts, and pathological changes. The chapter on lysosomal storage diseases is particularly useful for those rare occasions when you see them in clinical practice. The chapter provides a good overview of these diseases, the majority of which have CNS involvement. The chapter contains an array of electron micrographs demonstrating the ultrastructural findings of some of these diseases in skin biopsies, which are the most cost effective first line diagnostic tool in these cases.

cereus and the risk factors for the BSIs. None of the 26 isolates carried the emetic toxin (ces) gene, the NRPS gene or the nheBC gene, which CHIR-99021 manufacturer are usually

detected in isolates associated with food poisoning in Japan (Dohmae et al., 2008), while the genes encoding enterotoxins (EntFM and EntS) and the piplc gene were commonly found. These results support the hypothesis that virulence factors may be different between B. cereus isolates causing systemic infections and those causing food poisoning (Schoeni & Wong, 2005; Dohmae et al., 2008). Thirteen (50.0%) isolates harbored the cytK gene, although Dohmae et al. (2008) reported that this gene was rarely detected in isolates recovered from blood cultures. The diversity of the virulence gene patterns was found to be wide in both the isolates from BSIs and the isolates from contaminated blood cultures. Among 26 B. cereus isolates from blood cultures, the PFGE patterns were different, except for two Torin 1 molecular weight isolates (strains 17 and 25) that showed identical PFGE genotypes and had the same virulence gene profile (group C in Table 2). Nosocomial infections caused by B. cereus have been reported (Bryce et al., 1993; Gray et al., 1999; Van Der Zwet et al., 2000; Dohmae et al., 2008; Kalpoe et al., 2008) and transmission of B. cereus in the healthcare

setting is a serious problem. In this study, no cases of potential nosocomial transmission were found through retrospective else review of the medical records, although the two isolates had identical PFGE genotypes and the same virulence gene profile. The accuracy of antimicrobial susceptibility testings for B. cereus isolates has already been evaluated in some previous studies (Luna et al., 2007; Mérens et al., 2008). Antimicrobial susceptibility determined by the Etest method has shown broad agreement (81.8% for amoxicillin to 96.4% for ciprofloxacin and clindamycin) with broth microdilution data (Mérens et al., 2008). Luna et al. (2007) concluded that

data obtained with the Sensititre automated broth microdilution method were nearly identical to those with the Etest method, except for trimethoprim/sulfamethoxazole. However, only limited information is available concerning the clinical utility and the performance limitations of broth microdilution and Etest methods for determining the antimicrobial susceptibility of clinical isolates of B. cereus. In this study, therefore, we evaluated the antimicrobial susceptibility results obtained with the reference agar dilution, MicroScan broth microdilution and Etest methods. The MicroScan method showed essential agreement and/or categorical concordance with the reference method for levofloxacin, linezolid, and vancomycin, while the Etest method showed the same for clindamycin, gentamicin, imipenem, levofloxacin, and linezolid.

We found no clear difference between the efficiencies of propagation of each strain in NA cells (Fig. 5a). In addition, the growth curves of the RC-HL and R(G 242/255/268) strains in other neural cell lines, such as human neuroblastoma SYM-I and SK-N-SH cells, were almost identical (data not shown). These results indicate that the propagation efficiency of the RC-HL strain in vitro is almost identical to that of the R(G 242/255/268) strain. On the other hand, inconsistent with these IDH phosphorylation results, it was found that the RC-HL strain grew less efficiently in the mouse brain than did the R(G 242/255/268) strain (18),

suggesting that another factor is involved in their different efficiencies in in vivo propagation. Interestingly, we found that infection with the RC-HL strain induces inflammation in the

infected mouse brain more strongly than does infection with the Nishigahara strain (unpublished data). Therefore, it is possible that infection with the R(G 242/255/268) strain induces host immune responses less efficiently than does infection with the RC-HL strain, resulting in more restricted propagation of the RC-HL strain in the mouse brain. We conclude that amino acid substitutions at 242, 255 and 268 in rabies virus G protein affect the efficiencies of cell-to-cell spread, resulting in different distributions of RC-HL and R(G 242/255/268) strain-infected cells in the mouse brain and, consequently, distinct pathogenicities. Although the molecular mechanisms find more Glycogen branching enzyme remain to be elucidated, we clarified here important biological characteristics related to the different pathogenicities of the Nishigahara and RC-HL strains. We believe that this study provides basic information for understanding the pathogenicity of rabies virus, and also for establishing

an antiviral therapy for rabies. This study was partially supported by a grant (Project Code No., I-AD14-2009-11-01) from the National Veterinary Research & Quarantine Service, Ministry for Food, Agriculture, Forestry and Fisheries, Korea in 2008 to M.S. “
“To express the 56-kDa protein of O. tsutsugamushi strain Karp, this protein gene was cloned into pET30a(+) before transforming into host bacteria, E. coli Rossetta. Specificity of the recombinant protein was assessed by ELISA using rabbit sera against common members of the order Rickettsiae and 10 other pathogenic bacteria. After IPTG induction, SDS-PAGE analysis of isolated protein demonstrated a band at approximately 46-kDa. Western blot and mass spectrometry analysis proved that the recombinant protein was expressed successfully. Specificity analysis demonstrated that all sera were negative, except sera against O. tsutsugamushi strains TA763, TH1817 and Kato, B. quintana, A. phagocytophilum, E. chaffeensis and B. bacilliformis.

Conceivably, under conditions of high antigen concentration, the duration of T-cell–APC contacts is longer and sufficient to elicit a chronic inflammatory response. Hence, it has been suggested that the presence of antigen at a relatively low concentration may be protective against inflammation.[54] Further experimentation is required to address this question, as well as the questions of how long are cytokines produced by T cells in antigen-rich versus antigen-poor Maraviroc tissue environments and are effector cytokines retained locally or can they be delivered to several different distant sites. Similar

to the above-described patterns of recirculation and migration of naive, effector and memory CD4+ T cells, recent studies have

also analysed the patterns of recirculation and migration of NKT cells in vivo in mice (Table 4).[60] The pathogenic and protective effects of NKT cell subsets following agonist stimulation in vivo are determined mainly by their timing of activation, structures of lipid antigens recognized, interactions with different Staurosporine nmr DCs and profiles of cytokine secretion. Using structural variants of αGalCer that do not interfere with TCR recognition, it was recently shown that distinct types of CD1d-bearing DCs may regulate the different profiles of cytokines secreted, e.g. Th1-type (IL-12, IFN-γ), Th2-type [IL-4, IL-9, IL-10, IL-13, granulocyte–macrophage colony-stimulating factor (GM-CSF)] or

Th17-type (IL-17A, IL-21, IL-22), by NKT cells in vivo.[32, 60] The list of cytokines secreted by NKT cells include IL-2, IL-4, IL-5, IL-6, IL-10, IL-13, IL-17, IL-21, tumour necrosis factor-α, IFN-γ, transforming growth factor-β and GM-CSF. Hence, depending on the type of specific interactions between subsets of NKT before cells and DCs, the cytokines secreted by activated NKT cells may either activate or suppress adaptive immune responses. Since the strength of a TCR signal may influence the cytokine profile (Th1- or Th2-type) produced, understanding how the TCRs of NKT cell subsets bind to their ligands and subsequently cross-regulate each other’s activity is essential for the development of improved strategies of immune regulation for intervention in autoimmune diseases (Table 5). Considerable recent evidence in favour of a regulatory function of both type I and type II NKT cells suggests that both NKT cell subsets are attractive targets to test in novel immunotherapeutic protocols.[7-14, 61-63] A valuable animal model in which to study the pattern of recirculation and migration of NKT cells in vivo is a mouse in which the green fluorescent protein (GFP) gene is knocked into a lineage-specific gene yielding a heterozygous mouse in which certain leucocytes are fluorescently labelled.[61] The salient features of NKT cell recirculation and migration obtained in such a mouse model are highlighted in Table 4.

Together, these results suggest that there may be a complex relationship between the homeostatic and inflammation-associated production of LPC by APCs and the resulting activation

of iNKT cells and other CD1d-restricted subsets. Another mechanism by which iNKT cell responses may be physiologically modulated is via the regulation of CD1d cell surface expression levels. It has been shown that CD1d is up-regulated on murine macrophages following exposure to IFN-γ and one other signal, which can come from inflammation-associated cytokines SAHA HDAC ic50 such as tumour necrosis factor (TNF)-α, or from microbial infection of the macrophage, or simply from exposure to microbial products.131 As the up-regulated CD1d expression was associated with enhanced iNKT cell activation, this observation suggests that infected and non-infected bystander macrophages might similarly stimulate increased iNKT cell responses. Expression levels of CD1d on human myeloid DCs have been found to be regulated by a type of nuclear hormone receptor called peroxisome proliferator-activated receptor γ (PPAR-γ). Receptors of this family are known to regulate see more the expression of genes involved in energy management (e.g. genes relating to lipid storage, metabolism and transport), as well as genes involved

in inflammatory processes and wound healing.132 Like other receptors of this type, PPAR-γ resides in the cytoplasm in an inactivated state until it binds a specific ligand, generally a hydrophobic or lipidic molecule, whereupon it translocates to the nucleus and acts as a transcription factor for genes that include the appropriate response element sequences.132 Szatmari et al.133 have shown that exposure of DCs to oxidized low-density lipoprotein (LDL) results in the activation of PPAR-γ and transactivation of genes that turn on the retinoic acid synthesis pathway. The resulting production of all-trans retinoic acid eventually leads to activation of retinoic acid receptor-α

(RAR-α), which in turn transactivates CD1d mRNA synthesis.133 Thus, CD1d expression levels are directly modulated by RAR-α, but this pathway can be indirectly activated by exposure to PPAR-γ ligands, including lipids associated with oxidized LDL. As oxidized LDL is an inflammation-associated danger signal Branched chain aminotransferase that may be generated even in the absence of a pathogenic microbial challenge, these results suggest that CD1d expression by myeloid APCs, and consequently NKT cell activation, may be linked to broad pathways of endogenous inflammatory activation. Investigations over the last 15 years have revealed a surprising complexity and variety to the range of interactions between iNKT cells and myeloid APCs. It seems that iNKT cells can induce DCs to become highly stimulatory, but they can also cause them to gain a more tolerizing phenotype.

e. able to induce full T-cell differentiation 27, 38, 39. BALB/c ByJ and OT-I TCR-transgenic (Charles Rivers), C57BL/6J (Janvier), and ubiquitin–GFP-expressing mice 23 (Jackson) were housed and bred R788 in our SPF animal facility. Unless otherwise specified in the legend of the figures, wt C57BL/6 mice were used in the experiments. This study was carried out in strict accordance with the recommendations in the Guide

for the Care and Use of Laboratory Animals of the Commitee of Animal Care and Use of the Regional Cote d’Azur. The protocol was approved by the Committee on the Ethics of Animal Experiments of the Institut de Pharmacologie Moléculaire et Cellulaire (Permit Number: B-06-152-5, delivered by the Veterinary Services of the Alpes-Maritimes Prefecture) and by the animal use committees at the Albert Einstein

College of Medicine. All efforts were made to minimize suffering and provide humane treatment to the animals included in the study. We used the L. monocytogenes 10403s background strain in all experiments, either wt or deleted in the secA2 gene, expressing or not GFP 16. Wt Lm-OVA was a kind gift from Hao Shen (University of Pennsylvania, PA, USA). For infections, Lm were grown to log phase (OD600∼0.05–0.15) in broth heart infusion (BHI) medium (Sigma-Aldrich), diluted in PBS and injected in the lateral tail vein. For Lm titers, organs were Metformin in vitro dissociated on metal screens (water 0.1% Triton X-100), and serial dilutions plated onto broth heart infusion plates. Spleens were digested 20 min at 37°C in HBSS (Invitrogen) containing 4000 U/mL collagenase I (Invitrogen) and 0.1 mg/mL

DNase I (Roche). Red blood cells were lysed for 5 min in 170 mM NH4Cl, 17 M Tris-HCl and pH 7.4. All fluorochrome-labeled mAbs are listed in the Supporting Information Table S1. PE-conjugated LLO91-99/H2-Kd Florfenicol tetramers were obtained from the NIH tetramer core facility. Splenocytes were stained with the specified antibodies in PBS containing 0.5% BSA (FACS buffer). For surface staining, cells were incubated for 20 min on ice. For intracellular staining, splenocytes were incubated for 4 h at 37°C, 5% CO2 in RPMI1640 (Invitrogen) 5% FBS, 2 μg/mL Golgi Plug (BD) with or without 100 nM LLO91–99 peptide (Mimotopes), fixed in 1% paraformaldehyde/FACS buffer 10 min, incubated 20 min in 1× Perm/Wash (BD). Cells were analyzed on a FACSCalibur cytofluorometer (BD). When indicated, cells were sorted on a FACSVantage SE cell sorter (BD). Organs were homogenized in PBS containing a complete protease inhibitor cocktail (Roche), centrifuged 10 min 12 000×g. The supernatants were incubated with the BD Cytometric Bead Assay Flex Sets and analyzed using a FACS Array (BD).

50.3%, p < 0.001) than normal shunts. The possibility of shunt infection was highest of AVG, second of AVFT and lowest of AVF by Kaplan-Meier

survival analysis (p < 0.001). Being older (HR = 1.024, 95% C.I. = 1.001–1.047, p = 0.04) and using AVG (HR = 19.9, 95% C.I. = 4.872–81.25, p < 0.001), AVFT (HR = 6.323, 95% C.I. = 1.066–37.5, p = 0.043) were at significantly higher possibility of developing shunt infection. Patient who had the history of liver cirrhosis had nearly significant higher possibility of developing shunt infection (HR = 2.742, 95% C.I. = 0.995–7.554, p = 0.052). After adjusted by stepwise multivariate Cox proportional hazards regression analysis, using AVG (aHR = 20.04, 95% C.I. = 4.906–81.82, p < 0.001), AVFT (aHR = 6.293, 95% C.I. = 1.061–37.32, p = 0.044), and having liver I-BET-762 purchase cirrhosis (aHR = 2.918, 95% C.I. = 1.059–8.041, p = 0.039) were independent risks factor for shunt infection. Conclusion: For maintenance HD patients, receiving shunt creation with AVG or AVFT and

having liver selleck compound cirrhosis were independent predictors for further possibility of shunt infection. TAKAHASHI RYO1, KASUGA HIROTAKE1, KAWASHIMA KIYOHITO1, MORISHITA REIKO1, MATSUBARA CHIEKO1, KIMURA KEIKO1, TERASHITA YUKIO3, ASAKURA YUSUKE4, HORI HIROSHI2, KAWAHARA HIROHISA1, ITO YASUHIKO5, MATSUO SEIICHI5 1Department of Nephrology, Nagoya Kyoritsu Hospital; 2Department of General Internal Medicine, Nagoya tuclazepam Kyoritsu Hospital; 3Department of Surgery, Nagoya Kyoritsu Hospital; 4Department of Anesthesiology, Nagoya Kyoritsu Hospital; 5Departments of Nephrology and Renal Replacement Therapy, Nagoya University Graduate School of Medicine Introduction: Acquired cystic disease of the kidney (ACDK) is common findings to be seen in chronic dialysis patients, and hemorrhage by spontaneous rupture is rare but it is important as fatal complications.

We report two cases about the spontaneous rupture of renal cysts in ACDK with long-term dialysis patients. Methods/Results: One case was developed for sudden right side back pain in 41-year-old man and carried out emergency right nephrectomy because it presented a shock state. Another one was complained of left lumbago in 42-year-old woman and perinephric hematoma showed a tendency to reduce with conservative treatment. Conclusion: It had developed in each case that we experienced for sharp pain without any cause, and it is necessary to take account of the possibility of spontaneous rupture of renal cysts in ACDK when a dialysis patient is complaining about a sudden pain in one’s back, flank or abdomen. GOH SHI MIN, LIM LYDIA WEI WEI, ONG SIEW KWAN, CHOONG HUI LIN Singapore General Hospital Introduction: Vascular access malfunctions (VAMs) have been one of the main reasons for renal admissions through the Department of Emergency Medicine (DEM) of the Singapore General Hospital (SGH). Inadequate flow problems can be identified early to prevent complete access failure.

2), a time-point at which we found previously that T cells were already primed but anti-TSHR antibodies or hyperthyroidism were not induced [26]. Albeit slightly less effective

selleck chemical than pretreatment (Fig. 3), only 33% of immunized, anti-mCD20 mAb-treated mice became hyperthyroid compared with 73% in immunized, untreated mice (Fig. 4a). Again, the levels of anti-TSHR antibodies were significantly lower in mice that received anti-mCD20 mAb (Fig. 4b). In the third approach, anti-mCD20 mAb was administered to hyperthyroid mice (experiment 3 in Fig. 2). This treatment proved to be ineffective. Thus, the incidences of hyperthyroidism were decreased from 90% in the immunized, untreated mice to 54% in the immunized, anti-mCD20 mAb-treated mice (Fig. 5a), which were statistically insignificantly different. Moreover, the differences in levels of anti-TSHR antibodies check details and TSAb activities were also insignificant between two groups (Fig. 3b,c). Of interest,

immunization with Ad-TSHR289 increased serum concentrations of IgG significantly (Figs 3d and 5d). However, anti-mCD20 mAb had no effect on the basal IgG levels (Fig. 3d). TSHR antigen-specific splenocyte secretion of IFN-γin vitro was used as a measure of T cell activation because we have found previously that this cytokine is indispensable for the pathogenesis of Graves’ disease [27]. In the first experiment, splenocytes were prepared 2 weeks after a single injection of AdTSHR289 from mice which received anti-mCD20 mAb 5 days before immunization (experiment 1 in Fig. 2). Controls were splenocytes from immunized but not B cell-depleted mice, as well as splenocytes from unimmunized mice. In a T cell recall assay, splenocytes from Ad-TSHR289 immunized mice, but not from immunized

and B cell-depleted mice, produced significantly increased amounts of IFN-γ in response to TSHR antigen (Fig. 6a). Thus, anti-mCD20 mAb suppressed antigen-specific IFN-γ synthesis by ∼50%. In the second experiment, T cell recall responses were studied in mice which received anti-mCD20 mAb 10 days after immunization with Ad-TSHR289 (experiment 2 in Fig. 3). Splenocytes were prepared 2 weeks after immunization from these B cell-depleted mice Nutlin-3 mouse and from immunized but not B cell-depleted mice, as well as from unimmunized mice. In this case, splenocytes from both the immunized mice and the immunized and B cell-depleted mice produced comparably increased amounts of IFN-γ in response to TSHR antigen (Fig. 6b). Overall, our findings indicate that B cells are important for disease initiation by stimulating T cell function and antibody production. However, B cell depletion prevents disease induction but is not efficacious once disease is manifested clinically. This study was designed to evaluate the prophylactic and therapeutic potentials of B cell depletion on Graves’ hyperthyroidism in a mouse model.

Hong et al. assessed the risk factors of BPH in 641 South Korean men in a community-based cross-sectional study of male participants aged 50–79 years.21 Age was the only significant demographic risk factor of BPH. The presence of chronic bronchitis and a high prostate specific antigen (PSA) level increased the risk by threefold and twofold,

respectively. The risk decreased find more as drinking frequency increased. Physical activity three to five times a week reduced the risk relative to being active less than twice a week; however, engaging in physical activity nearly every day increased the risk 1.7-fold relative to being active up to twice per week. Interestingly, the risk was decreased as drinking frequency was increased.

However, physical activity three to five times a week reduced the risk relative to less or too much activity. In other studies LUTS have also been associated with lifestyle factors. In the Massachusetts Male Aging Study, 1019 men without prostate cancer were followed up for a mean period of 9 years and it was revealed that high levels of physical activity (top vs bottom quartile kcals/day OR 0.5, CI 1.1–3.0), cigarette smoking (OR 0.5, CI 0.3–0.8) decreased the risk of BPH.22 Total or fat calorie intake, sexual activity Ganetespib mouse level, alcohol intake, BMI, waist-hip ratio (WHR), diastolic blood pressure, history of diabetes, hypertension, vasectomy, or serum levels of androgens or estrogens did not individually predict clinical BPH. However, Rohrmann et al.23 reported that moderate alcohol consumption and physical activity had protective effects against LUTS in older men, but current cigarette smoking was not consistently associated in their studies from the Third National Health and Nutrition Examination Survey (NHANES III) on 2797 men aged ≥60 years. Data from NHANES III also showed a relationship Niclosamide between markers of MS and LUTS, defined as having three of four urinary symptoms (nocturia, incomplete bladder emptying, weak stream, hesitancy).9,23 There is much evidence that BMI or WHR (abdominal obesity) increase the risk of BPH.

The Boston Area Community Health (BACH) survey is a population-based epidemiological survey of a broad range of urological symptoms and risk factors in a randomly selected group of 1899 men.24 Using ATP III guidelines to characterize MS and American Urological Association (AUA) symptom index (AUASI) to assess LUTS, the authors found the interesting result that there is a significant association between MS and voiding symptoms rather than with storage symptoms of LUTS. In the present study, the prevalence of MS increased as AUASI score increased in the mild symptom range (2–7), but stabilized with higher scores (Fig. 1). According to the BACH survey, the overall prevalence of MS was 29% and demonstrated the association of each LUTS and individual components of MS.

gov). Furthermore, a dose-escalating Dabrafenib supplier phase I clinical trial was carried out in on-pump cardiac surgery patients undergoing coronary artery bypass or valve repair, who

were at high risk of developing postoperative acute kidney injury (http://www.clinicaltrials.gov; NCT00733876). Preliminary results have demonstrated that the MSC therapy resulted in no adverse effects. The postoperative length of stay and readmission rate of MSC-treated patients compared to historical matched controls was reduced by approximately 40%. All MSC-treated patients exhibited normal renal function in comparison to approximately 20% of the historical matched controls that developed acute kidney injury.53 Clinical trials investigating the use of MSC transplantation for the prevention of kidney transplant rejection and graft tolerance (http://www.clinicaltrials.gov; NCT00752479, NCT00658073 and NCT00734396), and the treatment of lupus nephritis (http://www.clinicaltrials.gov;

NCT00698191 and NCT00659217) are also currently underway. Despite the current data showing clinical efficacy, the precise manner in which MSC confer renoprotection is not understood. Initial experimental studies carried out PD332991 by Morigi et al.54 and Herrera et al.55 reported that the exogenous administration of MSC to mice with acute renal injury could promote both structural and functional renal repair via the transdifferentiation of MSC into tubular epithelium. However, follow up studies revealed that only 2.0–2.5% of the injected MSC showed engraftment,56 Pembrolizumab clinical trial opposed to a previously reported 22% of cells.55 These reports demonstrate that the direct engraftment of exogenously administered, transdifferentiating MSC is not the predominant

mechanism in which MSC enhance renal repair. There is increasing evidence that MSC can elicit repair through paracrine and/or endocrine mechanisms, where they release trophic growth factors that modulate the immune response and consequently mediate repair.57–64 The ability of MSC to inhibit the release of pro-inflammatory cytokines and secrete a variety of trophic growth factors that, promote angiogenesis, mitogenesis and proliferation while reducing apoptosis may collectively mediate the protective and regenerative effects in the kidney of laboratory rodents (summarized in Table 1).54–70 Recent studies,60,62 have shown that the administration of MSC following ischemia-reperfusion (IR) injury result in a significant downregulation of the expression of pro-inflammatory cytokines such as IL-1β, TNF-α, IFN-γ and suppression of inducible nitric oxide synthase (iNOS) at 24 h post-IR injury. This was coupled with an upregulation of the anti-inflammatory cytokines IL-4, IL-10, basic fibroblast growth factor (bFGF), transforming growth factor (TGF)-α and Bcl-2, which resulted in a reduction in renal injury, increased tubular epithelial proliferation and improved renal function.