7B). In addition, the proliferation of LPL knock-down T cells was attenuated (Fig. 7C). Since the shorter calcium signal of knock-down Fulvestrant datasheet T cells is the consequence of a reduced contact time with APC (Fig. 7A and B), it was tempting to speculate that antibody stimulation of T cells neutralizes this effect as this kind of stimulation is independent on T-cell/APC contact time. This was indeed the case (Supporting Information Fig. 8). In marked contrast to stimulation via APC, stimulation via antibodies induced an equal calcium influx in both control and LPL knock-down T cells. Furthermore, there was no inhibition

of proliferation if LPL knock-down T cells were stimulated via crosslinked antibodies (Supporting Information Fig. 8). Thus, the attenuated proliferation of LPL knock-down T cells upon stimulation with APC may at least rely in part on the reduced contact time and the short calcium signals. The activation of antigen-specific T cells is initiated by interaction of T cells with APC bearing the cognate antigen. Thereby, an ordered contact zone, called IS,

is established. The actin cytoskeleton is indispensable for spatial arrangements of a multitude of receptors and proteins that finally define a mature IS at the T-cell/APC contact zone 9, 30. Intracellular proteins regulating the selective spatio-temporal receptor accumulation to the IS were, however, so far not known. Employing RNAi-guided experiments here, we demonstrate that the actin-bundling BEZ235 order protein LPL is crucial for the stabilization of LFA-1 in the IS, the duration of T-cell/APC contact formation and sustained calcium signaling. Thus, LPL is an important regulator for the temporal organization of IS formation and T-cell

activation. There are a couple of evidences that the initial relocalization of LPL in the IS is dependent on actin polymerization. Thus, LPL completely colocalized with F-actin in the IS and deletion of the actin-binding domains of LPL interfered with its relocalization. Moreover, it was described that T-plastin binds only to newly formed actin Anidulafungin (LY303366) filaments, a process which can be considered as actin–plastin copolymerization 14, 15. Therefore, it is likely that the actin/LPL copolymerization in the IS is the major force that brings LPL in the IS. Vice versa, LPL seemed to stabilize F-actin since LPL knock-down T cells had a reduced amount of total F-actin. Given that LPL might protect F-actin from being depolymerized by cofilin 16, F-actin depolymerization may be enhanced in LPL knock-down cells, whereas actin polymerization may be comparable with control cells. In this scenario, F-actin fibers were smaller, which could contribute to the reduced synapse size. Our data show that actin polymerization and accumulation in the T-cell/APC contact zone are required but not sufficient to establish a mature IS.

Among them, SUI was the most common. Moreover, OAB symptoms in women might relate to BOO. Detailed history taking and sophisticated urodynamic studies are required for a substantial group of female patients with OAB symptoms to make the correct diagnosis and provide optimal therapy. “
“Objectives: The present study investigated CHIR-99021 research buy the early efficacy of naftopidil against lower urinary tract symptoms (LUTS) suggestive of benign prostatic hyperplasia (BPH). Methods: Subjects comprised patients with LUTS suggestive of BPH who were followed prospectively

for 8 weeks. Inclusion criteria were: (i) international prostate symptom score (IPSS) ≥8; (ii) no previous treatment for BPH; and (iii) eligibility for naftopidil monotherapy. IPSS and quality of life index were evaluated, and uroflowmetry and residual urine volume were determined optionally. In the previous study, patients who demonstrated a decrease in total American Urological Association symptom score of 25% or more from baseline were considered responders. The ratio of onset of efficacy of naftopidil was calculated by the ratio of the number of responder in each group with the starting dose. Results: Naftopidil efficacy was analyzed for 243 patients. Significant improvement of IPSS was achieved within 1–3 days after medication. Starting dosage and average dosage were identified as factors associated with the period until onset of

naftopidil efficacy. Onset of efficacy was significantly quicker with a starting dosage of 50 mg/day as compared with 25 mg/day Akt inhibitor (P = 0.0047). However, ratios of onset of efficacy with starting dosages of 25, 50 and 75 mg/day were 77.9, 76.7 and 85.7%, respectively, showing no significant difference between groups (P = 0.7463). Duration to onset of efficacy with naftopidil dosage ≥50 mg/day was 11.2 days, significantly early compared to dosage <50 mg/day. Incidence of adverse effect Cytidine deaminase was 3.8%. Conclusion: Naftopidil showed early effects against LUTS suggestive of BPH within a few days. “
“Objectives: We assessed the efficacy and safety of two α1-adrenoceptor antagonists, tamsulosin and silodosin, in the treatment of male lower

urinary tract symptoms. Methods: Men aged 50 years or older who had a total International Prostate Symptom Score (IPSS) of 8 or higher were enrolled in this study. Forty-six patients were randomized into two groups. Twenty-three patients were initially prescribed tamsulosin 0.2 mg once daily for 3 months, followed by silodosin 4 mg twice daily for 3 months (group T); the other group of 23 patients were initially prescribed silodosin, followed by tamsulosin (group S). Patients then switched to the alternative treatment after a 1-month clearance period. Evaluations included clinical determination of IPSS, quality-of-life index, maximum flow rate and postvoid residual urine volume before and after treatment. Results: A total of 46 men, 23 in group T and 23 in group S, were treated and 41 (89.

SNP information was utilized from NCBI dbSNP Build 126. For each article, abstract and related information such as PMID numbers, journal name, authors’ name and title also were stored in dbPTB. We used the ingenuity pathway analysis (IPA, Ingenuity® Systems, BGJ398 in vitro www.ingenuity.com) to identify pathways and networks involving the genes we identified with significant evidence for their roles in preterm birth. We included the genes and genetic variants identified by curation

and in public databases, largely transcriptome wide array data sets[5, 6] and some proteomic analyses related to preterm birth.[7] The genes identified by the ingenuity pathway analysis were entered into the Kyoto NVP-BEZ235 datasheet Encyclopedia of Genes and Genomes (KEGG) database. We extracted 31,018 articles dealing with PTB from PubMed using SciMiner.

The ‘filtered set’ included 980 articles with likely information from 1200 genes. We ‘accepted’ 142 articles described by a total of 960 unique MeSH terms. These articles provided associations of 186 genes with preterm birth that were accepted as statistically valid by the publishers and the curation team. We next imported 215 genes from both published and public databases containing array data and data from other proteomic analyses. Lastly, we identified and included an additional 216 genes based on the interpolation from pathway analysis. These genes were contained in 173 unique pathways. The work flow supporting retrieval of genes from the literature and public pheromone databases and gene interpolation from pathway analysis is shown in Fig. 1. These results are all retrievable from the publicly available database for preterm birth http://ptbdb.cs.brown.edu/dbPTBv1.php. We have also included the 156,963 SNPs contained with the genomic and flanking regions of each gene in dbPTB. We physically mapped the genomic location for genes in dbPTB. The chromosomes and the number of genes mapped to each are

shown in Fig. 2. We identified a total of 25 networks. Several networks including ‘Inflammatory Response, Small Molecule Biochemistry, Cellular Development, Hematological System Development and Function, Cellular Function and Maintenance, Cardiovascular Disease, Connective Tissue Development and Function, Drug Metabolism, Genetic Disorder’ represented the largest portion of interaction domains among the major networks detected. Database for preterm birth allows investigators interested in preterm birth to pursue several query strategies to search related articles, genes, SNPs, chromosomes or keywords against the MeSH terms and abstracts of the curated articles. This includes the authors, the title of the articles, name of the published journal and the link to the original source. There are links to Online Mendelian Inheritance in Man (OMIM), the UCSC Genome Bioinformatics and HGNC.

The tissue fragments were collected with 4-mm punch and fixed in formalin 10%, pH 7·2, and processed by the usual techniques for optical microscopy. At 4th and 8th weeks PI, biopsies from the hind footpads were collected, soaked in OCT medium (Easy Path, Brazil), and immediately frozen in liquid nitrogen. The fragments were stored in freezer at −80°C. Sections from skin were prepared using a cryostat microtome (Leica

Microsystems, Wetzlar, Germany), and fixed in acetone–chloroform (1 : 1) for 10 min at room temperature. After washing in PBS (for 10 min), the endogenous peroxidase and nonspecific binding were blocked with a solution of hydrogen peroxidase 0·3% (10 min) and skimmed milk 6% (1 h),

respectively. Fragments of PF-02341066 cell line skin were Dabrafenib concentration incubated overnight with monoclonal antibodies rat anti-mouse CD207 (BD Bioscience, San Diego, CA, USA) at 1 : 100, CD4 and CD8α (BD Pharmingen, San Diego, CA, USA) at 1 : 160 and 1 : 40, respectively, and hamster anti-mouse CD11c (BD Pharmingen) at 1 : 10 dilution in PBS plus 1% BSA. The biotinylated secondary antibody goat anti-rat immunoglobulin (BD Pharmingen), at 1 : 50 dilution, incubated for 1 h at 37°C was used for CD4, CD8, and CD207, and mouse anti-hamster IgG cocktail (BD Pharmingen) at 1 : 50 dilution for CD11c. The sections were incubated with streptavidin–HRP (Dako, Carpinteria, CA, USA) for 45 min at 37°C. Afterwards, the sections were incubated with diaminobenzidine solution from Liquid DAB+Substrate Chromogen System (Dako) for 5–10 min. The sections were counterstained with Harris Hematoxylin, and the slides were mounted using cover slides and

resin. For quantitative analysis, ten different fields of each section were photographed, and the cell numbers were evaluated with a Carl Zeiss microscope coupled to a computer using the axion vision 5·0 software (Axion Vision, Carl Zeiss Microscopy GmbH, Munich, Germany). The cellular densities were expressed by cells per square millimetre. The paraffin-embedded skin sections were dewaxed and rehydrated, and the antigen retrieval why was performed by steaming in 10 mm citric acid solution (pH 6·0) for 30 min at 95°C in a water bath. Endogenous peroxidase activity was blocked with 3% hydrogen peroxide and nonspecific interactions with a solution of 6% powdered skimmed milk solution. The reaction was developed using, as a primary antibody, rabbit anti-NOS2 polyclonal antibody (Santa Cruz Biotechnology, Santa Cruz, CA, USA) at 1 : 1000 dilution in PBS plus 1% BSA and, as a detection system, NovoLink Max Polymer (Novocastra, Newcastle Upon Tyne, United Kingdom). The sections were counterstained with Harris Hematoxylin, and the slides were mounted using cover slides and resin.

In response to tissue stress, TCR-proximal signals undergo relocalisation toward the basal epidermis and Langerhans cells [4]. This immunological synapse-like activating interaction is uniquely sustained in healthy epidermis and suggests the recognition of physiologically expressed molecules find protocol at steady state. A series of papers was dedicated to the recognition of the

microbial ligand HMB-PP ((E)-4-hydroxy-3-methyl-but-2-enyl pyrophosphate) and related ‘phosphoantigens’ by human Vγ9/Vδ2+ T cells [5], the major γδ T-cell population in peripheral blood and unique to higher primates. Martin Davey from Matthias Eberl’s lab (Cardiff, UK) demonstrated that HMB-PP-producing live bacteria stimulate Vγ9/Vδ2 T cells when phagocytosed by human neutrophils. Traces of soluble HMB-PP

released by neutrophils are then taken up by accessory monocytes and ‘presented’ to Vγ9/Vδ2 T cells, and crosstalk of the three cell types leads to the activation and expansion of Vγ9/Vδ2 T cells as well as survival and differentiation of monocytes and neutrophils (Figure 1). In a related study, Marianne Guenot from Charlotte Behr’s lab (Bordeaux, France) provided evidence that human erythrocytes infected with the malaria parasite Plasmodium falciparum similarly release soluble HMB-PP into the microenvironment where it becomes accessible to Vγ9/Vδ2 T cells [6] (Figure 1). With respect to the molecular IKBKE see more mechanism of ‘phosphoantigen’ recognition by Vγ9/Vδ2 T cells, Emmanuel Scotet and Stéphane Nedellec (Nantes, France) identified an unexpected, but pivotal role for the B7-related protein butyrophilin-3A (CD277) [7, 8]. Agonist antibodies against CD277 sensitise resistant tumour cell lines to Vγ9/Vδ2 T-cell–mediated cytotoxicity, while anti-CD277 blocking antibodies abrogate the response of Vγ9/Vδ2 T cells to aminobisphosphonate-pulsed or Mycobacterium bovis BCG-infected target cells, and exogenous ‘phosphoantigens’ (Figure 1). Cordula Gründer from Jürgen Kuball’s lab (Utrecht, The Netherlands) showed data from an extensive

mutagenesis screening to map the key determinants of phosphoantigen recognition by the Vγ9/Vδ2 TCR, providing important molecular insight into the recognition process and allowing the design of an “ideal” Vγ9/Vδ2 TCR with significantly improved responsiveness both in vitro and in vivo in a humanised mouse model [9]. David Vermijlen (Gosselies, Belgium) showed that the majority of human foetal blood γδ T cells at mid-gestation expresses a semi-invariant public Vγ9/Vδ2 TCR and responds readily to HMB-PP. Interestingly, this population is later on replaced by other γδ T-cell subsets so that Vδ1+ T cells predominate at birth. Another dynamic area of research is γδ T-cell development, with a particular focus on IL-17-producing γδ T cells.

Thus it is conceivable that pathogens control and modulate one, more or even all effector functions of the activated host complement cascade [[7, 8]]. A series of recent studies, in combination with past reports summarized in [[6]] have identified an important role for the activated complement cascade as a central defense element of the human innate immune response [[3, 9-12]]. Predominantly, the C3 effector level of selleck chemical the cascade is considered important for this immediate, first-line response. The C3 effector response is induced by the enzymatic cleavage of the soluble human plasma protein C3 to the effector molecules C3a and C3b (Fig. 1). The activation peptide C3a has antifungal as well as bactericidal activity

and displays chemotactic and inflammatory activities [[13]]. Newly formed C3b is deposited onto a nearby fungal surface and — when not properly controlled and inactivated — surface-deposited C3b initiates the complement amplification loop [[14]]. This loop serves to form additional C3 convertases, which cleave soluble C3 to generate more effector molecules. As a consequence more antifungal

C3a is generated and the fungal surface becomes decorated with C3b. This opsonization is aimed at recognition, engagement, and phagocytosis of the microbial intruder by human immune effector cells, particularly macrophages and neutrophils. Cheng et al. [1], in this issue of the European Journal of Immunology, now demonstrate that Candida infection also activates www.selleckchem.com/products/BIBW2992.html complement via the C5 level, a powerful inflammatory response that acts downstream of C3 (Fig. 1). The C5 complement effector level is reached by the generation of C5 convertases that cleave the plasma protein C5 into C5a and C5b. C5a is a strong inflammatory component that induces a proinflammatory host response and recruits and activates host immune effector cells including macrophages, neutrophils eosinophils, basophils and mast

cells, and other inflammatory cells [[14]]. Newly formed Gefitinib C5b can subsequently initiate and trigger the terminal pathway of complement, which forms the membrane inserting terminal complement complex, (TCC), which is also termed as MAC (membrane attack complex). The article by Cheng et al. [1] now shows that C5a is generated in response to the fungal pathogen C. albicans and induces an inflammatory cytokine response in PBMCs. The inflammatory pathway offers a new concept for understanding the role of the host’s innate immune recognition and defense against C. albicans. Interestingly, the authors study this aspect of this immunological arms race from both sides, from side of the human host and also from side of the fungal pathogen. On the host side, the authors demonstrate a complement-mediated inflammatory cytokine response by PBMCs; furthermore, by identifying host genetic susceptibility factors, they define which step of the cascade mediates this response.

See accompanying article: http://dx.doi.org/10.1002/eji.200940085 “
“Toll-like receptors (TLRs) recognize Selleckchem PD332991 pathogen-associated molecular patterns and results in innate immune system activation that results in

elicitation of the adaptive immune response. One crucial modulator of the adaptive immune response is CD40. However, whether these molecules influence each other’s expression and functions is not known. Therefore, we examined the effects of TLRs on CD40 expression on macrophages, the host cell for the protozoan parasite Leishmania major. While polyinosinic-polycytidylic acid [poly (I:C)], a TLR-3 ligand, lipopolysaccharide (LPS), a TLR-4 ligand, imiquimod, a TLR-7/8 ligand and cytosine–phosphate–guanosine (CpG), a TLR-9 ligand, were shown to enhance CD40 expression, CD40 stimulation enhanced mTOR inhibitor only TLR-9 expression. Therefore, we tested the synergism between CD40 and CpG in anti-leishmanial immune response. In Leishmania-infected macrophages, CpG was found to reduce CD40-induced extracellular stress-regulated kinase (ERK)1/2 activation; with the exception of interleukin (IL)-10, these ligands had differential effects on CD40-induced IL-1α,

IL-6 and IL-12 production. CpG significantly enhanced the anti-leishmanial function of CD40 with differential effects on IL-4, IL-10 and interferon (IFN)-γ production in susceptible BALB/c mice. Thus, we report the first systematic study on CD40–TLR cross-talk that regulated the experimental L. major infection. “
“The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor that mediates immunosuppression caused by a variety of environmental contaminants, such as polycyclic aromatic hydrocarbons or dioxins. Recent evidence suggests that AhR plays an important role in T-cell-mediated

immune responses by affecting the polarization GBA3 and differentiation of activated T cells. However, the regulation of AhR expression in activated T cells remains poorly characterized. In the present study, we used purified human T cells stimulated with anti-CD3 and anti-CD28 Abs to investigate the effect of T-cell activation on AhR mRNA and protein expression. The expression of AhR mRNA increased significantly and rapidly after T-cell activation, identifying AhR as an immediate-early activation gene. AhR upregulation occurred in all of the T-cell subtypes, and is associated with its nuclear translocation and induction of the cytochromes P-450 1A1 and 1B1 mRNA expression in the absence of exogenous signals. In addition, the use of an AhR antagonist or siRNA-mediated AhR knockdown significantly inhibited IL-22 expression, suggesting that expression and functional activation of AhR is necessary for the secretion of IL-22 by activated T cells. In conclusion, our data support the idea that AhR is a major player in T-cell physiology.

TAMs in the colorectal cancer model were also found to produce chemokines that attract T cells (Fig. 3B and C). The attraction of T cells is particularly important Apoptosis inhibitor since T cells are known to be the major effectors in anti-tumour immune responses 11, 13. Amongst these chemokines, CXCL9 and CXCL10, both IFN-γ inducible chemokines, are strong chemoattractants for TH1 cells 26. TH1 cells are important for promoting the killing of tumour cells by cytotoxic T cells 27, 28, and the presence of TH1 cells in colorectal tumours has been correlated with good clinical outcome 11. In addition, TAMs isolated from the co-culture spheroids were capable of stimulating allogeneic T-cell proliferation and activating type-1

T cells (Fig. 4). Taken together, the data suggest that TAMs in colorectal cancers create a type-1 inflammatory microenvironment. These new findings establish the link between clinical observations where (i) a high macrophage infiltration and

(ii) a type-1 adaptive immunity in human colorectal tumours independently have been correlated with beneficial clinical outcomes www.selleckchem.com/products/17-AAG(Geldanamycin).html 11, 29. Importantly, the in vitro findings were also observed in primary colorectal tumour tissues (Figs. 5 and 6). TAMs in vivo were pro-inflammatory, the number of tumour-infiltrating T cells correlated well with the number of TAMs and T cells of the type-1 inflammatory phenotype were present. Notably, the two patients with metastasis of the primary colorectal tumour (25271 and 25316) had the lowest TAM (23–35 TAMs per FOV) and T-cell infiltration (37–55 T cells per FOV, Table 1). Amongst these two patients, the one who isothipendyl had more metastasis and did not survive beyond 5 years (25316) had a lower percentage of IFN-γ-positive TAMs (6.6%) and T cells (45%). This supports our hypothesis that the attraction and activation of type-1 T cells into the tumour by pro-inflammatory TAMs play a crucial role in suppressing tumour progression.

For the first time, we have dissected the potential tumour-suppressive roles of TAMs in human colorectal tumours. The data suggest that in vivo, pro-inflammatory TAMs recruit T cells to the tumour site, present antigens and provide co-stimulating signals to activate the T cells, and subsequently promote the type-1 inflammatory response that leads to downstream anti-tumour immune activities. These findings explain the observation that high macrophage infiltration into colorectal cancers correlates with good patient prognoses. Besides helping us to understand how TAMs execute their tumour-suppressive role, these novel findings will contribute towards the rational design of therapeutic strategies to harness the power of TAMs for cancer treatment in future. It is noteworthy that the tumour types in which TAMs have been observed to exert a tumour-suppressive effect are located in the barrier organs of the body, namely the colon, stomach and skin.

There was a correlation between CD28null/IFN-γ/CD8+ and CD28null/CD137+/CD8+ (Fig. 6)

and CD28null/TNF-α/CD8+ and CD28null/CD137+/CD8+ (r = 0·563, P = 0·015, but no other correlations between any other groups including CD4+ and CD28+ subsets) (all P > 0·05). There was a correlation between BOS grade and CD28null/CD137/IFN-γ/CD4+ (r = 0·518, P = 0·021); CD28null/CD137/IFN-γ/CD8+ (r = 0·861, P < 0·001) (Fig. 7); CD28null/TNF-α/CD4+ (r = 0·487, P = 0·037); CD28null/TNF-α/CD8+ (r = 0·692, P < 0·001), but Deforolimus no other correlations between any other groups, including CD28+ subsets (all P > 0·05). There was a correlation between CD28null/CD8+ T cells and FEV1 (r = −0·675, P = 0·001). There was a significant increase in the percentage of CD28nullCD4+ and CD8CD28null T cells producing IFN-γ and TNF-α than CD28+ subsets (Fig. 8). CD28nullCD4+ and CD8CD28null T cells were more resistant to the inhibitory effects of 10−6 M methylprednisolone on TNF-α and IFN-γ production in vitro compared with CD28+CD8+ T cells. This is the first study to show that CD28 down-regulation on peripheral blood CD8 T cells is associated drug discovery with BOS. Persistent

antigenic stimulation has been shown to down-regulate CD28 expression progressively and irreversibly on CD8+ T cells and also CD4+ T cells, although at substantially lower frequencies, findings consistent with our current selleck chemicals study [16]. We have shown that stable transplant patients have decreased numbers of CD28null/CD4+ T cells compared with healthy aged-matched control subjects, although there were no differences in CD28null/CD8+ cells between these groups, suggesting that current therapeutics may be more effective at inhibiting persistent antigenic stimulation of CD4

rather than CD8+ T cells. However, BOS was associated with increased percentages of both CD28null/CD4+ and CD28null/CD8+ T cells, suggesting that therapeutics fail to prevent oligoclonal stimulation and proliferation of both CD28null/T cell subsets. Furthermore, these CD28null T cells are relatively resistant to a commonly used steroid to treat these patients. Consistent with these findings, a previous study showed that CD28null/CD4+ cells were increased in patients with BOS and that these cells were relatively resistant to the anti-proliferative effects of cyclosporin A [17]. However, although this study showed that CD28null/CD4+ cells were associated with increased granzyme, perforin and proinflammatory cytokines, they did not study CD28null/CD8+ cells nor did they examine other co-stimulatory molecules that may play a role in driving the proliferation and cytotoxic potential of CD28null T cell subsets.

Soluble and insoluble

(guanidine-extractable) pAβ level was measured by ELISA in the midfrontal and parahippocampal cortex in sporadic AD (N = 20, 10 with Braak tangle stages of III-IV and 10 of stages V-VI), DLB (N = 10), VaD (N = 10) and age-matched controls (N = 20). We found pAβ to be associated with only a subset of Aβ plaques and vascular deposits in sporadic and familial AD, with absent or minimal immunohistochemically detectable pAβ in control, DLB and VaD brains. In both brain regions, insoluble pAβ level was significantly elevated only in advanced AD (Braak tangle stage of V or VI) and in the parahippocampus soluble and insoluble pAβ level increased with the number of APOE ε4 alleles. GSK-3 assay These results indicate that

pAβ accumulation in the parenchyma and vasculature is largely restricted to late-stage AD (Braak tangle stage V – VI). “
“Lipoprotein lipase (LPL) is a key enzyme involved in lipid metabolism. Previous studies have shown that the levels of brain LPL mRNA, protein and activity are up-regulated after brain and nerve injury. The aim of this study was to determine the response of expression and activity of brain LPL following acute cerebral ischemia-reperfusion. Adult male Sprague-Dawley rats were subjected to surgical occlusion of the middle cerebral artery. The expression of brain LPL was assessed by immunohistochemical staining and the enzyme activity of brain LPL was evaluated by colorimetric method. Increase of LPL immunopositive cells in the cerebral cortex around the infarction area was observed at 4, 6, 12 h ischemia, 2 h ischemia 2 h reperfusion, and 4 h ischemia 2 h reperfusion. LPL activity this website was significantly decreased in the ischemic side cortex at 2 h ischemia, and then significantly increased at 4 and 6 h ischemia. Our results showed that LPL immunopositive cells were increased in the cortex around the infarction area, and activity of LPL first decreased and then increased following acute cerebral ischemia-reperfusion. These results may suggest that LPL plays a potential role in the pathophysiological response of the brain to cerebral ischemia-reperfusion. “
“Post-polio syndrome

(PPS) characterized next by new neuromuscular problems can appear many years after acute poliomyelitis in polio survivors. We report a 77-year-old man with antecedent poliomyelitis who newly developed neuromuscular disease with a clinical course of 27 years, the final 10 years of which were characterized by apparent progression, thus raising doubt as to the clinical diagnosis of amyotrophic lateral sclerosis (ALS) following PPS. Pathologically, plaque-like, old poliomyelitis lesions were found almost exclusively in the lumbosacral cord, showing complete neuronal loss and glial scars in the anterior horns. Although less severe, neuronal loss and gliosis were also evident outside the old lesions, including the intermediate zone.