The objective of the present study is to examine whether L-carnitine supplementation may improve the muscle symptom, cardiac function and renal anemia in hemodialysis (HD) patients. Cobimetinib order Methods: L-carnitine of 600 mg/day was administrated to 80 HD outpatients in our dialysis center for 6 months. The incidence of muscle spasm was obtained by the questionary survey,

the cardiac function was examined by echocardiography. Hemoglobin levels (Hb) and dosages of ESA (Erythropoiesis Stimulating Agents) were also obtained from personal data. Results: The blood concentration of total carnitine was significantly increased from 45.4 ± 6.58 μmol/l to 170.4 ± 6.92 μmol/l (normal range: 45–91 μmol/l) (p < 0.01), that of free carnitine was also significantly increased from 27.9 ± 4.20 μmol/l to 107.2 ± 4.42 μmol/l (normal range: 36–74 μmol/l) (p < 0.01). That of TAM Receptor inhibitor acyl carnitine was significantly increased from 17.4 ± 2.55 μmol/l to 63.2 ± 2.68 μmol/l (normal range: 6–23 μmol/l) (p < 0.01). As a result of questionary survey about the muscle spasm, 39% of patients who had HD for more than 4 years have felt the improvement of leg cramps. We didn't obtain any significant findings in echocardiography. The Hemoglobin levels were significantly elevated from 10.3 ± 0.12 g/dl to 10.8 ± 0.13 g/dl (p < 0.05), but dosage of erythropoietin resistance

index (dosage of ESA / body weight / Hb) was not significantly changed. Conclusion: This study showed that the blood concentration of carnitine was significantly increased by administration of L-carnitine. It appears that L-carnitine may improve the muscle spasm and hemoglobin levels in HD patients. TSAI MIN-SUNG1, SHAW HUEY-MEI2, LI YI-JEN3, LIN MENG-TE1

1KUO General Hospital, Tainan City, Taiwan; 2Chia-Nan University of Pharmacy and Science, Tainan City, Taiwan; 3Chang-Jung Christian University, Tainan City, Taiwan Introduction: Tocopherols are potent antioxidants and are effective in significantly reducing the production of membrane lipid peroxidation. Previous studies disclosed that the concentrations of alpha tocopherol (AT) in chronic kidney disease (CKD) patients were varies. There was no benefit of using tocopherol in CKD patients if the goals based Cell press on the decreasing cardiovascular disease events, slowing progression of proteinuria or decreasing progression of CKD. The level of alpha-tocopherol is highly associated with triglyceride. Furthermore, the increase of triglyceride-rich lipoproteins in CKD patients leads to the high prevalence of hypertriglyceridemia. Therefore, the effective tocopherol level needs to adjust the triglyceride level. AT is also associated with metabolic syndrome (MetS). MetS, characterized by insulin resistance, can be improved by supplements rich in tocopherols. However, the application of tocopherol in CKD with MetS had not been demonstrated before. Methods: There was a total 64 CKD patients enrolled in the cross sectional study.

Glycocalyx thickness is reduced, glomerular endothelial cell pore size is increased, glomerular charge selectivity is reduced and

podocyte cell foot processes are fused. These changes are associated with reductions in glomerular cell production this website of proteoglycans and glycosaminoglycans contained within the glycocalyx produced by the glomerular endothelial cells.11 Further evidence for a direct effect of Adriamycin on the kidney comes from a study in which clipping of the renal artery of one kidney protects it from injury.20 Additional studies have examined the molecular mechanisms for Adriamycin-induced renal injury. Increased free radical production has been proposed as a pathogenetic mechanism. This is supported by isolation perfusion studies of hagfish (Myxine glutinosa) glomeruli Dinaciclib ic50 in which

Adriamycin was found to reduce glomerular ATPase activity in association with a reduction in water permeability, an effect reversed by the sulfhydryl donor N-acetylcysteine. In addition, depleted levels of glutathione (an anti-oxidant) and elevated levels of lipid peroxide levels in liver, kidney and heart developed after Adriamycin administration.60 Evidence for the role of advanced glycation end products comes from studies of receptor for advanced glycation end product (RAGE)-null mice. These mice are protected from Adriamycin-induced podocyte damage and proteinuria. Adriamycin induced generation of RAGE ligands, an effect reversed by treatment Miconazole with soluble RAGE. The mechanism for RAGE ligand-induced renal injury involved the activation of nicotinamide adenine dinucleotide phosphate-oxidase and p44/p42 MAP kinase signalling, and upregulation of pro-fibrotic growth factors.61 The changes associated with the slit diaphragm in Adriamycin-induced nephropathy have been studied by Otaki, Kawachi and colleagues.62 Early after Adriamycin administration (day 7), expression of the slit diaphragm

molecules nephrin, podocin and NEPH1 (but not ZO-1- and CD-associated protein) is altered from a continuous to a discontinuous dot-like pattern consistent with podocyte injury. In particular, NEPH1 was disproportionately affected. Using immunoprecipitation and western blot studies of glomerular lysates from animals 7 days after Adriamycin injection, Kawachi’s laboratory found that a large proportion of nephrin lost its affinity with NEPH1. While these data are observational in nature, they do point to slit diaphragm abnormalities as critical early events in the pathogenesis of Adriamycin-induced proteinuric renal injury. Gene profiling using microarray chip technology has identified gene networks that are potential drivers of tubulointerstitial fibrosis in AN.

Results: The mean daily salt excretion was 9.9 ± 2.6 g. BP and eGFR were not different among for groups. However, incidence of overt proteinuria was significantly higher in the first quartile (Q1: 23%, Q2: 9%, Q3: 2%, Q4: 2%, p < 0.001). Conclusion: Low daily salt excretion was correlated with proteinuria in non-diabetic patients. Although the cause and effect relationship between salt intake and proteinuria could not be determined in Y-27632 mouse this study, low daily

salt excretion could be a marker for proteinuria in non-diabetic outpatients. AHMAD ISABEL1, YANG YATING ADONSIA1,2, LAU TITUS1,2, SETHI SUNIL1,2, TEO BOON WEE1,2, LIN TINGXUAN1,2, TOH QI CHUN1,2, CHONG YUE TING1,2, LI JIALING1,2 1National University Health System, Singapore; 2National University of Singapore, Singapore Introduction: Clinical practice guidelines recommend using 2 or more anti-hypertensive agents to control blood pressure (BP) to targets in chronic kidney disease (CKD) patients. The impact of the number of medications on the components of BP (systolic, SBP; diastolic, DBP) in Asian CKD patients is unclear. We assessed the effects of the number of anti-hypertensive agents on BP components

Crizotinib in a multi-ethnic Asian population of stable CKD patients. Methods: We prospectively recruited 613 patients (male 55.1%, Chinese 74.7%, Indian 6.4%, Malay 11.4%, Others 7.5%; 35.7% diabetes) with mean age 57.8 ± 14.5 years. BP was measured according to guidelines using calibrated automatic manometers. Glomerular filtration rate (GFR) was estimated using the CKD-EPI equation. ANOVA was used to compare means of BP components with number of anti-hypertensive medications, and Tukey-Kramer HSD for pairwise comparisons. Linear regression was used to assess associations of BP with continuous variables. Non-normally distributed data was natural log-transformed for analyses. Results: The mean SBP was 139 ± 21 mmHg, DBP

74 ± 11 mmHg, serum creatinine 166 ± 115 μmol/L, and GFR 53 ± 32 mL/min/1.73 m2. SBP increased with lower GFR (p < 0.001), whereas DBP decreased with lower GFR (p = 0.0052). Mean SBP increased with increasing number of antihypertensive agents used (p < 0.001), whereas mean DBP decreased with ≥3 antihypertensive Amino acid agents used (p = 0.0020, Table 1). Conclusions: Clinical practice guidelines recommend different component BP targets for CKD patients. Increasing number of antihypertensive agents use results in a divergence in the achievement of targets. Further research into improved methods of monitoring and treatment is required to better achieve targets. SHIMIZU HIDEKI, KANAME SHINYA, KAWASHIMA SOKO, IKEGAYA NORIKO, HAYAKAWA SATOSHI, FUKUOKA KAZUHITO, KARUBE MIHO, KOMAGATA YOSHINORI, ARIMURA YOSHIHIRO, YAMADA AKIRA First Department of Internal Medicine, Kyorin University School of Medicine Introduction and Purpose: We aimed to examine the hypothesis that renoprotective effect of angiotensin II (AngII) receptor blocker telmisartan may be associated with obesity.

The authors thank Dr. G. Brennan, Queen’s University of Belfast, for his help in proof reading and language corrections. None of the authors has any conflicts of interest associated with this study. “
“Cry1Ac protoxin from Bacillus thuringiensis is a potent mucosal immunogen and adjuvant. When delivered BAY 80-6946 concentration intranasally (i.n.) Cry1Ac elicits significant antibody response and is able to improve vaccination against Naegleria

fowleri infection, but the functional effects occurring in nasal lymphocytes when this protein is administered alone have not been determined. Here, we investigated the effects of i.n. immunization with Cry1Ac on antibody production, lymphocyte activation and cytokine production in lymphocytes from nasal-associated lymphoid tissue (NALT) and nasal passages (NP). Our results show that i.n. immunization with Cry1Ac induced significant specific IgA and IgG cell responses, especially in NP. Besides, it increased the proportion of lymphocytes expressing the activation markers CD25 and CD69 in both nasal tissues, selleck chemical but differently. CD25 was increased in B cells along with CD4 and CD8 T cells from NALT and

NP, while CD69 was increased in B cells from both tissues but only in CD4 T cells from NP. Finally, we found that Cry1Ac augmented especially a Th2 profile of cytokines, as the proportion of T cells that spontaneously

produced IL-4, IL-5 and IL-10 was increased and this effect was higher in NP than in NALT. Fluorouracil mw These data contribute to explain the potent immunogenicity of Cry1Ac via i.n. route. The nasal mucosa is an important site for host defence against invading pathogens as it is the first site of contact with inhaled antigens [1]. In addition to its role in the defence of the upper and lower respiratory tracts, the nasal lymphoid system cooperates with the systemic immune system and affects immune reactions at distant mucosal sites, such as the urogenital tract and the gut [2, 3]. Consequently, new vaccination strategies based on nasal application have been designed and have proven to be effective procedures for the induction of antigen-specific immunity in respiratory and reproductive tissues [4]. There is much evidence to suggest that nasal-associated lymphoid tissue (NALT) may have an important role in the induction of mucosal immune responses after nasal immunization [5], while nasal passages (NP) and their associated lymphocytes are considered effector sites. However, only a few studies have systematically analysed the distinctive phenotypic and functional features existing in the lymphocyte populations residing at the different nasal compartments [5–8].

3C). Collectively, these data clearly demonstrate that Mal modulates IFN-β gene induction whereby the TIR domain of Mal inhibits the PRDI-III reporter gene. Given that TRIF is essential for poly(I:C)-mediated signalling via TLR3 17, we tested the ability of Mal to modulate TRIF-dependent gene induction. Correlating with the previous reports 25, ectopic expression of TRIF potently activated the IFN-β reporter gene (Fig. 4A). We found that although ectopic expression of Mal or the TIR domain of Mal dose-dependently inhibited TRIF-induced activation of the IFN-β reporter gene, the N-terminal

Compound Library datasheet region of Mal did not inhibit, but rather, augmented IFN-β reporter gene activity (Fig. 4A). Further, we found that Mal-TIR inhibited the induction of the IFN-β reporter gene by Mal-N-terminal. As a control, we found that the TLR adaptor TRAM did not inhibit TRIF-induced activation of the IFN-β reporter gene (Fig. 4A). To preclude the possibility that Mal may exert its effects through poly(I:C)-mediated activation of the RLR, retinoic acid-inducible gene I (RIG-I) or melanoma differentiation-associated antigen 5 (Mda-5), rather than through TLR3/TRIF, cells were co-transfected with a plasmid encoding either RIG-I or Mda-5 and increasing amounts of Mal. Although ectopic expression of

RIG-I and Mda-5 activated the IFN-β reporter gene, Mal did not inhibit, but rather augmented RIG-I/Mda-5-mediated IFN-β reporter gene activity (Fig. 4E). As expected, although TRIF activated the NF-κB and the PRDIV reporter Selleck BGB324 genes (Fig. 4B and C), Mal and its variants did not inhibit TRIF-induced activation of the NF-κB (Fig. 4B) and PRDIV reporter genes (Fig.

4C). Also, although Mal and the TIR domain of Mal inhibited TRIF-induced activation of the PRDI-III reporter gene (Fig. 4D), the N-terminal region of Mal did not (Fig. 4D). Taken together, these data clearly demonstrate that Mal modulates TRIF-mediated IFN-β gene induction whereby the TIR domain of Mal inhibits the TRIF-induced activation of the PRDI-III reporter gene. Moreover, Cepharanthine the inhibitory role of Mal in poly(I:C)-mediated induction of IFN-β is TLR3/TRIF dependent and involves the PRDI-III enhancer element of the IFN-β promoter. Given that the data presented thus far provide compelling evidence that Mal negatively regulates IFN-β induction by blocking the PRDI-III element, we sought to establish whether this effect was mediated through IRF3 or IRF7. To this end, we transfected HEK293 cells with either the IFN-β or the PRDI-III luciferase reporter constructs and plasmids encoding either IRF3 or IRF7. Given that both IRF are weak activators of the IFN-β promoter 27, we opted to co-transfect the cells with TRIF (10 ng) to enhance the signal output and to aid in the engagement of auxiliary molecules necessary for IFN-β and PRDI-III gene induction. In addition, cells were co-transfected with increasing amounts of Mal, Mal-TIR or N-Mal.

This study evaluates MGMT promoter methylation in meningeal HPCs to determine its role in HPC oncogenesis and its association with patient outcome. Meningeal HPCs diagnosed between 2002 and 2011 were retrieved and clinicopathological features reviewed. MGMT promoter methylation status was assessed by methylation-specific polymerase chain reaction (MSP) and immunohistochemistry (IHC) for MGMT protein. HPCs accounted for 1.1% of all CNS tumors. Forty cases were analyzed; the majority were adults (mean age = 41.4 years). Seventy percent were primary and 30% were recurrent tumors; 60% were grade II and 40% were grade III. MGMT promoter methylation was identified in

45% of cases, buy SAHA HDAC including Grade II (54.2%) and Grade III (31.3%) (P = 0.203). Promoter methylation was significantly (P = 0.035) more frequent in primary (57.1%) than in recurrent (16.7%) tumors. No correlation was noted between MGMT promoter methylation by MSP and MGMT protein expression by IHC, or with progression-free survival. Thus, a significant proportion

of HPCs demonstrate MGMT promoter methylation, suggesting possible susceptibility to TMZ. As promoter methylation is more frequent in primary tumors, TMZ may serve as a therapeutic option in residual primary tumors. Epigenetic inactivation of MGMT in HPCs necessitates check details the assessment of prognostic and predictive value of MGMT promoter methylation in HPCs in larger clinical trials. “
“This chapter contains sections titled: Introduction Ocular Anatomy Nonneural Structures in The Eye Clinical Assessment of the Retina and Optic Nerve Specimen Acquisition and Processing for Ocular Neuropathology Bumetanide Studies Electron Microscopy Quantitative Analysis Ocular Processing Recommendations for Routine

Toxicological Neuropathology Studies Principles of Ocular Toxicological Neuropathology Categories of Lesions in Ocular Toxicological Neuropathology References “
“Dysembryoplastic neuroepithelial tumor (DNT) is a benign glioneuronal tumor, occurring in children and adolescents, typically associated with drug-resistant partial seizures. Pathologically, DNT is characterized by a specific glioneuronal element that is comprised of oligodendroglia-like cells (OLC) and floating neurons. The definition of DNT is currently controversial and the incidence of DNT varies among institutions. In this study we characterize the morphologic profiles of OLC and floating neurons by performing immunohistochemical and morphometric studies on seven cases of a simple form of DNT. While a majority of OLC was positive for oligodendrocyte transcription factor 2 (Olig2), only floating neurons and a few small cells were positive for neuronal nuclear antigens (NeuN). Double immunofluorescence studies revealed co-localization of Olig2 and galectin 3 in OLC, but no co-localization of Olig2 and NeuN.

We therefore reviewed current practices and surgical procedures currently available for women with recurrent or persistent SUI after initial MUS. The success rates of MUS surgeries for female SUI vary according to the definition of outcome. Objective outcome measures include cough stress tests, pad tests, and urodynamic evaluation, whereas subjective measures include patient self-assessment, validated questionnaires, voiding diaries, patient satisfaction, and quality of life measures.15 Sling failure is defined as the

persistence or recurrence of SUI after a procedure to remedy it. Persistent SUI has been regarded as leakage within 6 weeks of a previous MUS procedure and recurrent SUI as a leakage more than check details 6 weeks after the initial success of MUS.16 Sling failure has also been defined as re-treatment any time after surgery and the other criteria at any time more than 6 months post-operatively.17 Little is known about the optimal time for surgical intervention after initial MUS, making it difficult for surgeons to effectively prepare secondary procedures. A rigorous evaluation of recurrent or persistent SUI is important in determining its underlying pathophysiology, which may direct further treatment.

First, it is necessary to determine whether urine leakage is due to the bladder (urinary urgency incontinence) or outlet causes (urethral hypermobility or ISD). A detailed history should be taken of storage and voiding symptoms and physical examinations

should include assessments for the presence of a prolapsed pelvic organ, urethral hypermobility, see more suture or sling extrusion, and pelvic muscle strength. Moreover, leakage can be assessed using the cough provocation test. Although routine urodynamic tests for simple SUI may not be indicated, urodynamic evaluations before interventions are indicated in patients who failed previous treatment or surgery, as well as for click here those with mixed incontinence, obstructive symptoms, increased post-voided residual urine volume, and neurologic diseases.18 The goal of these urodynamic tests is to determine whether the incontinence is due to bladder-related causes, such as detrusor overactivity or impaired compliance, or to outlet-related causes, such as ISD or bladder outlet obstruction and overflow incontinence. Determination of valsalva leak point pressure may confirm stress leakage. Cystoscopy in patients who have undergone previous anti-incontinence surgery may exclude the presence of intravesical or intraurethral sling materials. Most women who fail surgery for SUI are unwilling to undergo additional surgical procedures. In the management of persistent or recurrent SUI, however, there is little evidence for the efficacy of non-surgical treatment options while awaiting surgery.

Our study suggests that Bcl-3 may be an effective target for promoting regeneration of the epithelium in the colon. Bcl3−/−C57BL/6 (B6) mice were generated as described previously [15, 16]. All mice were group-housed in individually ventilated cages (IVCs) under specific pathogen-free conditions. Standard mTOR inhibitor housing and environmental conditions were maintained (temperature

21°C, 12 h light/12 h darkness with 50% humidity). Animals were fed sterile standard pellet diet and water ad libitum. Animal husbandry and experimental procedures were approved by the University College Cork Animal Experimentation Ethics Committee (AEEC). Mice were administered 2% DSS (45 kDa; TdB Consultancy, Uppsala, Sweden) ad libitum in their drinking water to induce colitis, as described previously [18]. DSS solutions were prepared freshly

and administered on a daily basis for 6 days. This was followed by water up to day 8 to induce acute disease. Body weight, stool consistency and posture/fur texture were recorded daily to determine the daily disease activity index (DAI). DAI scoring was assessed blinded with a maximum score of 10, as described previously [18, 19]. DAI scoring combined scoring from weight loss (% change) 0–4, stool consistency 0–4 and posture/fur texture 0–2. Briefly, a percentage weight loss score of 0 = no loss, 1 = 1–3% loss, 2 = 3–6% loss, 3 = 6–9% loss and 4 = greater than 9% loss in body mass. A stool

consistency score of 0 = no change, 1 = mild change, 2 = loose stool, 3 = loose stool and rectal bleeding, 4 = diarrhoea and rectal 3-deazaneplanocin A bleeding. A fur and posture score 0 = no change, 1 = mild hunched posture, 2 = hunched posture and reduced movement. Mice were killed at day 8 with colons removed from anus to caecum and washed in phosphate-buffered saline (PBS). Colons were measured and cut longitudinally dividing into the distal and proximal colon. Both proximal and distal colons were weighed and processed for histology, protein and quantitative reverse transcription–polymerase chain reaction (qRT–PCR) Avelestat (AZD9668) analysis. Distal colons (3 cm) were cut longitudinally and into three sections. One section was rolled in a ‘swiss roll’ fashion and frozen in optimal cutting temperature (OCT) tissue-freezing medium (Tissue Tek, Sakura Finetek, Torrance, CA, USA) using liquid nitrogen. Frozen sections (6 μm) were fixed in ice-cold acetone/ethanol 3:1 solution and stained with haematoxylin and eosin (H&E) according to standard histological staining procedures. Stained sections were analysed and scored using a light microscope (Olympus BX51; Olympus, Hamburg, Germany). Images were captured using Cell F software (Olympus). Images captured are representative of greater than seven fields of view at ×20 magnification per mouse. Histological scoring was performed in a blinded fashion.

Administration of IL-25 to mice elicited the release of high levels of IL-5 and IL-13 from a population Acalabrutinib of RAG-independent, γ-common-chain dependent, non-T, non-B innate lymphoid cells in the gut. Later studies identified several cell populations with similar, but not identical, phenotypes in various organs. These cell populations were lineage negative (Lin−) Sca-1+IL-7R+Thy1+T1/ST2+, and served as critical mediators

of parasite expulsion in the murine intestine [[15, 61, 62]]. Transcriptional analysis revealed a number of transcription factors, including Id2, Notch1, Notch2, RORα and GATA3 [[6, 15, 61, 63]] that could potentially control the development and function of these cells. Like NK cells and RORγt-dependent ILCs, development of type 2 ILCs depends on the transcriptional repressor Id2 [[4, 15]], suggesting, as discussed above, that they are derived from a common precursor; however, type 2 ILCs develop independently of RORγt, as Rorγt−/− mice exhibit numbers of type 2 ILCs comparable to those in wt mice [[15]]. Recently, it was reported that ILC2s could be generated from a bone marrow Lin−IL7Rα+Flt3+ CLP, differentiating under the influence

of Notch1 signaling [[6, 64]] ILC2s failed to differentiate in mice with a spontaneous deletion in the gene for RORα, the so called staggerer (Rorasg/sg) mice [[6]]. In line with this observation, staggerer mice either injected with IL-25 or infected with the helminth parasite N. brasiliensis failed to either generate ILC2s or expel the parasites respectively. GATA3 is highly BMN 673 molecular weight expressed by ILC2s [[15, 63, 65]], and mice

in which GATA3 was deleted only in IL-13-producing cells, of which the majority were ILC2s during N. brasiliensis infection, are phenocopies of IL13-deficient mice [[66]]. Fludarabine cost These mice exhibited reduced worm clearance, suggesting that GATA3 is critical for IL-13 production in ILC2s. Together, these findings emphasize the striking similarity between Th2 cells and ILC2s, with both cell types relying on GATA3 for their function. Collectively, the studies described in this section indicate that the development and function of ILC2s are controlled by several transcription factors including Id2, RORα, Notch1 and GATA3. ILC-related transcription factors are potential targets for therapy in those diseases in which ILCs play either a prominent detrimental or beneficiary role. Two recent papers describe the potent effects of RORγt antagonism in inhibiting Th17-cell differentiation and reducing the severity of experimental auto-immune encephalomyelitis (EAE)[[67, 68]]. First, Huh et al reported that digoxin, and the two synthetic, non-toxic, derivatives 20,22-dihydrodigoxin-21,23-diol and digoxin-21-salicylidene, inhibit the differentiation of mouse and human Th17 cells[[67]]. Digoxin was shown to specifically inhibit RORγt transcriptional activity.

In the motor cortex, loss of Betz cells was also confirmed. Synaptophysin immunostaining of the lumbosacral cord also revealed decreased expression outside the old lesions, excluding the posterior horn. Interestingly, decreased expression of synaptophysin was also evident in the cervical anterior horns, where no old lesions were observed. No Bunina bodies, TDP-43 inclusions, or Golgi fragmentation were found. Neurogenic atrophy was evident in the iliopsoas and scalenus muscles, and inclusion body myositis-like changes were also observed in these muscles and the tongue. Was it possible to have diagnosed this patient as having ALS? We consider that

the features in this case may have represented the pathology of long-standing and/or fatal PPS itself, and not ALS. “
“We describe a 78-year-old Japanese woman with early-stage progressive supranuclear palsy (PSP). She had a 3-week find more history of postural instability and gait disturbance. On examination, upper vertical gaze palsy, akinesia, hyperreflexia with pathological reflexes, hesitation, and postural instability were observed. Rigidity and resting tremors were not apparent. Brain MRI revealed atrophy of the frontotemporal GS-1101 purchase lobes and dilatation of the third ventricle. A month later, she died of cerebral infarction. The total duration

of her clinical course was approximately 2 months. The brain weighed 1180 g after fixation. Macroscopically, mild atrophy of the frontal lobes and mild depigmentation Tyrosine-protein kinase BLK of the substantia nigra were observed. The conspicuous findings included degeneration confined to the subthalamic nucleus and substantia nigra and widespread but infrequent tau-positive neurofibrillary tangles/pretangles and glial fibrillary tangles (tuft-shaped astrocytes, coiled bodies and argyrophilic threads)

in the brain. It has been reported that the most affected areas in PSP are the globus pallidus, subthalamic nucleus and substantia nigra. We suggest that degeneration in PSP would start with involvement of the substantia nigra and subthalamic nucleus. “
“Y. Liu, X. Zhang, Y. Liang, H. Yu, X. Chen, T. Zheng, B. Zheng, L. Wang, L. Zhao, C. Shi and S. Zhao (2011) Neuropathology and Applied Neurobiology37, 395–405 Targeting X box-binding protein-1 (XBP1) enhances sensitivity of glioma cells to oxidative stress Aims: Reactive oxygen species (ROS) and oxidative stress are tightly linked with cancers including gliomas. We previously reported the protective role of X box-binding protein-1 (XBP1) against oxidative stress in both mouse embryofibroblasts and human Hela cells. This study was to investigate XBP1-mediated protection against oxidative stress in the treatment of gliomas. Materials and methods: XBP1 expression levels were knocked down by siRNA transfection in the U251MG cell line.