After the initiation of highly active anti-retroviral therapy, one patient presented disseminated lesions, whereas

the other patient’s preexisting lesions worsened and became more extensive. Simultaneously, their CD4 T cell counts increased and HIV viral loads decreased. “
“We report on a dermatophyte infection acquired by a young woman from Germany who had worked in Ghana. The strain isolated from her skin lesions showed morphological and physiological features compatible with Microsporum audouinii but a clearly positive hair perforation test made its definite identification by conventional methods equivocal. A genetic analysis finally unambiguously revealed Microsporum audouinii. This is the first observation of a Microsporum audouinii strain with a positive hair perforation test. The ability to perforate hair may be related to attributes favouring an inflammatory host response. “
“Trichophyton mentagrophytes JQ1 supplier is one of selleck kinase inhibitor the most common dermatophytes causing cutaneous human fungal disease

worldwide. Pubic and/or vulvar localisation of dermatophytosis has rarely been reported and may often be misdiagnosed as bacterial infections. We present a connubial case of severe inflammatory tinea in the genital region caused by T. mentagrophytes. The case illustrates the importance of getting material for cultivation before treatment and emphasises the difficulty of diagnosis selleck chemicals llc and treatment of fungal infections in the genital region. “
“Obwohl nur mäßig immunkompromittiert, erkrankte eine ältere Patientin an Pleuritis, die auf einer Aspergillus fumigatus-Mykose beruhte. Trotz annähernd 6 Monaten Therapie mit oralem Itraconazol erlag die Patientin schließlich der CNPA. Chronische Pleuritis ist offenbar häufig mit dieser seltenen Verlaufsform der Aspergillose assoziiert, die häufig eine schlechte Prognose aufweist. Though not overtly immunosuppressed, an elderly female patient suffered from chronic pleurisy due to Aspergillus

fumigatus. In spite of nearly six months of itraconzole-therapy, she eventually succumbed to CNPA. Pleurisy may be a typical manifestation of this rare mycosis which is often ill fated. “
“A 31-year-old male patient complained of having follicular and brownish red maculopapules along the Blaschko’s lines on the right chest for 2 days. On examination, follicular brownish maculopapules were present on the chest with a uniform size of about 3 mm in diameter. The lesions were isolated without a tendency to merge, giving several S-shaped, band-like appearances. Direct mycological examination of the skin flakes revealed many pseudomycelial hyphae and yeast cells with typical spaghetti and meatball appearance. Wood’s light examination of the lesion revealed a golden yellow fluorescence. A diagnosis of blaschkoid pityriasis versicolor was suggested because of blaschkoid distribution of the lesions in this new variant of PV.

6 Databases searched: The terms used to define ARAS were ‘Renal Artery Obstruction’ (as a MeSH term and text word) and ‘renal artery stenosis’, ‘renovascular disease$’ and ‘renal artery occlusion$’ as text words. To define this further, the terms ‘Atherosclerosis’ and ‘Arteriosclerosis’, as both MeSH terms and text words along with text words ‘angioplasty$’ and ‘stent$’ were searched. In addition, various text words were searched to find references pertaining to distal protection devices. These were combined with the previous search, yielding 27 results. Ovid

MEDLINE (1950–April 2009) was the database searched. The Cochrane Central Register of Controlled Trials and Database of Systematic Reviews were Silmitasertib research buy searched for trials and reviews not indexed in Medline. In addition, the reference lists of manuscripts retrieved by the above method were manually reviewed for additional studies. Date of searches: 2 April 2009. There are no systematic reviews of randomized controlled trials comparing the use of distal protection devices with renal artery stenting to stenting alone. There has been one

PI3K activator randomized controlled trial that compared renal artery stenting with and without a distal protection device (Tables 1–4).7 The ‘RESIST’ study had a 2 × 2 factorial design and randomized patients to an open-label distal protection device or not, and to double blind use of the platelet glycoprotein IIb/IIIa inhibitor abciximab or placebo. The sample

size was based on providing 80% power to detect a difference in glomerular filtration rate (GFR) of 5 mL/min per 1.73 m2 with a standard deviation of 8. The investigators required 85 participants and recruited 100 to allow for 15% loss to follow up. The primary outcome was change in GFR at 1 month measured by the 4-variable Modified Diet in Renal Disease (MDRD) equation and creatinine was measured by an isotope dilution mass spectrometry-traceable assay. In total, 390 patients were screened to achieve 100 randomized patients. Data were available for 91 patients; 5 refused follow up and 4 had insufficient sample to enable analysis. There was a significant decline in GFR in all groups except the group given the combination of distal protection device and abciximab. There was a significant interaction for these therapies at P < 0.05, indicating that the addition of Bupivacaine abciximab to stenting with distal protection was more effective in preventing a decline in GFR than either therapy alone. Analysis of all patients randomized to the distal protection device demonstrated a percent change in GFR of –1 ± 28% compared with –10 ± 20% in those not receiving the device (P = 0.08). For abciximab, this was 0 ± 27% compared with –10 ± 20% in those receiving placebo (P < 0.05). This trial does not provide evidence that the use of distal protection devices prevents decline in GFR but suggests the possibility when used with abciximab.

The current

study examined how attention toward an angry-looking gorilla mask in a room with alternative opportunities for play in 24-month-old toddlers predicted social inhibition when children entered kindergarten. Analyses examined attention to threat above and beyond and in interaction with both proximity to the mask and fear of novelty observed in other situations. Attention to threat interacted with proximity to the mask to predict social inhibition, such that attention to threat most strongly predicted social inhibition when toddlers stayed furthest from the mask. This relation occurred above and beyond the predictive relation between fear of novelty and social inhibition. Results are discussed within the broader literature of anxiety development and attentional check details processes in young children. “
“We explored the role that exogenous and endogenous competitors for attention play in infants’ abilities to encode and retain information over a 6-month period. Sixty-six children visited the laboratory at 15 months, and 32 returned for a second

visit at 21 months. Children observed models of conventional- relation and enabling-relation action sequences. Half the children were distracted by a “Mister Monkey” mechanical toy during the conventional-relation sequence, while the other half was distracted during the enabling-relation sequence. The Early Childhood Behavior Pexidartinib cell line Questionnaire indexed endogenous factors at both ages. Immediate postmodel production of target actions indexed encoding efficiency, and 6-month production Protein tyrosine phosphatase of target actions indexed

long-term recall. The exogenous distracter impacted encoding efficiency (i.e., immediate recall), but not long-term recall. Endogenous factors (i.e., temperament) were primarily associated with long-term recall. Of special interest was our finding that endogenous factors, especially surgency, moderated the effect of the exogenous distracter. It appears that when learning conventional-relation sequences in the presence of exogenous distracters, surgency mobilizes attentional resources toward the learning objective; however, when learning enabling-relation sequences under the same conditions, surgency either boosts the saliency of the distracters or boosts children’s susceptibility to them. “
“Mental rotation involves transforming a mental image of an object so as to accurately predict how the object would look if it were rotated in space. This study examined mental rotation in male and female 3-month-olds, using the stimuli and paradigm developed by Moore and Johnson (2008). Infants were habituated to a video of a three-dimensional object rotating back and forth through a 240° angle around the vertical axis. After habituation, infants were tested both with videos of the same object rotating through the previously unseen 120° angle, and with the mirror image of that display.

The central role of Treg cells in maintaining immune self-tolerance has generated the concept that both Treg number and function represent key factors required for the efficient regulatory effect

of Tregs. Thus, a decrease in the number and/or function of these cells is associated with autoimmunity in many instances,6–8 and an abnormal increase in Treg number and/or function may lead to immunosuppression and defective clearance of pathogens or tumours.9,10 In this study, we found that IFN-α alters the balance between Tregs and Teffs by affecting the number of aTregs that are generated upon T-cell activation. Interestingly, in preliminary studies using purified Tregs and Teffs in in vitro suppression assays, we found that

EMD 1214063 IFN-α had no effect on the function of Tregs (data not shown). Similarly, it has also been found that IFN-I does not account for inhibition of Treg function by TLR-ligand-activated dendritic cells.45 Thus, in contrast to other cytokines such as TNF-α which down-modulate Treg function by directly affecting its activity,46 IFN-α appears to modulate Tregs indirectly by containing their activation/proliferation. Indeed, the finding that IL-2 is substantially down-regulated by IFN-α, and that the exogenous addition of IL-2 reverses IFN-α-induced suppression of aTregs, strongly supports the conclusion that IFN-α restrains Treg expansion indirectly via inhibition of IL-2 production, selleck probably from Teffs. Metabolism inhibitor In this regard, whereas common γ-chain cytokines such as IL-15 and IL-7 may somewhat compensate for lack of IL-2 in thymic development of Tregs, IL-2 remains the dominant cytokine necessary for maintenance, activation, FoxP3 induction and expansion of Tregs in the periphery.34,35,47–49 Thus, although we cannot discount the possibility that other cytokines relevant for Treg homeostasis may also be inhibited by IFN-α, as our assays are based on activation/expansion of peripheral Tregs (but not thymic Treg development) in which IL-2 (but

no other cytokine) appears to play a dominant role,35,47 we strongly believe that IL-2 inhibition is a major mechanism by which IFN-α suppresses Treg activation. Furthermore, as IL-2 is not mandatory to establish Teff functions,35 it may explain the selective effect of IFN-α in suppressing Treg but not Teff activation. In recent years, the study of patients with SLE has revealed a central role for IFN-α in autoimmune disease pathogenesis. Specifically, it has been proposed that IFN-α causes differentiation of monocytes into myeloid-derived dendritic cells39 and activation of autoreactive T and B cells.19 In a parallel manner, cumulative studies have found that Tregs are decreased in subjects with active SLE,8,50,51 and more recently a fine analysis of CD4+ FoxP3-expressing cells demonstrated that aTregs, but not rTregs, are the prominent population of regulatory T cells that is decreased in SLE.

All samples included junctional and sulcular epitheliums and connective gingival tissue. The gingival biopsies were divided into two portions. One portion was immediately placed in microcentrifuge tubes containing 250 μl phosphate-buffered saline and protease inhibitor cocktail (Sigma-Aldrich), and homogenized (Kinematica Polytron PT3100, Littau-Luzern, Switzerland), and then centrifuged at 13,000 g for 5 min at 4 °C. The resulting supernatants, devoid of debris, were stored at −70 °C until subjected to cytokine measurements by ELISA. The additional portion was stored in a tube containing RNA later (Ambion Inc., Austin, TX, USA) and stored at −20 °C for subsequent assays. Enzyme linked

immunosorbent assay (ELISA).  learn more Total levels of IgA were determined by ELISA using microtiter plates (Costar STA-9090 molecular weight 3590, Corning, NY, USA)

coated for 24 h at 4 °C with 2 μg/ml of goat IgG anti-human IgA (Southern Biotech, Birmingham, AL, USA) in carbonate-bicarbonate buffer, pH 9.6. After being coated, plates were washed and blocked for 1 h at room temperature with bovine serum albumin (0.1%) in phosphate-buffered saline (PBS), pH 7.5. Diluted saliva samples (1:200 in PBS) were applied in triplicate, and plates were incubated for 2 h at room temperature. All experiments included serial dilutions (1.0, 0.5, 0.25, and 0.125 μg/ml) of a standard sample of human IgA antibody purified from serum (Southern Biotech). The secondary antibody was biotin-conjugated goat IgG anti-human IgA (Southern Biotech) at a dilution of 1:14,500. After incubation with a solution of streptavidin, conjugated with alkaline phosphatase (Southern Biotech) (1:500 in PBS, pH 7.5), antibody reactions were revealed by incubation with the substrate p-nitrophenyl phosphate disodium. In order to obtain the A405 units, plates were read in an ELISA plate reader (Epoch, Biotek, Winooski, VT, USA). Negative controls included the uncoated wells without saliva and primary antibody. For determination of IgA concentrations, absorbance values were plotted

Thalidomide against the standard curve obtained for the serial dilutions of the purified human IgA within a linear range. IgA levels were expressed as pg/ml of saliva. The gingival biopsies were analyzed by ELISA for IL-4 and IL-10 using commercially available ELISA kits (Quantikine; R&D Systems Inc., MN, USA). Assays were carried out according to the manufacturer’s recommendations using human recombinant standards. The optical density was measured at 450 nm according to recommendation. Results are reported as total amount (pg/mg) of each cytokine. Sites with cytokine levels below the detection limit of assay were scored as 0 pg. RNA extraction.  The gingival biopsies stored in RNA later (Ambion) were evaluated for mRNA levels of IL-4, IL-10, IL-21, IL-21R, CD40L and glyceraldehyde-3-phosphate dehydrogenase (GAPDH).

We conclude that SD-4 is a negative regulator of T-cell allo-reactivity responsible for acute GVHD in animal models. SD-4 selleck kinase inhibitor differs from CTLA-4 and PD-1 by an inability to alter the intrinsic ability of T cells to respond to TCR-activation signals and by lack of influence on Treg-cell function. These attributes support the concept of SD-4 as a new therapeutic mechanism for treating GVHD by blocking allo-reactivity of effector T cells while sparing Treg-cell activity. We thank Irene Dougherty and Megan Randolph for technical and secretarial assistance. This research was supported by National Institutes of Health grant (AI064927-05)

and a Pilot and Feasibility Study Grant from Galderma. The authors declare no competing financial interests. “
“With the introduction of the Haemophilus influenzae serotype b (Hib) vaccine, invasive Hib disease has decreased substantially, but nontypeable H. influenzae (NT Hi) disease appears to be increasing. In order to understand the origin of NT Hi strains and their relationship

with serotypeable strains, we analysed 125 NT Hi isolates collected from individual patients with either invasive disease (70 isolates) or Ribociclib purchase respiratory tract infections (55 isolates). Serotype-specific and capsular transport genes were absent by PCR analysis, confirming their nonencapsulated status, which also suggested the NT Hi isolates were not encapsulated strains that shed their capsules. Multilocus sequence

typing confirmed the NT Hi isolates did not have the same genetic background as serotypeable strains, including Hib. Despite the genetic heterogeneity found, two major genetic clusters were identified, both containing Montelukast Sodium invasive and respiratory isolates. Fourteen invasive isolates and nine respiratory isolates produced β-lactamase and were ampicillin resistant. More invasive (26.8%) than respiratory isolates (10.9%) showed decreased susceptibility towards ampicillin by a mechanism unrelated to β-lactamase production. Besides a change in the capsule status of invasive Hi strains, the burden of invasive Hi disease, which used to be mainly a childhood disease, has now shifted to involve both adults and infants. Haemophilus influenzae (Hi) is an obligate parasite of the human respiratory tract and causes a variety of systemic and localized infections. One of the virulence factors of Hi is the polysaccharide capsule. Six different capsular types, a through f, were identified based on specific antisera that recognize antigenic specificities of the different capsular structures. Strains that lack the polysaccharide capsule (nonencapsulated) are termed nontypeable H. influenzae (NT Hi).

, 2007). Taken together, these results indicate that both OspA and OspB play a role in persistence of B. burgdorferi in the arthropod vector. EX 527 in vitro OspD was initially described by Norris et al. (1992) as a 28-kDa surface lipoprotein encoded on B. burgdorferi plasmid lp38. OspD is downregulated in response to temperature and host signals, and OspD expression reaches its peak on the B. burgdorferi surface shortly after tick feeding and detachment (Brooks et al., 2003; Ojaimi et al., 2003; Tokarz et al., 2004; Li et al., 2007; Stewart et al., 2008). Recombinant OspD can bind tick gut extracts, suggesting that OspD is involved in adherence to the

tick midgut (Li et al., 2007). The role of OspD has been examined in vivo, and OspD was not required for infection of mice by needle inoculation or tick infestation (Li et al., 2007; Stewart et al., 2008). Interestingly, at least one report indicates a defect in colonization of the tick midgut by the OspD-mutant strain, but this defect did not

interfere with ability of the OspD-mutant strain to infect naïve mice via tick infestation (Li et al., 2007). Additionally, clinical isolates have been collected that lack OspD providing further evidence that OspD is not required in the natural life cycle of B. burgdorferi (Marconi et al., 1994). BptA (Borrelial persistence in ticks A) is encoded on plasmid lp25 by open reading frame (ORF) BBE16, and proteinase K surface accessibility assays revealed that this lipoprotein is surface exposed (Revel et al., 2005). BptA is upregulated when Selleck Panobinostat grown in dialysis membrane chambers that mimic the mammalian environment (Revel et al., 2002, ID-8 2005). A B. burgdorferi BptA-mutant strain was attenuated compared with wild type after needle inoculation of mice (Revel et al., 2005). While engorged larvae were able to acquire the BptA mutant from infected mice, the mutant spirochetes were significantly reduced in the tick midgut after molting to the nymphal stage, and no BptA-mutant

spirochetes were detected in tick midguts after the ticks fed to repletion (Revel et al., 2005). These data suggest that BptA is important for B. burgdorferi persistence in ticks. OspC is a 22-kDa immunodominant B. burgdorferi lipoprotein that is encoded by circular plasmid (cp) 26 (Fuchs et al., 1992; Marconi et al., 1993; Sadziene et al., 1993; Fraser et al., 1997). Although OspC has been the focus of intense research for over 15 years, the biological role of OspC in the B. burgdorferi enzootic cycle is still under investigation. To date, OspC is widely known for its reciprocal production to OspA and OspB, which has become a prototypical model for the differential gene expression that mediates spirochete transmission from the arthropod to the mammalian host (Radolf & Caimano, 2008).

This could imply a signalling Selleck R788 defect in both pathways or, alternatively, it could indicate that B cells from CVID patients die in culture after stimulation. In this study we evaluated the effect of IL-21 on spontaneous and TLR-9-, CD40- or BCR-induced apoptosis or proliferation of CD27– and CD27+ B cells from CVID patients. The aim of the study was

to ascertain if differences in response between controls and patients could determine a different fate of CD27– and CD27+ B cells and explain the imbalanced B cell homeostasis and finally immune deficiency in CVID patients. Twenty-two CVID patients were selected according to diagnostic criteria of the International

Union for Immunological Societies scientific group for primary immunodeficiency diseases. Patients were classified into three groups according to Piqueras et al. [8]: (i) CVID patients with a low percentage of CD27+ (memory selleck products phenotype) B cells or MB0; (ii) patients with normal IgD+CD27+ (non-switched-memory phenotype) and a low percentage of IgD–CD27+ (switched-memory phenotype) B cells or MB1; and (iii) patients with normal percentages of CD27+ B cells or MB2. Patients received intravenous gamma globulin therapy every 21 days and did not suffer from infections at the time of the study. Peripheral blood samples were collected before gamma globulin replacement.

Table 1 summarizes the patients’ age, gender and percentages of B cell subpopulations. Twenty-two age- and sex-matched healthy blood donors were included as controls. The study was conducted according to the ethical guidelines of the 1975 Declaration of Helsinki and Adenylyl cyclase approved by CEIC (Balearic Islands Clinical Research Ethics Committee; IB 1564/11 PI). Informed consent was obtained from all subjects. Peripheral blood mononuclear cells (PBMC) were isolated from 40 ml of heparinized blood by density gradient centrifugation. B lymphocytes were obtained from PBMC by negative selection using the Dynabeads UntouchedTM human B cells separation kit (Dynal; Invitrogen, Carlsbad, CA, USA), according to the manufacturer’s instructions. CD27– and CD27+ B cells were sorted from 4 × 106 purified B cells using a Coulter Epics Altra HypersortTM system (Beckman Coulter, Brea, CA, USA). Purified B cells or sorted CD27– and CD27+ B cells were resuspended in RPMI-1640 medium supplemented with 10% heat inactivated fetal calf serum (FCS), glutamine (2 mM) and antibiotics (penicillin and streptomycin). Purified B cells (1 × 106/ml) were labelled during 5 min at room temperature (RT) (25°C) with 1 μg carboxyfluorescein succinimidyl ester (CFSE) (Invitrogen), following the manufacturer’s instructions.

[74] AngII facilitates inflammatory cell chemotaxis and upregulates genes that encode pro-inflammatory proteins, including nuclear factor (NF)-κB and monocyte chemoattractant protein (MCP)-1.[75] Thus, mast cells may contribute to inflammation in ADPKD by facilitating chymase and AngII production. Although macrophages are typically recruited during infection,[76] they have been identified in both infected and non-infected ADPKD kidneys.[11] Moreover, interstitial inflammation has been observed in adult ADPKD patients with Maraviroc nmr no history of renal infection and in newborn ADPKD infants.[77] Although this does not exclude infection as a

cause of macrophage infiltration, it indicates that macrophage infiltration probably is an intrinsic feature of ADPKD pathophysiology rather than an anti-microbial response. If so, pro-inflammatory chemoattractants and cytokines may be the chief mechanisms promoting inflammatory cell accumulation in PKD. MCP-1 (or Ccl2) is a chemokine that recruits monocytes and other cells to regions of inflammation,[78, 79] and mediates cell infiltration in renal inflammatory states including diabetic nephropathy[80] and glomerulonephritis.[81] MCP-1 has been detected in the cyst fluid

of ADPKD patients.[82] Furthermore, urinary MCP-1 levels were higher in ADPKD patients compared with non-ADPKD individuals (mean 511 pg/mL vs 194 pg/mL).[82] Higher MCP-1 was associated with worse renal function (as assessed by serum creatinine).[82] More recently, the longitudinal CRISP (Consortium for Radiologic check details Imaging Studies of PKD) study identified that a urinary MCP-1 level above 410 pg/mg was a predictor of stage 3 chronic kidney disease in ADPKD (sensitivity 0.80, specificity 0.62; P = 0.02).[83] Animal models Forskolin cell line of ADPKD display abnormalities in MCP-1 that parallel those observed in humans. In Han:SPRD rats, renal MCP-1 mRNA was elevated in homozygous rats compared with wild-type controls.[35] Homozygous animals consistently

displayed higher MCP-1 mRNA expression compared with heterozygous and wild-type rats until postnatal week 3, whereby the homozygous animals died of renal failure. Heterozygotes displayed higher MCP-1 mRNA expression compared with wild-type rats at all stages of life.[35] Heterozygous males also displayed higher MCP-1 mRNA than females, in whom disease progression was slower and less severe.[35] Furthermore, the elevations in MCP-1 mRNA coincided with increased numbers of CD68-positive macrophages,[35] suggesting that the chemoattractant may have induced inflammatory cell infiltration. Preliminary data also show that cpk mice with a knockout of Ccl2 have improved renal function as assessed by BUN, compared with cpk/Ccl2+/+ mice.[84] An in vitro model also confirmed that Pkd1−/− (PC1-deficient) tubular cells have significantly higher expression of MCP-1 mRNA than Pkd1fl/− cells.

As shown in Figure 1A, apomorphine-induced rotations reached seven turns per min at 2 weeks and increased gradually from week 2 to week 5 after a LY294002 ic50 unilateral injection of 6-OHDA into the right MFB. No rotations (0 turns per 30 min) were observed during 5 weeks of testing in the sham group. To evaluate alterations of dopaminergic neurones in substantia nigra, immunostaining and Western blot

analyses were performed to examine TH expression. In the sham group, TH expression remained relatively stable at several time points after operation; therefore, we utilized saline-lesioned rats at 2 weeks after lesion as a control for the PD group. FEZ1 and GFAP performed similar comparison. Western blot analysis showed that in 6-OHDA-lesioned rats, TH immunoreactivity gradually decreased, in a statistically significant manner, from week 2 to week 5 in striatum (Figure 1B,C) and in substantia nigra (Figure 1D,E) selleck chemicals llc of the lesioned hemisphere when compared with the TH immunoreactivity of the sham-operated rats. Relative density of TH/β-actin in 6-OHDA-lesioned rats (0.39 ± 0.02 in striatum and 0.35 ± 0.04 in substantia nigra) at 5 weeks after injury was markedly lower than it in sham-operated rats (0.87 ± 0.07

in striatum and 1.06 ± 0.05 in substantia nigra). The decrease in TH immunoreactivity was further confirmed by Nissl staining (Figure 1F) and TH immunostaining (Figure 1G). 6-OHDA lesions induced a dramatic unilateral loss of dopaminergic neurones in substantia nigra pars compacta of PD rats (F″ and G″) but not in sham-operated rats (F′ and G′). The mRNA expression of FEZ1 in rat striatum and substantia nigra was analysed by real-time PCR. Compared with the sham-operated rats (relative value was 0.033 ± 0.002), the FEZ1 mRNA level in striatum was markedly increased during the initial post-injury period, reached peak level (0.038 ± 0.002) at 2 weeks after

injury, and then gradually decreased (Figure 2A). However, in substantia nigra, FEZ1 mRNA expression levels were significantly enhanced at 2 weeks after injury, peaked at 3 weeks after injury (0.63 ± 0.002 compared with 0.46 ± 0.004 in the sham-operated rats), and then decreased (Figure 2B). FEZ1 mRNA expression level Edoxaban was higher in striatum of the PD group at 2–3 weeks after lesion than in striatum of the sham group. However, in substantia nigra, FEZ1 expression levels were higher in the PD group at 2–5 weeks after lesion when compared with the sham group. We next examined FEZ1 protein expression by Western blot analysis. As shown in Figure 2C,D, FEZ1 protein levels mirrored mRNA levels, as FEZ1 protein levels were significantly increased in striatum at 2 weeks (0.82 ± 0.07 compared with 0.75 ± 0.06 in the sham-operated rats) after surgery compared with the sham group and then decreased to normal levels at 4 weeks after surgery (0.62 ± 0.03).