Figure 3 shows the mean values of baseline, early peak, nadir, an

Figure 3 shows the mean values of baseline, early peak, nadir, and plateau SkBF. The visual impression conveyed by Figure 2, was confirmed by the statistical analysis of these parameters. From T0 to T2, the mean decrease in the plateau SkBF and increase in early peak were, respectively, −9% to −16% and +10% to +18% of the value at T0 (p values below 0.05 for all conditions). As occurred with the plateau, the nadir tended to be lower at T2 than at T0 in the

four conditions tested, but the difference reached statistical significance only in the case of the custom-made chamber probed with LDI. Finally (and not obvious in Figure 2), the baseline SkBF, in all conditions, was slightly and significantly lower at T2, in comparison

with T0. At T2, the higher peak response was associated with a higher mean BP and therefore could reflect a change in perfusion pressure rather than in vascular tone. Against this interpretation, cutaneous vascular conductance (i.e., SkBF divided by mean BP) consistently increased from T0 to T2 (LDI EPZ-6438 purchase custom-made chamber: from 4.7 ± 1.5 to 5.8 ± 1.9 PU/mmHg, p < 0.001; LDI commercial chamber: from 4.0 ± 2.0 to 5.3 ± 2.6 PU/mmHg, p < 0.001; LDF custom-made chamber: from 6.8 ± 4.0 to 8.3 ± 4.7 mV/mmHg, p = 0.001; LDF commercial chamber: from 6.2 ± 2.7 to 7.7 ± 3.4 mV/mmHg, p = 0.001). Finally, the plateau response was somewhat lower with the custom commercial, when compared with the custom-made chamber. Although statistically significant, this effect was minor and could have been related to small differences in heating rate and temperature reached. The present study confirms our previous observation that the repeated application of a local thermal stimulus on the same skin patch,

at least when carried out within two hours, leads to a reduction in the elicited vasodilatory response. However, two studies [4,20] have not noticed this phenomenon. Therefore, the questions that must be asked are the reasons for this apparent discrepancy and whether differences in methods could be involved. The major difference relates to the equipment, both for measuring SkBF (LDF vs LDI) and for local heating (commercially available vs PD184352 (CI-1040) custom-made chambers, which may not have the same surface area and heating rate). Any of these factors could have contributed to the discrepancy between our previous observations [3] and those made by these other groups [4,20]. However, in the present study, desensitization clearly occurred in all tested conditions, supporting its independency from the measuring equipment and heating system used in the experiment. In the work by Shastry et al., 10 subjects participated, five men and five women. The laser-Doppler flowmeter (PF 5010; Perimed) was single point at 780 nm, based on exactly the same technology as the less recent Perimed 4001 used in the present study.

Our study was designed using a case–control approach Sixty pre-e

Our study was designed using a case–control approach. Sixty pre-eclamptic patients, 60 healthy pregnant women with uncomplicated pregnancies and 59 healthy non-pregnant women were involved in the AZD1152-HQPA study. The study participants were enrolled from the First Department of Obstetrics and Gynecology and from the Department of Obstetrics and Gynecology of Kútvölgyi Clinical Center, at the Semmelweis University, Budapest, Hungary. All women were Caucasian and resided in the same geographic area in Hungary. Exclusion criteria were multi-fetal gestation, chronic hypertension,

diabetes mellitus, autoimmune disease, angiopathy, renal disorder, maternal or fetal infection and fetal congenital anomaly. The women were fasting; none of the pregnant women were in active labour, and none had rupture of membranes. The healthy non-pregnant women were in the early follicular phase of the menstrual cycle (between cycle days 3 and 5), and none of them received hormonal contraception. Pre-eclampsia was defined by increased blood pressure (≥140 mmHg systolic or ≥90 mmHg diastolic on ≥2 occasions at least 6 h apart) that occurred after 20 weeks of gestation in women with previously normal

blood pressure, accompanied by proteinuria (≥0·3 g/24 h or ≥1 + on dipstick in the absence of urinary tract infection). Oxalosuccinic acid Blood pressure returned to normal by 12 weeks postpartum in each pre-eclamptic study patient. Pre-eclampsia was regarded as severe if any of the following criteria was present: blood pressure ≥ 160 mmHg BAY 57-1293 systolic or ≥110 mmHg diastolic, or proteinuria ≥ 5 g/24 h

(or ≥3 + on dipstick). Pregnant women with eclampsia or HELLP (haemolysis, elevated liver enzymes and low platelet count) syndrome were not enrolled into this study. Early onset of pre-eclampsia was defined as onset of the disease before 34 weeks of gestation (between 20 and 33 completed gestational weeks). Fetal growth restriction was diagnosed if the fetal birth weight was below the 10th percentile for gestational age and gender, based on Hungarian birth weight percentiles. The study protocol was approved by the Regional and Institutional Committee of Science and Research Ethics of the Semmelweis University, and written informed consent was obtained from each patient. The study was conducted in accordance with the Declaration of Helsinki. Blood samples were taken from an antecubital vein into plain tubes, as well as ethylenediamine tetraacetic acid (EDTA) or sodium citrate anti-coagulated tubes, and then centrifuged at room temperature with a relative centrifugal force of 3000 g for 10 min. The aliquots of serum and plasma were stored at −80°C until the measurements.

This might be an important prerequisite to children’s ability to

This might be an important prerequisite to children’s ability to cope with imperfect input and to recognize words under more challenging circumstances. “
“Previous research has found that young children recognize an adult as being acquainted with an object most readily when the child and adult have previously engaged socially with that object together. In the current study, we tested the hypothesis that such social engagement is so powerful that it can sometimes lead children to overestimate what has been shared. After having shared two objects with HDAC inhibitor an adult in turn, 2-year-old children played with a third

object the adult could not see. In three out of four conditions, the adult remained co-present and/or communicated to

the child while she played with the third object. Children falsely perceived the adult as being acquainted with the third object when she remained co-present (whether or not she also communicated) but not when she clearly terminated the interaction by disengaging and leaving. These results suggest that when young children are engaged with a co-present person they tend to overestimate the other’s knowledge. “
“Quinn and Liben Selleck BVD-523 (2008) reported a sex difference on a mental rotation task in which 3- to 4-month-olds were familiarized with a shape in different rotations and then tested with a novel rotation Telomerase of the familiar shape and its mirror image. As a group, males but not females showed a significant preference for the mirror image, a pattern paralleled at the individual level (with most males but less

than half the females showing the preference). Experiment 1 examined a possible explanation for this performance difference, namely, that females were more sensitive to the angular differences in the familiarized shape. Three- to 4-month-olds were given a discrimination task involving familiarization with a shape at a given rotation and preference testing with the shape in the familiarized versus a novel rotation. Females and males preferred the novel rotation, with no sex difference observed. This finding did not provide support for the suggestion that the sex difference in mental rotation is explained by differential sensitivity to angular rotation. Experiment 2 revealed that the sex difference in mental rotation is observed in 6- to 7-month-olds and 9- to 10-month-olds, suggesting that a sex difference in mental rotation is present at multiple ages during infancy. Mental rotation refers to the ability to rotate an image of an object in one’s mind.

[53, 54] It is interesting to note that the average murine pMHCI–

[53, 54] It is interesting to note that the average murine pMHCI–CD8 interaction is substantially stronger (KD = 49–69 μm) (Table 1b,c) than the equivalent human interaction (KD = 145 μm) (Table 1a) [15] but does not result

in non-cognate CD8+ T-cell activation. Despite differences in TCR and CD8 binding (the average murine TCR–pMHCI and pMHCI–CD8 binding affinities are KD = 3·3 μm[17, 55-59] and KD = 59 μm, respectively, compared with the average human TCR–pMHCI and pMHCI–CD8 binding affinities of KD = 8·7 μm[45, 59-65] KD = 145 μm did, respectively[37, this website 45, 66]) the ratio of TCR and CD8 binding affinity is maintained between the two species (murine = 1 : 17, human = 1 : 18), so that the TCR binds with around 17–18 times stronger affinity than CD8. Therefore, the relationship between the binding affinity of the CD8 co-receptor compared with the TCR could represent a fundamental mechanism by which T cells maintain peptide antigen specificity through the TCR while retaining the required level of antigen sensitivity via CD8. Thus, pMHCI–CD8 interactions may have evolved in a highly constrained manner dictated by the need to balance high levels of T-cell cross-reactivity with non-specific T-cell activation, of which the latter could instigate auto-immunity. It

should also be noted that the ratio of TCR : CD8 binding affinity may be different in the thymus because positively selecting pMHC ligands have been shown to have a very weak binding affinity for cognate TCRs.[55, 67] Hence, CD8 has been implicated as an important player Metformin mouse during thymic selection of immature thymocytes.[19] Although the weak binding affinity of the pMHCI–CD8 interaction excludes the possibility that CD8 plays a major role during T-cell/target cell adhesion, experiments using mutated pMHCI tetramers with altered CD8 binding properties have shown that CD8 can Carnitine dehydrogenase profoundly affect TCR–pMHCI avidity.[11, 23, 53, 68] Accordingly, mutations in the α3 domain of HLA-A*0201 (D227K/T228A) that abolish CD8 binding (CD8-null) decreased both

tetramer association rate and tetramer half-life compared with wild-type HLA-A*0201 tetramers[23] (Fig. 5a,b). Furthermore, the shift in mean fluorescence intensity (MFI) using weakly binding pMHCI variants was substantially reduced using CD8-null tetramers compared with wild-type reagents (Fig. 5c,d). These data show that, although the interaction is weak, pMHCI–CD8 binding has an important role in stabilizing the TCR–pMHCI complex at the cell surface. In support of this notion, two-dimensional binding affinity measurements have shown that the TCR and CD8 bind pMHCI co-operatively to modulate T-cell antigen discrimination.[69] Disrupting the pMHCI–CD8 interaction clearly impacts the ability of T cells to recognize antigen.

73 m2) and who wish to fall pregnant be advised that they can pro

73 m2) and who wish to fall pregnant be advised that they can provided their blood pressure is well controlled (2C). Note: The degrees of increased risk of each outcome in pregnant women with CKD are difficult to precisely quantify, although have generally been reported in each study to be at least 2-fold higher than in pregnant women without CKD. d. We recommend that patients with CKD planning to fall pregnant should have their medications reviewed and modified prior to conception. The CP673451 anticipated benefits of

each medication should be weighed against its potential risks. In particular, angiotensin converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) should be discontinued (1D). Chronic kidney disease is a significant contributor to morbidity and mortality, and represents a major expense to the healthcare system. Early intervention selleck screening library with appropriate medical therapies is essential to address this public health burden and may reduce the progression of CKD and cardiovascular risk by up to 50%.[9] Important risk factors for CKD include diabetes mellitus, hypertension, obesity and smoking. Modification of lifestyle habits (e.g. healthy diet, physical exercise, smoking cessation, moderate alcohol consumption

and weight loss in obese people) may therefore be of value in retarding the progression of CKD. In addition, restriction of dietary protein[31] and augmentation of fluid intake[32] have been recommended as a treatment for retarding CKD progression for over 50 years. While the National Health and Medical Research Council (NHMRC) Dietary Guidelines for Australian Adults (

provide useful generalized, evidence-based information about healthy food choices, patients with CKD often require individualized diet prescription by an appropriately qualified dietitian. Diabetes mellitus, particularly type 2, is increasing in prevalence and associated with significant cardiovascular morbidity and mortality. It also represents HSP90 the leading cause of CKD worldwide. Evidence from large, prospective trials indicates that tight glycaemic control in type 1[33] and, to a lesser extent, type 2[34, 35] diabetic patients results in clinically significant preservation of renal function. The optimal level to which glycosylated haemoglobin (HbA1c) should be targeted (<7.0%) is largely based on the Diabetes Control and Complications Trial (DCCT) and UKPDS trials[33-35] but the threshold below which the benefit is lost or at which the incidence of side-effects becomes unacceptable is not clear. Chronic kidney disease is also a well-established independent cardiovascular risk factor. Evidence[36, 37] for anti-platelet therapy suggests that low-dose aspirin reduces the risk of CVD by 25–33%, particularly in patients with established CVD (secondary prevention) or those at high risk (primary prevention).

001) The viral loads of all of these discordant samples were low

001). The viral loads of all of these discordant samples were low copy numbers. Indeed, complete concordance was observed in the quantitative results for the samples with ≥36 copies/ml in the prototype assay. Comparison of the prototype assay and each home-brew assay for all positive samples according to both assays had a high degree of correlation (Fig. 3). Longitudinal monitoring of five representative EPZ015666 datasheet individual transplant recipients is demonstrated in Figure 4. The dynamics of the CMV load in all patients were similar, although some discrepancies were observed within the follow-up period.

Standardized calibration materials and commercially available assays have been developed for standardized quantification for specific viruses, such as HIV and hepatitis C virus (12–14). Standardization is necessary for consensus guidelines in patient management. Hayden et al. (7) reported a multicenter comparison of different real-time PCR assays for EBV. This study was carried out at eight sites using three panels consisting Pexidartinib mw of serial dilutions of commercially available EBV DNA and extracts from 19 whole blood specimens. Strong concordance among laboratories was observed with respect to the qualitative results, whereas quantitative discordance was seen at a maximum of 4 log-units. This discrepancy decreased when a common reference standard was used to obtain quantitative results. Preiksaitis et al.

(15) reported an international comparison of EBV DNA quantitative assays. They distributed a panel of samples to 28 laboratories. The panel of samples consisted

of seven constructs using EBV-positive cell lines and three clinical plasma samples. Half of the quantitative results were within ±0.5 log-units, whereas the maximum variation was approximately 4 log-units. With regard to CMV quantification, Pang et al. (16) recently reported an international comparison of CMV viral load assays. They distributed a panel of samples to 33 laboratories. The panel of samples consisted of seven constructs using purified CMV stock and three Dichloromethane dehalogenase clinical plasma samples. Fifty-eight percent of the quantitative results were within ±0.5 log-units whereas the maximum variation was approximately 4 log-units. In the present study, five independent laboratories were involved in comparing the quantitative values for EBV and CMV from each home-brew assay and the prototype assay. The maximum variations were 4.15 for EBV and 3.03 for CMV, which is acceptable in comparison with previous reports (7, 15, 16). Additionally, the dynamics of the EBV load in 12 patients and the CMV load in five patients were found to be similar, and this comparison may be unique. Even the inter-laboratory variation appears to be small; however, it is uncertain whether this variation is a problem for treating patients. The development of a prototype assay may help eliminate concern related to variability.

Total RNA from pre-treated monocytes was isolated using the RNA M

Total RNA from pre-treated monocytes was isolated using the RNA Miniprep Kit from Stratagene (La Jolla, CA), according to the recommendations of the manufacturer. One microgram of total RNA was reverse transcribed using the High Capacity cDNA Reverse Transcription Kit (Applied Biosystems, Foster City, CA) to generate cDNA. To identify the housekeeping genes that maintain constant expression levels in our experimental settings, the expression stability of 32 housekeeping genes was pre-evaluated using human TaqMan Gene Expression Endogenous Control Plate (Applied Biosystems). For both TaqMan Gene Expression CP-673451 purchase Endogenous Control and Multigene

TaqMan arrays the real-time PCR were performed in the format of 96-well plates on ABI PRISM 7900HT Fast Real-Time PCR System (Applied Biosystems). The cDNA was amplified with TaqMan Universal PCR Master Mix (Applied Biosystems) for 40 cycles using universal cycling conditions (95° for 10 min followed by 40 cycles at 95° for 15 seconds and 60° for 1 min). For profiling of individual control genes such as tumour necrosis factor-α (TNF-α) and interleukin-12p40 (IL-12p40), the primers were designed using primer express 2.x software (Applied Biosystems). Sequences of primers to detect TNF-α were described previously,[14]the

sequences of primers for IL12p40 were forward: CTTCTTCATCAGGGACATCAT CAA, reversed: JQ1 GGGAGAAGTAGGAATGTGGAGTACTC,probe: FAMCAGGTGGAGGTCAGCTGGGAGTACCC-Tamra. For relative quantification, data were analysed by the ΔΔCT method using SDS 2·3. (Applied Biosystems) and by Data Assist v2·0. Expression levels of target genes were normalized to the average of housekeeping genes. Ingenuity Pathway Analysis (ipa) software ( is a proprietary web-based database that provides information on gene and protein interactions based on the published literature. In this study, the data-driven, n-butyrate-affected HSP90 eicosanoid-associated gene network was delineated using the ipa software; core analysis was used to identify the

most significantly affected biological processes. For intracellular determination of COX-1 and COX-2 by flow cytometry, stimulated monocytes were fixed with 2% formaldehyde, permeabilized with 0·1% saponin, and stained with anti-COX-1-FITC/anti-COX-2-phycoerythrin (BD, San Jose, CA). For analysis of mitogen-activated protein kinase (MAPK) activation cells were incubated after fixation and permeabilization with antibodies to the phosphorylated forms of the kinases: anti-p-p38 MAPK (pT180/pY182) (BD Biosciences, Franklin Lakes, NJ), anti-p-p44/42 MAPK (Erk1/2) (Thr202/Tyr204), anti-p-SAPK/JNK (Thr183/Tyr185), (both Cell Signaling Technology, Boston, MA). The cells were analysed on a FACSCalibur (BD Biosciences).

13 However, the growth cycle can be slowed or arrested depending

13 However, the growth cycle can be slowed or arrested depending on intracellular nutrient availability, leading to bacterial persistence within host cells.14,15 This is a key survival feature of these organisms and is a major determinant of disease pathogenesis as discussed more fully in the following sections. C. abortus typically causes reproductive failure and abortion in ruminants and swine and has a world-wide distribution, with the exception of Australia and New Zealand. C. abortus is also a well-recognized and potentially

fatal zoonosis, presenting a major hazard to pregnant women who come in contact with livestock, particularly at lambing.16 Although OEA is a reproductive disease, the principal route of transmission to naïve sheep is thought to be via an oro-nasal route, most likely from heavily infected placentas from ewes that have aborted and contaminate the environment.17,18 A typical example Selleck AZD8055 of a placenta with characteristic thickened HDAC inhibitor membranes from an ewe that aborted as a result of OEA is shown in Fig. 2. Abortion is thought to be because of inappropriate inflammatory cytokine and chemokine production in the placenta that leads to placentitis.18,19 The success of C. abortus as a reproductive pathogen in a species that is only pregnant for 5 months

and only gives birth once a year is because of its ability to establish a persistent, subclinical infection in non-pregnant sheep.20 Thus, when naïve, non-pregnant sheep are infected, protective immunity does not develop. Ewes then abort in the subsequent pregnancy. Sheep that have aborted do develop strong protective immunity (but not necessarily sterile immunity) and reproduce normally in subsequent pregnancies.20,21 The Methamphetamine epidemiology and pathogenesis of OEA both indicate that a systemic phase of infection occurs after the primary infection of the oro-nasal mucosa. Neither the site of persistence of C. abortus nor the timing or duration of the systemic phase of infection has been identified. Therefore, the paradigms relating to reproductive immunology and to host immune control of intracellular bacteria are useful frameworks for addressing questions regarding

the pathogenesis of OEA. Furthermore, in addressing these paradigms in sheep, we can test their predictions and assess their relevance for a species other than mouse or human. In doing so, we should advance our knowledge of comparative immunology and reproduction. The first description of helper T-cell clones expressing distinctive cytokine profiles was made by Tim Mosmann, Robert Coffman and co-workers22 in 1986 in a paper that has had a profound impact on our understanding of how CD4+ve T cells orchestrate and regulate immune responses. They discovered that mitogen-activated murine CD4+ve T-cell clones were mutually exclusive in their expression of IL-2/IFN-γ (TH1) and what we now know to be IL-4 (TH2), whereas both sets of clones made IL-3.

These observations suggest that TNF-α -308 polymorphism plays a c

These observations suggest that TNF-α -308 polymorphism plays a central role to the TNF release, and it may also be a genetic factor for the susceptibility to MHC-associated autoimmune and infectious AG-014699 order diseases [30]. In this report, we have examined which influence the polymorphisms IL-2 -330 (T/G) and TNF-α -308 (A/G) has on the cytokines IL-2 and TNF-α and whether glutamine can influence or change the cytokines synthesis within the scope of immunonutrition. Blood samples from healthy probands were used. All blood samples were taken from a collective of probands consisting

of both genders. The samples were stored frozen at −20 °C. For the determination of IL-2 and TNF-α concentrations, a 7.5 ml sample of venous blood was collected from each proband in a sodium-heparinate tube. In addition to this, another 10 ml sample of venous blood was collected in a sodium-heparinate

tube for the IL-2 and TNF-α genotyping. Before starting the measurements of concentrations of IL-2 and TNF-α, the samples were adjusted to two different glutamine concentrations and then activated in vitro. The DNA was extracted from the samples, and the IL-2 -330 and TNF-α -308 polymorphisms were determined. In the first step, the BTK inhibitor ic50 whole blood was diluted with glutamine-free RPMI-1640 in a ratio of 1:1. After that, each of the samples was adjusted to two different glutamine concentrations with l-alanyl-l-glutamine, which is broken down by hydrolases in the blood within minutes, so that the free glutamine can be found. Objective criteria were concentrations of 2000 and 250 μm, which is about halving of the physiological glutamine concentration. The adjusted Sitaxentan concentrations were verified by HPLC. The in vitro activation was performed with 10 ng/ml phorbol 12-myristate-13-acetate (PMA) and 1 ng/ml ionomycin.

PMA and ionomycin stimulate mainly the lymphocytes. Both agents activate the intracellular, signal-induced cascade and stimulate the production of cytokines. The stimulation was carried out in an incubator at 37 °C for 8 h. Subsequently, the mixture was centrifuged for 5 min at 500 G. The supernatant of the samples was removed and frozen at −80 °C until the determination of the levels of IL-2 and TNF-α with an “enzyme-amplified sensitivity immunoassay (EASIA). We used a standard EASIA kit from Biosource Europe, Belgium. To read out the plate, the microplate reader EL 311 from Behring (Behringwerke, Germany) was used. The software used was Behring ELISA software V2.0.2. The absorption was determined at a wavelength of 450 nm and a reference wavelength of 630 nm. After creating a standard curve, the concentrations were calculated. DNA was extracted from the collected blood samples with the Genomic DNA Purification kit, D-5000, Gentra Systems, Valencia, CA, USA.

The vascular wall presented only slight to mild hyalinosis We as

The vascular wall presented only slight to mild hyalinosis. We assumed a common pathogenesis to the cortical

lesions and the white matter change. The pathogenesis of the present diffuse cerebral lesions may not be just secondary to circulatory disturbance but partly due to metabolic abnormality. “
“L. Chadwick, L. Gentle, J. Strachan and R. Layfield (2012) Neuropathology and Applied Neurobiology38, 118–131 Unchained maladie – a reassessment of the role of Ubb+1-capped polyubiquitin chains in Alzheimer’s disease Molecular misreading allows the formation of mutant proteins in the absence of gene mutations. A mechanism has been proposed by which a frameshift mutant of the ubiquitin protein, Ubb+1, which accumulates in an age-dependent manner as a result of molecular misreading, contributes to neuropathology

in Alzheimer’s disease (Lam et al. selleck chemical 2000). Specifically, in the Ubb+1-mediated proteasome inhibition hypothesis Ubb+1‘caps’ unanchored (that is, nonsubstrate linked) polyubiquitin chains, which then act as dominant inhibitors of the 26S proteasome. A review of subsequent literature indicates that this original hypothesis is broadly supported, and offers new insights into the mechanisms accounting for the age-dependent accumulation of Ubb+1, and how Ubb+1-mediated proteasome inhibition may contribute to Alzheimer’s disease. Further, recent studies have highlighted a physiological role for free endogenous

unanchored polyubiquitin chains in the direct activation of certain protein kinases. This raises the possibility that Ubb+1-capped unanchored polyubiquitin chains could also exert harmful effects through the aberrant activation of tau or other ubiquitin-dependent kinases, neuronal NF-κB activity or NF-κB-mediated neuroinflammatory processes. “
“J-R. Liu, Y. Zhao, A. Patzer, N. Staak, R. Boehm, G. Deuschl, J. Culman, C. Bonny, T. Herdegen and C. Eschenfelder (2010) Neuropathology and Applied Neurobiology36, 211–224 The c-Jun N-terminal kinase (JNK) inhibitor XG-102 enhances the neuroprotection of hyperbaric oxygen after cerebral ischaemia in adult rats Aim: Both hyperbaric oxygenation (HBO) and inhibition of the c-Jun N-terminal kinases Baf-A1 mw (JNKs) by the peptide inhibitor XG-102 (D-JNKI-1) are efficient protective strategies against ischaemia-induced neurodegeneration. The present study investigated whether the combination of HBO and JNK inhibitor, XG-102, provides additive neuroprotection against cerebral ischaemia. Methods: Rat middle cerebral artery was occluded (MCAO) for 90 min. XG-102 [2 mg/kg, intraperitoneally] or HBO (3 ATA, 60 min) was applied 3 h after the onset of MCAO. For the combination treatment, HBO was started 10 min after the injection of XG-102.