CXCL12 was shown to play an important role in NK cell migration to the decidua.11,67 CXCR4, which is highly expressed on both peripheral blood CD56bright CD16− and dNK cells seems to be essential for CD56bright CD16− migration, through its interactions with its ligand CXCL12, which is expressed by invasive trophoblasts.11 The CD56bright CD16− peripheral blood NK cells that were attracted to the decidua by the invasive trophoblasts further differentiate

in the decidual microenvironment and acquire dNK characteristics. Other chemokines were also shown to participate in the attraction of peripheral NK cells to the decidua. For example, it was suggested that cytotrophoblasts can attract CD56bright CD16− NK cells by producing MIP1-α.68 In mice, the origin of dNK cells is also not clear. www.selleckchem.com/products/Neratinib(HKI-272).html Murine studies indicate that dNK cells do not self-renew in the uterus, but are rather derived from secondary lymphoid tissue.69 Indeed, it was recently suggested that mouse dNK cells do not originate in the thymus, as they are negative for CD127,18 which

was suggested as a molecular marker of a pathway of mouse NK cell development that originates in the thymus.3 It is possible that mouse dNK cells originate in the Vemurafenib clinical trial small population of NK1.1+DX5+ NK cells that are found in the mouse decidua and resemble peripheral blood mouse NK Gefitinib nmr cells.18 The involvement of chemotaxis in the control of dNK accumulation is still not clear. Studies of CCR2−/−, CCR5−/−, MIP1-α−/− or MIP1-α−/−CCR2−/− null mice did not detect any changes in the localization or activation of NK cells.70 dNK cells might alternatively originate in hematopoietic progenitor cells that reside in the endometrium, proliferate and differentiate into dNK cells during early pregnancy. The presence of hematopoietic stem cells (HSC) in the human endometrium was demonstrated by Lynch et al.71 who showed the existence of a relatively mature HSC population in the endometrium that

does not express lineage-committed markers. Indeed it was shown that when human endometrium was transplanted into NOD/SCID/γcnull mice, there was an increase in NK cell levels by day 28 of the menstrual cycle.72 NOD/SCID/γcnull mice lack T and B lymphocytes, and have extremely low levels of NK cells. Therefore, migration of NK cells from the peripheral blood to the tissue cannot account for the observed increase in NK cell numbers, which was determined by the expression of CD56, which is expressed in human, but not in murine NK cells. Another finding that could support the concept that dNK cells might originate from local stem cells is the expression profile of chemokine receptors in dNK cells. dNK cells express high levels of CXCR3 and intermediate levels of CXCR4.

05, Fig. 1B). We compared the severity of inflammation in the airway between Derf-exposed CD44KO and WT mice. The numbers of total leukocytes, macrophages, and lymphocytes in the BALF of Derf-exposed CD44KO mice were lower than those of Derf-exposed WT mice (p<0.05, Fig. 1B). The number of eosinophils in the BALF of Derf-exposed CD44KO mice was marginally lower than that of Derf-exposed WT mice (p=0.0963, Fig. 1B). Furthermore, accumulation of Th1 and Th2 cells was investigated by counting the number

of CD4+Tim-3+ and CD4+T1/ST2+T cells, respectively, in the BALF. The accumulation of Th2 cells (p=0.0041), but not Th1 cells (p=0.6911), was suppressed in CD44KO mice compared with WT mice (Fig. 1C), after Derf challenge. Therefore, the lack of antigen-induced selleck chemicals llc AHR in CD44KO mice might be caused Ceritinib in vivo by the down-regulation of Th2 cell accumulation in the lung. To investigate the possible roles of various cytokines and chemokines in allergic airway inflammation, concentrations in BALF of Th1

(IFN-γ) and Th2 (IL-5, IL-13) cytokines, and chemokines (TARC, IP-10, and eotaxin) were measured by ELISA. The levels of these cytokines and chemokines in the PBS group of both CD44KO and WT mice were under the detection limits (data not shown). Elevated levels of Th1 and Th2 cytokines were observed in both CD44KO and WT mice after Derf challenge. Th2 cytokine (IL-5 and IL-13) concentrations in the BALF of CD44KO mice were lower than those of WT mice (p<0.05, Fig. 2A), while the amount of IFN-γ in the BALF of Derf-exposed CD44KO mice was higher than that of Derf-exposed WT mice (p<0.05, Fig. 2A). Levels of TARC and eotaxin in the BALF of Derf-exposed CD44KO mice were similar to those of Derf-exposed WT mice, while the IP-10 concentration in the BALF of Derf-exposed CD44KO mice was higher than that in Derf-exposed WT mice

(p<0.05, Fig. 2B). These data demonstrate the possibility that CD44 deficiency not only suppresses Th2-mediated airway inflammation, but also facilitates Th1 development in Derf-sensitized and challenged Vorinostat mouse model. To explore the role of CD44 in the development of Th1- or Th2-biased Th differentiation, antigen-specific antibody production, Derf-specific IgE, IgG1, IgG2c, and Th1, Th2 cytokine levels in the serum were determined by ELISA in Derf-immunized CD44KO and WT mice before and after antigen challenge. Serum levels of Derf-specific IgE (p=0.3472), IgG1 (p=0.1172), and IgG2c (p=0.2948) were not significantly different between CD44KO and WT mice before antigen challenge (Fig. 3A), whereas the serum levels of Derf-specific IgG2c (p=0.0109), but not IgE (p=0.5589) and IgG1 (p=0.8494), were significantly higher in CD44KO mice compared with WT mice after Derf-challenge (Fig. 3B). Before antigen challenge, serum levels of IL-5 (p=0.2347) and IL-13 (p=0.

This latter hypothesis is supported by the fact that in the TCRGV phylogenetic tree the clustering of orthologue TCRGV groups from different species is evident. However, orthology between multiple TCRGC genes is maintained in more closely related

Cetartiodactyla lineages. Within this clade, dromedary TCRGC genes group apart from the other suborders, for which a common ancestor gene can be hypothesized. The TCRGV genes of mammalian and avian species cluster in two main groups that can be further subdivided in distinct subgroups labeled A to H [20, 21]. Dromedary TCRGV1 gene belongs to the mammalian subgroup F (including primates, rodents, lagomorpha, and artiodactyls), and it is most closely related to some ovine and swine TCRGV. Dromedary TCRGV2 gene instead belongs to mammalian see more subgroup H (including carnivores and artiodactyls). Our results also show that dromedary TCRG locus lacks orthologues of the mammalian subgroups A, B, and D, containing ovine and swine gene belonging to ancient cassettes TCRG5 and TCRG1, respectively. Altogether the phylogenetic results for TCRGV and TCRGC genes are in line with the most recent super trees describing the phylogeny selleck products of present-day mammals, in which Camelids are placed in the basal position within Cetartiodactyla [22]. Based on TCRGC sequences, two different

primers were designed and used in a second 5′ RACE experiment to enlarge the variable domain (V-GAMMA) repertoire in spleen (Supporting Information Table 1). Analysis of the sequences shows that Florfenicol only two TCRGJ and two TCRGV genes are expressed in unique combinations: TCRGV1-TCRGJ1-1-TCRGC1 (only 5% of the in-frame clones) and TCRGV2-TCRGJ2-2-TCRGC2. The predominance of one rearrangement might indicate a probable bias in the expression of a single cassette, or alternatively, the expansion of particular clones of circulating γδ T cells. To obtain a larger cDNAs pool representative of the TCRGV1-TCRGJ1-1-TCRGC1 rearrangement, an RT-PCR experiment was conducted on the same Poly-C tailed ssDNA (Supporting Information Table 1). Different CDR3 sequences of the cDNA clones are shown in Figure 3. The CDR3 region is formed by the joining of TCRGV and

TCRGJ genes and by the nucleotide deletion and addition mechanisms typical of the junctional process. Its length varies between 5 and 17 aa (a very similar range of variation has been previously reported in mice and humans). The nucleotide additions detected, whose number varies between 0 and 16, could theoretically produce a diversity of nearly 108 sequences. However, this would probably be a significant overestimate of the actual diversity of the rearranged TCRGV2-TCRGJ2-2 cDNA, since according to our data the addition of G nucleotides (41.7%) is twice more frequent than the addition of A, T, and C nucleotides (19.4% each). Remarkably, when the cDNAs were compared with the parent genomic sequences base changes were observed at many positions especially in the variable domain.

21 Historically, groups of patients in early peritoneal dialysis (PD) programmes were dialysed incentre using intermittent PD. Because PD effluent from HBsAg positive patients is potentially infectious,22 this regular gathering of patients facilitated transmission of HBV. As a consequence, early infection risks were similar for PD and HD.23 With the development of PD as a predominantly https://www.selleckchem.com/products/icg-001.html home therapy, rates of HBV infection in this population have fallen, so that the prevalence of HBV

in PD populations is now heavily influenced by the underlying population prevalence. In countries with very high endemicity of HBV, both PD and HD programmes have similar rates of seropositivity, reflecting HBV acquired before the commencement of dialysis.24,25 Conversely, in countries with low background prevalence, present-day risk Gefitinib of HBV in PD patients is associated with exposure to blood products and previous time spent on HD. The latest US guidelines for HBV infection control in dialysis units were published in 2001.26,27 Other countries have also produced guidelines.28–30 Underpinning these are established infection-control principles. These include vaccination and screening of HD patients, and segregation of those that are infectious. Safe sharp handling is advised, as is avoidance of multidose

vials for intravenous drugs. Other developments that have contributed to a reduction in infection risk include a widespread move from reusable membranes towards disposable dialysers and the introduction of synthetic erythropoietin with a decrease in blood transfusion. Dialysis unit staff members are at risk of infection through exposure Metformin cell line during the dialysis procedure. Infection with HBV compromises their own health, and risks further staff-to-patient transmission of HBV. Vaccination of all dialysis unit staff is recommended by guidelines, and response rates are >90%.31 Non-responders who are

HBsAg positive should be counselled and assessed accordingly, those who are HBsAg negative should be warned to seek post-exposure prophylaxis in the event of contact with potentially infectious blood. Other steps that can be taken to prevent cross infection with HBV between patients and staff include barrier protection, such as wearing gloves and face shields. Cleaning hands and changing gloves between contacts prevents staff infecting one patient from another. Minimizing staff turnover and allocating dedicated staff to infectious patients is important. Full guidelines relating to management of occupational exposure to HBV, including needlestick injuries is available from the Centers for Disease Control.32 Despite the successes of these measures, HBV outbreaks continue to occur intermittently in HD units. These do not point to inadequacies in infection-control guidelines, but rather to shortcomings in following such recommendations.

GRP-78 is a glucose-regulated protein belonging to the HSP-70 family, which is mainly present in the endoplasmic reticulum where it mediates several cellular processes as a chaperon, including protein folding, degradation of misfolded proteins, regulation of calcium homeostatis and sensing the endoplasmic reticulum stress.[32, 37-41] Recent studies indicate that a fraction of GRP-78 is also translocated to the cell surface in many cell types,[41] wherein it acts as the receptor mediating penetration and damage of endothelial cells by Mucorales, leading to the observed angioinvasion.[32] Mice with diabetic ketoacidosis

have an increased expression of GRP-78 in sinus, lungs Apitolisib and brain, and anti-GRP-78 serum can protect such mice from mucormycosis, indicating a plausible role of GRP-78 overexpression in susceptibility of diabetics

to this disease.[32, 39] It is generally believed that distinct clinical presentations of mucormycosis are associated with specific underlying risk factors, with ROC, pulmonary, gastrointestinal and cutaneous types occur in patients with diabetes, haematological malignancies or neutropaenia, severe malnutrition, and trauma or burns respectively.[1, 4-7] However, uncontrolled diabetes has been found as the major factor in all types of mucormycosis in India except the isolated renal form, although ROC manifestation remains the most common clinical type and is significantly associated with uncontrolled diabetes.[1, 4-7, for 20, 21] As the CH5424802 price majority of Indian patients have diabetes and metabolic acidosis as the major risk factors, the principal management modalities in such cases include a control of hyperglycaemia and prompt reversal of ketoacidosis, along with surgical debridement and amphotericin B therapy.[3] It is hypothesised that a decrease in diabetes-associated mucormycosis in USA in recent years may be attributed to an increased use of statins

in diabetic patients and the inhibitory action of statins against mucoralean agents.[42] Although statins are regularly prescribed in Indian patients with diabetes, no fall in the number of diabetes-associated mucormycosis cases has been reported from this country.[3] Therefore, a detailed study is required for assessing the role of statins against mucormycosis. Among the different clinical types of mucormycosis, cutaneous and rhino-cerebral types have a better survival rate due to possibility of an early diagnosis. Though majority of the Indian patients have rhino-cerebral presentation, the mortality rate of mucormycosis remains high (nearly 50%) in India.[4] This is largely due to a delay in seeking medical attention, diagnosis and therapy.[3] Apart from the common clinical types, isolated renal mucormycosis in apparently healthy hosts is being reported as a new clinical entity in India.[4-6, 43] Although the kidney is involved in nearly 22% cases of disseminated mucormycosis,[44] isolated renal mucormycosis is described rarely in literature.

As seen in Figure 1, five RCTs involving 263 patients reported Ccr, the meta-analysis showed that the Ccr level was significantly higher in the groups receiving calcium disodium EDTA as compared with the groups receiving placebo (SMD,

0.68; 95% CI, 0.43 to 0.93; P < 0.00001). These results suggest that calcium disodium EDTA chelation therapy has a significant benefit of retarding the progression MK-1775 cell line of chronic kidney disease in patients with measurable body lead burdens. However, the pooled estimate showed that the calcium disodium EDTA treatment group did not have a significant decrease in urine protein level compared with that of the control group (SMD, −0.17; 95% CI, −0.46 to 0.11; P = 0.24, Fig. 1). The first reported case of nephrotoxicity associated with lead was described more than a hundred years ago. From then on, exposure to lead has been thought of as a risk factor for kidney injury. Because blood lead levels indicate only recent exposure to lead, see more the level of body lead burden is considered as a more accurate indicator

reflecting the lead load in the human body, and urinary lead excretion <600 μg/72 h after calcium disodium EDTA chelation therapy is considered as a normal body lead burden. However, it was found that lead has a direct toxic effect on the kidney even at ‘normal or acceptable’ levels.[2, 3] The pathogenesis of nephrotoxic effects of lead is mainly related to direct toxicity, inflammation and oxidative stress.[2,

13, 14] A growing body of research has shown that lead exposure is a reversible risk factor for CKD progression,[4-9] nonetheless, the optimal strategy to treat lead nephrotoxicity remains uncertain. Chelating agents such as calcium disodium EDTA are widely used to remove toxic metals, and this therapy could exert long-term antioxidant, anti-inflammatory effects.[15] However, lead chelation is controversial owing to the potential of its use in lieu of exposure reduction. In addition, cases of acute tubular necrosis have been reported following early clinical use of calcium disodium EDTA that involved very large doses.[16] Fortunately, adverse renal effects have not been observed Evodiamine at low levels of exposure such as in the trials included in our meta-analysis. The main finding of the current meta-analysis is that calcium disodium EDTA chelation therapy could effectively delay the progression of chronic kidney disease among patients with measurable body lead burdens by increasing the levels of GFR and Ccr. There is no conclusive evidence that chelation therapy with calcium disodium EDTA reduces proteinuria. However, our findings indicate the need to be confirmed by more larger randomized clinical trials. There are several important potential study limitations to this meta-analysis. First, most of the included studies were small-scale studies that may have had patient selection and treatment bias. Second, most studies were not blinded.

CXCR3 is preferentially expressed on encephalitogenic Th1 cells [13, 32, 33], and on T cells that infiltrate PLX4032 research buy MS and EAE lesions [4-6, 9-11], making it a logical therapeutic target for the suppression of Th1-mediated inflammatory demyelinating disease. We found that, even in that special circumstance, blockade of CXCR3, or neutralization

of its primary ligand, had no therapeutic impact on the clinical course of EAE. Similarly, CXCR3−/− Th1 cells were not compromised in their ability to transfer clinical EAE. In fact, WT recipients of CXCR3−/− Th1 cells, or CXCL10−/− recipients of WT Th1 cells, failed to recover following peak disease to the same extent as their WT counterparts (Fig. 2C and F). It is possible that widespread and diffuse parenchymal distribution of effector cells, as described by Muller et al. in MOG-immunized CXCR3−/− mice [17], results in increased axonal damage and long-term deficits. Of note, administration of a mAb specific for CXCR3 was found to be therapeutically beneficial in a Lewis rat model of EAE induced by the adoptive transfer of unpolarized myelin Crizotinib chemical structure basic protein reactive T cells [10]. As in our study, the investigators did not administer Bordetella pertussis toxin (PT) to transfer recipients. The discrepancy between their results and ours

further underscores the heterogeneity of encephalitogenic T cells and reinforces our contention that the importance of a specific molecule as a therapeutic target is context dependent. Other laboratories Pregnenolone have previously reported that Th17 “sentinel” cells traverse the blood–brain barrier at the inception of EAE and release vasoactive substances that permit the subsequent infiltration of Th1 cells [26, 34, 35]. This raises the possibility that in our experimental

paradigms, neuroinflammation is initiated by a minor subpopulation of Th17 contaminants within the pool of IL-12-polarized donor cells. We deem this unlikely since we were unable to detect IL-17+ cells among IL-12-polarized donor T cells. Furthermore, we did not detect RORγt transcripts in mRNA extracted from donor cells immediately prior to adoptive transfer (data not shown). It has also been reported that CNS expression of ELR− CXC chemokines leads to the local accumulation of CXCR3+ Tregs [17, 36]. By extension, mice with a disrupted CXCR3/CXC chemokine pathway could be relatively susceptible to EAE due to a dearth of Tregs in target organ infiltrates. However, we found no difference in the percentage of FoxP3+ T cells in the CNS of WT and CXCL10−/− hosts with Th1-mediated EAE. Similarly, FoxP3+ donor cells occurred at the same frequency in the adoptive recipients of CXCR3−/− and WT Th1-polarized cells (data not shown). We believe that the most likely explanation for the dispensability of CXCR3/CXC chemokine interactions in the manifestation of Th1-mediated EAE lies in the complexity of chemokine pathways that arise at sites of neuroinflammation.

Thyroglobulin elicited CD4+ T-cell proliferation kinetics characteristic of a memory response, but unlike TT the autoantigen provoked the persistent production of IL-10. Though monocytes were the primary producers of IL-10, their IL-10 release depended

on small numbers of IL-10-secreting CD4+ T cells, predominantly of the CD45RO+ memory phenotype. The implications of these findings are discussed. Blood samples were collected after obtaining informed consent in 10-ml PLX3397 BD Vacutainer™ heparin tubes and 10-ml BD Vacutainer™ non-coagulant containing tubes (BD Bioscience, Brøndby, Denmark) Ipilimumab in vivo from 19 healthy volunteers (seven women and 12 men; median age = 37 years, range 20–65) attending the blood banks of Odense University Hospital and Copenhagen University

Hospital, all of whom fulfilled the criteria recommended by the Council of Europe for blood donation. The study was approved by the local ethical committee. Tetanus toxoid (molecular weight 150 000) was purchased from the State Serum Institute, Copenhagen, Denmark. The crude TT extract was purified by filtration on Sephacryl S-300, sterile filtered and diluted to 1 mg/ml in phosphate-buffered saline (PBS). Lyophilized KLH (molecular weight 800 000–900 000), purchased from Sigma-Aldrich, (Vallensbæk, Denmark), was dissolved in

water at a concentration of 1 mg/ml. The TG (molecular weight 670 000), purified from human thyroid tissue, was purchased from Biogenesis Ltd. (Poole, UK). The preparation was > 99% pure with immunoglobulin G (IgG); < 0·4%), IgA (< 0·3%) and IgM O-methylated flavonoid (< 0·3%) as the primary contaminants. The TG was diluted to 1 mg/ml in either PBS or medium (RPMI-1640). Boiling TG has previously been shown to abrogate both the cell-proliferative and cytokine responses induced by this antigen, thereby excluding contaminant LPS as the causative agent.12,13 Phycoerythrin (PE) -conjugated anti-human CD3, peridinin chlorophyll-a protein (PerCP) -conjugated anti-human CD4 and CD14, allophycocyanin (APC) – conjugated anti-human CD45RO and fluorescein isothiocyanate (FITC) -conjugated anti-human CD45RA, all of mouse origin, were purchased from BD Biosciences (Brøndby, Denmark). Peripheral blood mononuclear cells (PBMC) were harvested by density centrifugation (814 g, 30 min) over Lymphoprep© (Axis-Shield Poc AS. Oslo, Norway).

Treg cells were also separated for further analysis of multiple genes important in their function with the use of real-time RT-PCR. We did not observe any difference in Treg percentages between study and control group but there was lower expression of some molecules including transforming growth factor-β and interleukin-12 family members in Treg cells separated from children with MS compared to the healthy subjects. Our study is the first to report significant disturbances in some gene expression in T regulatory cells separated from

children with MS. The results should be useful for further research in this field, including immunotherapeutic Selleck Roxadustat interventions. More than 20 years ago, Reaven has postulated the link between insulin resistance, hypertension and dyslipidemia with an increased risk of cardiovascular diseases in adults [1].

Since Autophagy activator that time, the metabolic syndrome (MS) has been defined as a cluster of risk factors including abdominal obesity, dyslipidaemia, glucose intolerance and hypertension that increase the risk for coronary heart disease. The three current definitions of MS in adults use similar components, but threshold values for those components are different, this is why Reaven disputes their clinical utility [2]. However, because of epidemic of childhood obesity in the last decades, there is increasing interest in identifying children who are at risk for developing cardiovascular diseases in adulthood. The latest definition of MS in children presented by International Diabetes Immune system Federation (IDF) considers the abdominal obesity as essential for the diagnosis; other components (two or more are required) include elevated triglycerides, low HDL cholesterol, high blood pressure and elevated blood glucose [3]. Immunological and

molecular aspects of obesity and MS have been recently intensively investigated (review e.g. in [4]). Many studies suggest that low-grade systemic inflammation plays a role in the pathology of MS (discussed in [5]). Cytokines and chemokines produced by T cells are crucial immune mediators in many pathophysiological obesity-related conditions including atherosclerosis [6, 7]. Recent research in this field concerns T regulatory cells [8]. In the last two decades, there have been tremendous advances in explication of molecular processes which control immune response. One of the most important players in this phenomenon seems to be the small subpopulation of T lymphocytes called T regulatory cells (Tregs). These cells are regarded as the primary mediators of peripheral tolerance and play a pivotal role in the pathogenesis of autoimmune and immunosuppressive diseases. The lack of Treg number and/or function leads to the appearance of autoimmune diseases like thyroiditis, gastritis, insulitis, glomerulonephritis, polyarthritis and others [9].

A schematic representation of “Injury Imatinib types and reconstruction algorithm” is shown in Figure 2. Experience on intraoperative vascular pedicle damage during axillary lymph-node dissection by general surgeon is reported and an algorithmic approach regarding types of injuries and available options to repair them in attempt to salvage the flap is developed. The knowledge of what to expect and what to do,

may reduce the incidence of flap loss and reconstruction failure, thus saving the patient from the additional stress of a second procedure. Every surgeon must be aware of such complications and of the available surgical strategies, being then adequately skilled in the different techniques of breast reconstruction including Autophagy inhibitor microvascular surgery which was required to re-establish blood flow in our cases. “
“The transjugular portosystemic shunt, widely used to treat portal hypertension today, may increase the risk of encephalopathy

and reduce effective hepatic flow. To address these issues, a strategy to produce a portocaval shunt (PCS) with hepatic function using intestinal grafts was conceived, and rat models were developed. We transplanted ileal grafts from wild-type and luciferase transgenic Lewis rats to wild-type Lewis rats, anastomosing the graft mesenteric artery (SMA) and portal vein (PV) to the recipient PV trunk and inferior vena cava, respectively. Recipient survival was significantly longer in the partial PCS model, Thiamet G in which the graft SMA was anastomosed to the recipient PV trunk in an end-to-side fashion, than in the total PCS model, with the end-to-end anastomosis. In the partial PCS model, histological and luminescence analyses showed graft survival for 1 month. These results suggest that intestinal grafts can be maintained in the particular conditions required for our strategy. © 2010 Wiley-Liss, Inc. Microsurgery,

2010. “
“The aim of this study was to evaluate long-term regenerative capacity over a 15-mm nerve gap of an autologous nerve conduit, the biogenic conduit (BC), 16 weeks after sciatic nerve transection in the rat. A 19-mm long polyvinyl chloride (PVC) tube was implanted parallely to the sciatic nerve. After implantation, a connective tissue cover developed around the PVC-tube, the so-called BC. After removal of the PVC-tube the BCs filled with fibrin (n = were compared to autologous nerve grafts (n = 8). Sciatic functional index (SFI) was evaluated every 4 weeks, histological evaluation was performed at 16 weeks postimplantation. Regenerating axons were visualized by retrograde labelling. SFI revealed no significant differences.