A 50-year-old woman, arriving directly from her village in the Kasai-province of the Democratic Republic of Congo was admitted in July 2010 to our department. She presented with painful abdominal distension that appeared 6 months before. Her past clinical history was unremarkable except for a Graves-Basedow disease discovered in 2008 and left untreated. She suffered from chronic weakness and severe dyspnea due to abdominal distention. She had neither ocular

complaint nor cutaneous itching. Physical examination was characterized by extreme cachexia (body weight: 33 kg; body mass index 12 kg/m2), clear lung auscultation, presence of ascites, and the absence of fever. Laboratory tests showed mild leukocytosis (11,490/µL) without peripheral eosinophilia (30/µL). She had moderate microcytic anemia (hemoglobin 10.8 g/dL; MCV 78 fL). C-reactive protein level was 9.3 mg/dL. The thyroid function tests demonstrated Graves’ disease [serum-free triiodothyronine BKM120 level, 9.4 pg/mL (reference range, 2.0–4.0 pg/mL); free thyroxine level, 3.3 ng/dL (reference range, 0.54–1.40 ng/dL); thyroid-stimulating hormone level, <0.003 microU/mL (reference range, 0.34–5.60 microU/mL); and thyrotropin receptor antibodies, 37.6 UI/L (reference value, <1 UI/L)] which was treated upon admission with thiamazol 10 mg b.i.d and levothyroxin 75 µg q.d. Biological liver and

kidney functions were normal. Albumin level was low (2.1 g/dL). Hepatitis B and C serology was not in favor of chronic infection and human immunodeficiency http://www.selleckchem.com/products/Cisplatin.html virus antibodies were absent. Initial cardiac ultrasound showed a mild reduction of the left ventricular ejection fraction (LVEF) at 40% which declined further during the hospital course (LVEF: 20%), despite adequate treatment of thyrotoxicosis. Metabolic and toxic liver disease was excluded (absence of alcoholism, diabetes, dyslipidemia, non-alcoholic steatohepatitis, alpha-1 antitrypsin deficiency, and absence of apparent autoimmune disease). Computed tomography of the abdomen failed to detect any intraperitoneal expansive process. However, large amounts of ascitic and pleural fluids were present. Positron

Emission Tomography did not show any pathological intraperitoneal Fludarabine datasheet activity. Abdominal and pleural paracentesis fluid was citreous and foamy with exudate parameters (protein levels were 39.9 and 42.2 g/L successively). No neoplastic cells were detected. Mycobacterium tuberculosis culture of peritoneal and pleural fluids remained negative beyond 6 weeks. Biopsy of peritoneal tissue showed chronic inflammation without granulomas. Polymerase chain reaction and culture of peritoneal fluid were both negative for M tuberculosis. Filarial serology using an enzyme-linked immunosorbent assay homemade assay (rat antibodies) was positive. Serologies for other helminths were negative. Smears of cytocentrifugated blood and pleural fluids showed the presence of L loa (Figure 1).

These guidelines have used the British HIV Association (BHIVA) standard grading for levels of evidence (see Table 1.1). The translation of data into clinical practice is often difficult even with the best possible evidence (i.e. that from two randomized controlled Selleck Ensartinib trials) because of trial design, inclusion criteria and precise endpoints. Furthermore, many opportunistic infection treatment studies were performed prior to the availability of HAART. A number of newer diagnostic tests and imaging modalities may help to expedite OI diagnosis and allow earlier initiation of specific therapy with

improved outcomes. Recommendations based upon expert opinion have the least evidence but perhaps provide an important reason for writing the guidelines: to produce a consensual opinion about current practice. It must, however, be appreciated that such opinion is not always correct and alternative practices may be equally valid. The recommendations contained in these guidelines should therefore be viewed as guidelines in the true spirit of the term. They are not designed to be restrictive nor should they challenge

research into current practice. Similarly, although the BHIVA Opportunistic Infection Guidelines Group seeks to provide guidelines to optimize treatment, such care needs to be individualized and we have not constructed a document www.selleckchem.com/products/ch5424802.html that we would wish to see used as a ‘standard’ for litigation. The impact

of HAART in preventing opportunistic infection is well established. Whilst HAART is the cornerstone of treatment that leads to resolution or improvement in certain PDK4 OIs, co-prescription of HAART with specific OI treatment is complicated by overlapping toxicities, drug–drug interactions and occasionally a severe immune reconstitution inflammatory syndrome (IRIS), which may complicate the management of both the OI and the underlying HIV infection. Whilst there are limited data with which to provide definitive guidance on when to start HAART in patients with OIs, these guidelines support early initiation of HAART and provide practical information regarding co-prescribing and management of common complications. The clinical care of patients with known or suspected OIs requires a multidisciplinary approach, drawing on the skills and experience of all healthcare professional groups. Moreover, these guidelines emphasize that inpatients with HIV-related disease often need rapid access to a variety of diagnostic tests and radiological interventions that may not be immediately available at local hospitals. Furthermore, expert interpretation of these tests by supporting specialties such as radiology, histopathology, microbiology and virology is often required.

The genomic DNA fragment flanking the transposon was cloned into the pBluescript II SK (+) (pBS, Stratagene) vector at the BamHI site and sequenced

with primers zhang-O and zhang-I (Tian et al., 2010) localized at the two ends of the Tn5 transposon. Using primers hfqT3 and hfqT7 (Table S1), which were designed according to the Tn5-flanking sequence in the PMphlA23 mutant, a cosmid p5-2 was screened out by PCR from a genomic DNA library of strain 2P24 (Wei & Zhang, 2005). A 3.2-kb BamHI fragment from p5-2 was subcloned into pBS, giving rise to the plasmid pBS-hfq. The entire hfq gene was identified by sequencing of this fragment (Fig. 1; accession number FJ960506). The hfq gene in-frame deletion mutant was generated using a two-step homologous recombination strategy. The detailed protocol and PCR primers (Table S1) are given in the online Supporting Information. The hfq gene with http://www.selleckchem.com/products/poziotinib-hm781-36b.html an in-frame deletion was cloned into the suicide plasmid pHSG299 (TaKaRa) see more to generate p299Δhfq (Table 1). Allelic exchange in the wild-type strain 2P24 using p299Δhfq resulted in the mutant PM107 (Δhfq), which was confirmed by PCR amplification (data not shown). For complementation of the strain PM107

(Δhfq), the full-length hfq gene was PCR amplified from P. fluorescens 2P24 with the primers hfq1 and hfq2 (Table S1) and cloned in the shuttle vector pRK415 to generate p415-hfq. For quantitative analysis of 2,4-DAPG production, Pseudomonas test strains were grown in KB liquid media at 30 °C for 30 h. The antibiotic 2,4-DAPG was extracted from the culture supernatant and assayed by HPLC using the method described by Shanahan et al. (1992). For extraction of AHL, P. fluorescens 2P24 and its derivatives were grown in LB liquid media at 30 °C for 30 h. The cell-free supernatants of culture samples (0.8 mL) were extracted with the same volume of ethyl acetate. The extracts were then dried and resuspended in 0.1 mL of methanol. For quantitative analysis of AHL, 3 μL of the samples (the equal volume of methanol as a control) were incubated with 0.2 mL of the AHL Molecular motor biosensor A. tumefaciens

NTL4 (pZLR4) (OD600 nm=0.8). The reaction mixture was incubated at 30 °C for 3 h, and the β-galactosidase activity of the biosensor cells was assayed using the Miller method (Miller 1972). In vitro biofilm formation assays were performed as described previously (Wei & Zhang, 2006). Briefly, test strains were grown to saturation in LB media and then diluted 1 : 1000 in fresh LB media. The diluted culture (0.5 mL) was transferred to a polyvinyl chloride (PVC) plastic Eppendorf tube and incubated without shaking for 12, 24 and 36 h at 30 °C. The resulting biofilm was stained with 0.1% w/v crystal violet for 20 min, and then unattached cells and residual dye were removed. The dye was dissolved in 95% ethanol, and the A570 nm of the dissolved dye was determined.

In addition, the presence of very low-copy plasmids (fewer than five copies) may be constrained by this approach. Plasmid restriction analysis showed a diverse plasmid pool in intI+ strains from wastewaters. In total, 45 different plasmid restriction patterns (similarity < 98%) were obtained (Fig. 1). No restriction

patterns were recovered from six strains (MM.1.10, MM.1.11, MM.1.12, MM.1.14, MM.1.15, MM.1.26), due to low plasmid DNA concentration, which may be due to lower plasmid DNA extraction efficiency and/or very low-copy plasmid number. Restriction patterns did not cluster by species, type of effluent or treatment stage, suggesting a high diversity of backbones and/or accessory elements present in these strains. The results reinforce that wastewaters are reservoirs Talazoparib of diverse mobile genetic elements and hotspots for HGT, as previously reported (Schlüter et al., 2007; Moura et al., 2010). Among donor strains, plasmids Roxadustat were assigned to FrepB (Aeromonas salmonicida, Aeromonas veronii, Aeromonas sp., E. coli, Enterobacter sp.), FIC (A. salmonicida, Aeromonas sp.), FIA (Shigella sp.), I1 (A. veronii, Aeromonas

sp., E. coli), HI1 (E. coli) and U (Aeromonas media) replicons (Table 1 and Fig. 1). Although the presence of broad-host-range IncN, IncQ, IncW and IncP-1 plasmids had been detected in total community DNA obtained from the same environments (Moura Autophagy activator et al., 2010), none of

the donor strains gave positive hybridization signals using probes targeting these groups. Other studies dealing with total community DNA and exogenous isolation of plasmids from urban wastewaters also suggested that broad-host-range plasmids, in particular those belonging to the IncP-1 group, are abundant in wastewater environments (Dröge et al., 2000; Heuer et al., 2002; Schlüter et al., 2007; Bahl et al., 2009). Thus, results obtained here suggest that the hosts of broad-host-range plasmids may probably be noncultivable bacteria and/or bacteria from other taxa than those focused in this study. To date, reported replicons in Aeromonas spp. have been limited to IncU and IncA/C, identified in different aquatic environments. IncU replicons have been reported in Aeromonas caviae, A. media, Aeromonas allosaccharophila, Aeromonas hydrophila and A. salmonicida strains isolated from rivers (Cattoir et al., 2008), lakes (Picão et al., 2008), fish farms and hospital sewage (Rhodes et al., 2000), often associated with tetracycline and/or quinolone resistance determinants. IncA/C plasmids have been reported in A. hydrophila and A. veronii strains isolated from fish carriage water (Verner-Jeffreys et al., 2009).

As the difference between the logarithms of two values is the logarithm of the ratio of these values, we interpreted the meaning of the regression parameters as the percentage increase of the titre per given unit (for continuous factors) or compared to the reference category (for categorical factors). A multivariate logistic model was further developed to analyse the association between given variables and an observed increase in HIV RNA levels between sera obtained ‘PRE’ and

‘POST’ dose [an ‘increase’ was defined as HIV RNA <20 copies/mL at baseline (PRE) and HIV RNA >20 copies/mL after the two immunization doses (POST)]. In addition, clinically significant variables, such as CD4 cell count (<350 and >500 cells/μL) and time since HIV infection, were introduced into the model. The significance Selleck RG7204 Acalabrutinib chemical structure level was defined as 0.05. Data were analysed using s-plus 8.0 (Insightful Corp., Seattle, WA). The clinical characteristics of the 121 HIV-infected patients and 138 healthy controls are described in Table 1. In comparison with the healthy controls, the HIV-infected population included a higher percentage of male (68.6 vs. 42.8% in the controls; P = 0.0001) and non-Caucasian (40.5 vs. 16.7% in the controls; P < 0.0001) participants. The median age of HIV-infected patients was lower than that of the controls (median 46.4 vs. 50.9

years, respectively; P = 0.0005), which was explained by the lower proportion of HIV-positive individuals above 60

years of age (9.9 vs. 28.3%, respectively). As the inclusion criteria for HIV-infected patients required either a very high or a very low CD4 T-cell count, differences in median CD4 cell count, CD4 cell count nadir and disease severity between these two subgroups were significant, as expected (CDC category; Table 1). At the time of enrolment, one-third of HIV-positive individuals with a CD4 count <350 cells/μL had been diagnosed with AIDS. Most patients (108 of 121; 89.3%) Sorafenib manufacturer were being treated with antiretroviral drugs and baseline HIV RNA levels were below the detection level in 88 of 121 patients (72.7%). More HIV-positive patients than healthy subjects had been previously immunized against seasonal influenza (P < 0.0001), in accordance with Swiss recommendations. Five HIV-positive patients declined the second vaccine dose and one left the study area, while 11 HIV-infected individuals and seven healthy subjects did not present themselves to the second study appointment and remained unreachable after three phone calls. Altogether, 104 of 121 (86.0%) HIV-positive patients and 131 of 138 (94.9%) healthy subjects completed enrolment and were included in the final analysis of vaccine antibody responses. During the following season of 2010/2011, 66 of the originally 121 patients (54.5%) agreed to participate in the follow-up study and provide plasma samples prior to and following one dose of nonadjuvanted trivalent seasonal influenza vaccine.

Hypertension was the most frequent type of CVD. However, the recorded frequency of CVD in high-altitude mountaineers is lower compared to hikers and alpine skiers. Mountain BTK inhibitor screening library sports have become very popular, and the number of tourists visiting altitudes above 2,000 m worldwide is estimated to be more than 100 million per year.1 The majority of them perform alpine skiing or hiking. High-altitude mountaineering represents a further popular mountain sport in high mountain areas. High-altitude mountaineering in this article is defined as (1) ascending

on foot to altitudes >3,000 m and (2) crossing glaciers using harness, rope, and, if necessary, crampons. High-altitude mountaineers hike on trackless terrain (eg, snow, rocky passages, and glaciers) with rather heavy equipment. The characteristics of high-altitude mountaineering challenge the technical skills and endurance of the participants and can elicit high exercise intensities. Therefore,

high-altitude mountaineering has to be distinguished from other mountain sports such as alpine skiing, hiking, or ski mountaineering. High-altitude mountaineering is associated with manifold risks (eg, slips and falls, breaking into crevasses), but about 50% of all Selleck AZD2014 fatalities during mountain sport activities are sudden cardiac deaths.2 Although sojourns at moderate altitude are well tolerated by persons with cardiovascular diseases (CVD),3 preexisting CVD are associated with an increased risk for fatal and nonfatal cardiac events during high-intensity exercise and mountain sports.2,4,5 Previous studies on different mountain sport activities have shown a mountain sport-specific prevalence of CVD. The frequency of persons with known CVD was 12.7% in hikers and 11.2% in alpine skiers,6 whereas it was considerably lower (5.8%) in disciplines with high psychophysiological demands such as ski mountaineering.7

This might also be assumed for high-altitude mountaineers. Despite the increasing popularity and the specific conditions of high-altitude mountaineering, epidemiological Unoprostone data on its participants are lacking. Therefore, the goal of this survey was to evaluate the prevalence of preexisting CVD among high-altitude mountaineers. We studied a cohort of high-altitude mountaineers (target sample size n = 500) using a standardized questionnaire (in German), which was tested previously and revised to improve clarity and time efficiency. The questionnaire was validated in patients with various diseases and healthy persons (n = 20). For this purpose, the medical diagnoses of the persons were compared with the results of the questionnaires. The calculated sensitivity and specificity amounted to 100 and 93%, respectively.

Caries experience also increased on buccal-lingual, mesio-distal, and occlusal primary dental surfaces among poor children aged 2–8 years and this increase may be attributed to an increase in the number of dental surfaces restored. In the mixed dentition, caries remains relatively unchanged. Caries continues to decline in the permanent dentition for many

children, but is increasing among poor non-Hispanic whites aged 6–8 years (8–22%) and poor Mexican-Americans aged 9–11 years (38–55%). Conclusions.  MI-503 cost For many older children, caries continues to decline or remain unchanged. Nevertheless, for a subgroup of younger children, caries is increasing and this increase is impacting some traditionally low-risk groups of children. “
“International Journal of Paediatric Dentistry 2011 Background.  Children who have caries in their primary teeth in infancy or toddlerhood tend to develop Selleck Metformin dental caries in their permanent dentition. Although risk indicators are helpful in identifying groups at risk, they give little information

about the causes of difference in caries experience. Aim.  To identify the association between maternal risk factors and early childhood caries among 3- to 5-year-old schoolchildren of Moradabad City, Uttar Pradesh, India. Design.  A total of 150 child–mother pairs participated in the study. The maternal risk factors were assessed by a pretested questionnaire. After obtaining the consent, the mothers and their children were clinically examined for dental caries using Radike criteria (1968). Saliva was collected from all the participating mothers for assessing the Streptococcus mutans level. Results.  Significant differences were found in mothers’ caries activity, high level of S. mutans, educational level, socioeconomic status, frequency of maternal sugar consumption, and

their child’s caries experience (P < 0.001). Conclusions.  Differences between children’s situations in these underlying factors play out as consequential disparities in both their health and the health care they Dimethyl sulfoxide receive. “
“The dental literature is replete with reports on the oral health surveys of normal children. Relatively few data exist for the oral conditions of mentally challenged children and adolescents with multiple disabilities in India. To assess the oral hygiene practices and treatment needs among 6–12-year-old disabled children attending special schools in Chennai, India, between 2007 and 2008. A cross-sectional study data were collected using WHO criteria, a questionnaire (for the parents/guardians) regarding demographic data and oral hygiene practices, medical record review, and clinical examination. Among 402 disabled children, majority of the children brushed their teeth once daily (89.7%) and with assistance from the caregiver (64.4%). The utilisation of the dental services was minimal (extractions 14.4%, oral prophylaxis 1.7%, and restorations 1.7%).

Caries experience also increased on buccal-lingual, mesio-distal, and occlusal primary dental surfaces among poor children aged 2–8 years and this increase may be attributed to an increase in the number of dental surfaces restored. In the mixed dentition, caries remains relatively unchanged. Caries continues to decline in the permanent dentition for many

children, but is increasing among poor non-Hispanic whites aged 6–8 years (8–22%) and poor Mexican-Americans aged 9–11 years (38–55%). Conclusions.  Ponatinib For many older children, caries continues to decline or remain unchanged. Nevertheless, for a subgroup of younger children, caries is increasing and this increase is impacting some traditionally low-risk groups of children. “
“International Journal of Paediatric Dentistry 2011 Background.  Children who have caries in their primary teeth in infancy or toddlerhood tend to develop Enzalutamide concentration dental caries in their permanent dentition. Although risk indicators are helpful in identifying groups at risk, they give little information

about the causes of difference in caries experience. Aim.  To identify the association between maternal risk factors and early childhood caries among 3- to 5-year-old schoolchildren of Moradabad City, Uttar Pradesh, India. Design.  A total of 150 child–mother pairs participated in the study. The maternal risk factors were assessed by a pretested questionnaire. After obtaining the consent, the mothers and their children were clinically examined for dental caries using Radike criteria (1968). Saliva was collected from all the participating mothers for assessing the Streptococcus mutans level. Results.  Significant differences were found in mothers’ caries activity, high level of S. mutans, educational level, socioeconomic status, frequency of maternal sugar consumption, and

their child’s caries experience (P < 0.001). Conclusions.  Differences between children’s situations in these underlying factors play out as consequential disparities in both their health and the health care they PRKACG receive. “
“The dental literature is replete with reports on the oral health surveys of normal children. Relatively few data exist for the oral conditions of mentally challenged children and adolescents with multiple disabilities in India. To assess the oral hygiene practices and treatment needs among 6–12-year-old disabled children attending special schools in Chennai, India, between 2007 and 2008. A cross-sectional study data were collected using WHO criteria, a questionnaire (for the parents/guardians) regarding demographic data and oral hygiene practices, medical record review, and clinical examination. Among 402 disabled children, majority of the children brushed their teeth once daily (89.7%) and with assistance from the caregiver (64.4%). The utilisation of the dental services was minimal (extractions 14.4%, oral prophylaxis 1.7%, and restorations 1.7%).

1b). However, lopinavir/ritonavir treatments severely

affected the growth of gingival epithelium in a dose-dependent manner when compared with control rafts (Fig. 1a, panels A–X). Further, in the 9.8, 13.5 and 16 μg/mL Cilomilast molecular weight lopinavir/ritonavir treatments, the growth of gingival epithelium was completely obliterated over time (Fig. 1a, panels V, Q, W, F, L, R and X). These results suggested that lopinavir/ritonavir treatments severely inhibited the growth and differentiation of gingival epithelium when the drug was present throughout the growth period. We then decided to start treating the rafts with lopinavir/ritonavir on day 8. Under normal conditions, a developing epithelium with all four strata (basal, spinosum, granulosum and corneum) can be visualized BMS-907351 concentration on collagen matrices by day 8 of tissue growth. Further, starting treatment on 8 day epithelium growth would provide the opportunity

to examine the effect of this drug on developing epithelium as present in the human oral cavity. The raft cultures treated with lopinavir/ritonavir were morphologically similar to control rafts at 2 days post treatment (Fig. 2a, panels A–F). However, at 4 and 6 days post treatment, the cell–cell contacts within the stratified layers appeared to be less tight in rafts treated with 6, 9.8, 13.5 and 16 μg/mL of lopinavir/ritonavir, compared with untreated controls (Fig. 2a, panels G–R). Further, lopinavir/ritonavir treatments at all concentrations interfered with the epithelial stratification and severely compromised gingival epithelial growth and structure at 8 days post treatment (Fig. 2a, panels T–X). these To

study in more detail the effect of this drug on tissue integrity, TEM studies were performed to analyse desmosome configuration in untreated and drug-treated tissue. TEM analysis showed that in untreated tissue the desmosomes were well organized and tightly configured between cells (Fig. 2b, panels A and B). However, in lopinavir/ritonavir-treated tissues desmosomal halves were separated in the intercellular region, which could potentially explain the loss of cell–cell adhesion in lopinavir/ritonavir-treated tissues (Fig. 2b, panels C–F). Upon commitment of gingival keratinocytes to terminal differentiation, a number of biochemical changes occur, namely, the expression of cytokeratins 5, 14 and 10 [28]. Cytokeratins 5 and 14 are normally expressed in the basal cells of gingival stratified epithelium and have been used as proliferative cell markers [28–30]. In our study, lopinavir/ritonavir treatments increased expression of cytokeratins 5 and 14 and altered their expression patterns in a time- and dose-dependent manner (data not shown). Lopinavir/ritonavir treatments dramatically compromised epithelium structure at 8 days post treatment, thereby making it difficult to observe the staining patterns (Fig. 2a, panels T–X).

“
“Agents such as sertindole and astemizole affect heart action by inducing long-QT syndrome, suggesting that apart from their neuronal actions through histamine receptors, 5-HT2 serotonin receptors and D2 dopamine receptors they also affect ether-a-go-go channels and particularly ether-a-go-go-related (ERG) potassium selleck products (K+) channels, comprising the Kv11.1, Kv11.2 and Kv11.3 voltage-gated potassium currents. Changes in ERG K+ channel expression and activity have been reported and may be linked to schizophrenia [Huffaker, S.J., Chen, J., Nicodemus, K.K., Sambataro, F., Yang, F., Mattay, V., Lipska, B.K., Hyde, T.M., Song, J., Rujescu, D., Giegling, I., Mayilyan,

K., Proust, M.J., Soghoyan, A., Caforio, G., Callicott, J.H., Bertolino, A., Meyer-Lindenberg, A., Chang, J., Ji, Y., Egan, M.F., Goldberg, T.E., Kleinman, J.E., Lu, B. & Weinberger DR. (2009). Nat. Med., 15, 509–518; Shepard, P.D., Canavier, C.C. & Levitan, E.S. (2007). Schizophr Bull., 33, 1263–1269]. We have previously shown that histamine H1 blockers augment selleck inhibitor gamma oscillations (γ) which are thought to be involved in cognition and storage of information.

These effects were particularly pronounced for γ induced by acetylcholine. Here we have compared neuronal effects of three agents which interfere with ERG K+ channels. We found that astemizole and sertindole, but not the Kv11 channel blocker E4031, augmented γ induced by acetylcholine in hippocampal slices. Kainate-induced γ were only affected by astemizole. Evoked responses induced by stratum radiatum stimulation in area CA1 revealed that only E4031 augmented stimulus-induced synaptic potentials and neuronal excitability. Our findings suggest that Kv11 channels are involved in neuronal excitability without clear effects on γ and that the effect of astemizole is related to actions on H1 receptors. “
“Extending the classical neurocentric view that epileptogenesis is driven by neuronal

alterations, accumulating experimental and clinical evidence points to the possible involvement of non-neuronal cells, such as glia, endothelial cells, and leukocytes in the pathophysiology of epilepsy, specifically by means of inflammatory mechanisms. Inflammatory responses, notably interleukin (IL)-1β signaling, have been shown to be associated Carnitine dehydrogenase with status epilepticus and seizure frequency (Marchi et al., 2009). As shown in experimental models and in tissue from patients with epilepsy, seizures evoke the release of cytokines not just from neurons but also from glial cells and endothelial cells (Ravizza et al., 2008). Furthermore, the contribution of non-neuronal cells to the induction of neuronal death following pilocarpine-induced status epilepticus has been demonstrated (Rogawsi, 2005; Ding et al., 2007). Several key events that lead to inflammatory responses following seizures have been identified.