Parkinson's disease and skin cancer risk: a nationwide population-based cohort study in Korea.

BACKGROUND: Previous studies have reported that patients with Parkinson's disease (PD) have a significantly lower risk of cancer. Studies reporting prevalence of skin cancers in Parkinson's disease mostly involve Caucasians. OBJECTIVE: A nationwide population-based study was conducted to determine the risk of skin cancer in patients diagnosed with PD in Korea. METHODS: Data obtained from National Health Insurance Claims records were used to retrieve information about 70 780 patients with newly diagnosed PD between January 2010 and December 2015. The control group included 353 900 sex- and age-matched patients without PD. In this nationwide population-based cohort study, we investigated the association between PD and skin cancer. RESULTS: The overall hazard ratio (HR) of skin cancers in patients with PD was 1.169 (95% CI, 1.005-1.359) compared with non-PD group. Among patients with PD, males aged above 65 had a 2.8-fold increase in the risk for melanoma development than the non-PD group (HR, 2.825; 95% CI, 1.395-5.721). In addition, female PD patients aged above 65 years showed a 1.3-fold increase in non-melanoma skin cancer risk than the non-PD group (HR, 1.305; 95% 1.073-1.589). CONCLUSION: Compared with the general population, Korean patients diagnosed with PD had a greater risk of skin cancer. Especially, male patients aged 65 years and above, and diagnosed with PD had a significant risk of melanoma development compared with control.

Silver nanoparticles induce Egr-1-dependent psoriasin expression via the ERK and p38 pathways.

BACKGROUND: Silver nanoparticles (Ag-NPs) can prevent bacterial infection and improve cutaneous wound healing owing to their antimicrobial activity. However, the mechanism of their antimicrobial activity is poorly understood. AIM: To determine the mechanistic relationship between Ag-NP treatment and expression of psoriasin. METHODS: Human epidermal keratinocytes, neonatal (HEKn) were used. Psoriasin mRNA expression was measured by reverse transcription PCR and real-time PCR. Western blotting was performed to verify expression of early growth response-1 (Egr-1) and psoriasin, and phosphorylation of mitogen-activated protein kinase (MAPK). Psoriasin promoter activity by Egr-1 was detected by a luciferase assay. RESULTS: Treatment of HEKn with Ag-NPs induced psoriasin mRNA and protein expression. Upregulation of psoriasin promoter activity was also observed in the luciferase assay. Ag-NPs increased Egr-1 expression, promoter activity and nuclear translocation in HEKn. Psoriasin luciferase activity was increased in HEKn transfected with Egr-1 pcDNA 3.1. Ag-NPs activated MAPK pathways including the extracellular signal-regulated kinase (ERK), p38, and c-Jun-N-terminal kinase (JNK) pathways. The upregulation of Egr-1 expression by Ag-NP stimulation was inhibited by ERK and p38 inhibitors, but not by a JNK inhibitor. Psoriasin expression was reduced in Egr-1 small interfering RNA-transfected HEKn. CONCLUSIONS: Ag-NP treatment induces upregulation of psoriasin expression through Egr-1 expression. We suggest that the ERK and p38 pathways are involved in Egr-1-dependent psoriasin expression.

Acquired enophthalmos with systemic lupus erythematosus.

Ocular involvement sometimes occurs with systemic lupus erythematosus (SLE) but enophthalmos with SLE is rare. We report a case of enophthalmos with SLE. A 25-year-old male was admitted for two weeks of fever, sore throat, arthralgia, chest pain and right arm weakness with pain. We diagnosed him with SLE with malar rash, arthritis, pleural effusion, proteinuria, leukopenia, positive antinuclear antibody, anti-dsDNA, and lupus anticoagulant. The patient was prescribed high-dose prednisolone and hydroxychloroquine 400 mg. One week after discharge, he complained about a sensation of a sunken right eye. CT showed right enophthalmos, a post-inflammatory change and chronic inflammation. Proteinuria increased to 3.8 g/day after the patient stopped taking prednisolone. Cyclophosphamide therapy was administered for three months without improvement. We decided to restart prednisolone and change cyclophosphamide to mycophenolate mofetil. Proteinuria decreased but enophthalmos remains as of this reporting.

Analytic parallel-polarized light imaging technique using various light-emitting diodes: a comparison with skin conductance values.

BACKGROUND: The quantitative difference of the light reflected from a skin surface can be analyzed using parallel-polarized light (PPL) photography when combined with an analytic technique similar to colorimetric photography. OBJECTIVE: To improve the PPL photography technique as an assessment tool for the evaluation of skin condition using light-emitting diodes (LED) of different colors. METHOD: Parallel-polarized light images were taken using white and green LED illuminators. The acquired images were transformed to CIELAB coordinates. An in-house skin conductance meter was constructed to assess skin hydration level. A dermatologist evaluated the clinical grading of dryness and glossiness. These clinical severities were also compared statistically with the CIELAB values. RESULTS: As with the green illuminator, the correlation analysis of whole sites showed that the L* value positively correlated with age (r = 0.18677, P < 0.05), and that the a* value has negative and positive relationships with age (r = -0.20528, P < 0.05) and glossiness (r = 0.20885, P < 0.05) respectively. CONCLUSION: The correlations between CIELAB values and multiple characteristics of skin were more significant when green LED was applied than when white light was applied. In addition, coherent relationships between the grade of dryness and skin conductance values showed that visual assessment could be appropriate for the study as with objective measurement.

Ascites associated with uterine leiomyoma in a 22-year-old woman with systemic lupus erythematosus.

Ascites in systemic lupus erythematosus (SLE) patients has a variety of etiologies, which usually require different treatment options. Our case was a 22-year-old patient with an unusual combination of ascites, uterine leiomyoma and SLE. The patient presented with painless ascites of an inflammatory nature. However, the ascites was not related to peritonitis and SLE disease activity. The ascites disappeared following laparotomy and tumor resection without additional medication. Gynecologic benign tumors including uterine leiomyoma can be the cause of ascites in SLE patients. Clinicians should be aware of that possibility in case painless ascites occurs in females with SLE.

Production and determination of the magnetic properties of the Fe-36Ni nanopowder via electrical explosion of wire in water and compacted alloy.

Fe-36Ni alloy nanopowder was prepared via electrical explosion of wire in DI water. The nanopowder was reduced in hydrogen at 500 degrees C for 30 min. Spark plasma sintering at 800 and 1000 degrees C for 10 min was used to obtain bulk samples from the hydrogen-reduced nanopowder. The sintered samples were annealed at 500 degrees C for 2 h. X-ray diffraction was used to analyze the phases of the nanopowder and sintered samples. The results showed that the sintered samples were formed in gamma-(Fe-Ni) solid solution. The particles sizes and morphologies of the as-synthesized and hydrogen-reduced nanoparticles were observed via transmission electron microscopy. The morphologies of the as-synthesized nanoparticles had spherical core-shell structures. Core was gamma-(Fe-Ni) and the shell was FeO. The nanoparticles of the as-synthesized and hydrogen reduced samples were found to be nearly spherical in shape, with average diameters of 32 and 70 nm, respectively. The hysteresis loops of the as-synthesized nanopowder, hydrogen reduced nanopowder, and sintered samples revealed ferromagnetic characteristics.

Potential roles of D-serine and serine racemase in experimental temporal lobe epilepsy.

To confirm the roles of D-serinergic gliotransmission in epilepsy, we investigated the relationship between spatiotemporally specific glial responses and the D-serine/serine racemase system in mesial temporal structures following status epilepticus (SE). In control animals, D-serine and serine racemase immunoreactivities were detected mainly in astrocytes. After SE, D-serine and serine racemase immunoreactivities were increased in astrocytes. Double-immunofluorescence study revealed that up-regulation of serine racemase immunoreactivity was relevant not to D-serine immunoreactivity but to nestin or vimentin immunoreactivity. Neither D-serine nor serine racemase was found in naïve or reactive microglia. In addition, phosphorylated N-methyl-D-aspartate (NMDA) receptor subunit 1 (pNR1-Ser896) immunoreactivity in the hippocampus was increased compared with controls. Increased D-serine immunoreactivity showed direct correlation with the phosphorylation of Ser896 of NR1. Given the findings of our previous study, these findings suggest that D-serine and serine racemase in astrocytes may play roles in neuronal hyperexcitability via a cooperative activation of NMDA receptors. Furthermore, serine racemase may be involved in migration and differentiation of immature astrocytes, which is relevant to reactive astrogliosis.

Genetic variations in the leptin and leptin receptor genes are associated with type 2 diabetes mellitus and metabolic traits in the Korean female population.

Type 2 diabetes mellitus (T2DM) is a metabolic disorder that is characterized by insulin resistance and hyperglycemia. Leptin inhibits the glucose-stimulated insulin secretion, and leptin receptors are present on beta cells as well as on fat cells, thus enabling leptin to modulate both insulin secretion and action. Therefore, leptin (LEP) and leptin receptor (LEPR) genes could play a role in the regulation of glucose and insulin after an oral glucose load. For the association study of LEP and LEPR with T2DM and metabolic traits, 752 women from Seoul National University Hospital (SNUH data) and 532 women from the Korean Health and Genome Study (KHGS data) were selected. Using the SNUH data, we identified that LEP-632G>A and +4998A>C polymorphisms were marginally associated with T2DM, LEP+4950G>A was significantly associated with several metabolic traits, and LEPR+5193G>A, +7187A>C, +27265G>A, +35861T>C, and +52289A>G showed strongly significant association with body mass index (BMI). We observed reproducibility of these results using the KHGS data; LEP+4950G>A and +4998A>C were significantly associated with systolic blood pressure and low-density lipoprotein cholesterol level, respectively. In conclusion, we observed that several polymorphisms in LEPR that had previous reports of association with BMI were significantly replicated in our samples and newly found that some variations of LEP were associated with T2DM and metabolic traits.

Effects of an intracellular Ca(2+) chelator on insulin resistance and hypertension in high-fat-fed rats and spontaneously hypertensive rats.

We explored the possibility that a sustained elevation of intracellular Ca(2+) concentration ([Ca(2+)](i)) may be a cellular abnormality common to both insulin resistance and hypertension. In high-fat diet (HFD) fed rats, the steady-state glucose infusion rate (GIR) during the euglycemic hyperinsulinemic clamp was reduced by 40% (P <.05) and mean arterial pressure (MAP) was elevated by 20 mm Hg (P <.01) in comparison to the normal chow-fed rats. Intravenous injection of 5,5'-dimethyl derivative of bis(o-aminophenoxy)ethane-N,N,N',N' tetraacetic acetoxymethyl ester (dimethyl-BAPTA/AM), an effective intracellular Ca(2+) chelator, 90 minutes before the clamp not only restored about 50% of the reduced GIR, but also normalized MAP in the HFD rats. The chelator injection also significantly increased GIR by 25% (P <.01) and reduced MAP about 30 mm Hg (P <.01) in the spontaneously hypertensive rats (SHR). In addition, we have recently shown in the HFD rats that an injection of dimethyl-BAPTA/AM normalizes elevated [Ca(2+)](i) in adipocytes. These results together demonstrate that lowering [Ca(2+)](i) simultaneously ameliorates both insulin resistance and hypertension and provide presumptive evidence that sustained high levels of [Ca(2+)](i) may play a common pathophysiologic role in these 2 diseases.

Improvement of insulin sensitivity by chelation of intracellular Ca(2+) in high-fat-fed rats.

It has been postulated that sustained high levels of intracellular calcium concentration ([Ca(2+)](i)) in the insulin target cells may cause insulin resistance. We evaluated this hypothesis by examining the effect of an intracellular Ca(2+) chelator, 5,5'-dimethyl derivative of bis (o-aminophenoxy) ethane-N,N,N',N' tetraacetic acetoxymethyl ester (dimethyl-BAPTA/AM), on insulin resistance. Insulin resistance was induced in rats by feeding a high-fat diet for 3 to 4 weeks. The whole body insulin sensitivity was determined by the steady state glucose infusion rate (GIR) under euglycemic hyperinsulinemic (6 mU x kg(-1) x min(-1)) clamps. Compared with control rats, the high-fat diet (HFD) fed rats showed significantly lower GIR (12.2 +/- 0.7 v 20.2 +/- 0.9 mg x kg(-1) x min(-1); P <.01). In the HFD rats, an intravenous injection of dimethyl-BAPTA/AM (6 mg/kg) 90 minutes before the clamps significantly increased GIR to 16.3 +/- 0.9 mg x kg(-1) x min(-1) (P <.02), reversing insulin resistance by about 50%; but this intervention had no effect in the controls. This increase in GIR by dimethyl-BAPTA/AM was observed without an increase in femoral artery blood flow, indicating that the chelator increased GIR directly through improving cellular responsiveness to insulin. The stimulatory effect of insulin on 2-deoxy glucose (2-DG) uptake by the isolated epididymal adipocytes was reduced by 35% in the HFD rats compared with the control rats (P <.01). Pretreatment of the HFD rats with dimethyl-BAPTA/AM restored 2-DG uptake to the level in the control rats. The direct measurement of [Ca(2+)](i) using fura-2/AM in isolated adipocytes showed that basal [Ca(2+)](i) was significantly higher in the HFD rats than in the control rats (145 +/- 11 v 112 +/- 9 nmol/L; P <.05). An injection of dimethyl-BAPTA/AM in the HFD rats lowered [Ca(2+)](i) to 127 +/- 11 nmol/L, which did not differ from the level in the control rats (P >.2). The present study clearly demonstrates that an injection of intracellular Ca(2+) chelator in the HFD rats reverses insulin resistance, as well as normalizes elevated [Ca(2+)](i) in the insulin target cells. The results strongly support that sustained high levels of [Ca(2+)](i) in the insulin target cells may play an important role in insulin resistance, at least in the HFD rats.

LIM kinase-2 induces programmed necrotic neuronal death via dysfunction of DRP1-mediated mitochondrial fission.

Although the aberrant activation of cell cycle proteins has a critical role in neuronal death, effectors or mediators of cyclin D1/cyclin-dependent kinase 4 (CDK4)-mediated death signal are still unknown. Here, we describe a previously unsuspected role of LIM kinase 2 (LIMK2) in programmed necrotic neuronal death. Downregulation of p27(Kip1) expression by Rho kinase (ROCK) activation induced cyclin D1/CDK4 expression levels in neurons vulnerable to status epilepticus (SE). Cyclin D1/CDK4 complex subsequently increased LIMK2 expression independent of caspase-3 and receptor interacting protein kinase 1 activity. In turn, upregulated LIMK2 impaired dynamic-related protein-1 (DRP1)-mediated mitochondrial fission without alterations in cofilin phosphorylation/expression and finally resulted in necrotic neuronal death. Inhibition of LIMK2 expression and rescue of DRP1 function attenuated this programmed necrotic neuronal death induced by SE. Therefore, we suggest that the ROCK-p27(Kip1)-cyclin D1/CDK4-LIMK2-DRP1-mediated programmed necrosis may be new therapeutic targets for neuronal death.

Utility of QuantiFERON-TB assay for prediction of tuberculosis development in kidney transplant patients in an intermediate-tuberculosis-burden country: lack of evidence for enhanced prediction for short-term tuberculosis development.

INTRODUCTION: Although a latent tuberculosis (TB) infection is a risk factor for active TB, the diagnosis of latent TB infection is difficult in end-stage renal disease patients. PATIENTS AND METHODS: We retrospectively compared the results of the QuantiFERON-TB (QFT) test and the tuberculin skin test in patients on the waiting list for kidney transplantation (KT), and investigated whether the QFT test can predict TB development in KT recipients in an intermediate-TB-burden country. RESULTS: The incidence of post-KT TB was 283 cases/100,000 patient-years among 1274 KT recipients at the Seoul National University Hospital. The overall standardized incidence ratio of TB was 4.358 compared with the general population. A past history of TB infection, smoking history, myocardial infarction after KT, and pneumocystis infection were significant predictors of subsequent TB development (adjusted odds ratios were 3.618, 2.959, 9.993, and 5.708, respectively). Among the 129 recipients who had the QFT test, 42 patients (32.5%) had positive a QFT. At a median follow-up of 8.4 ± 6.8 months, 1 patient with positive QFT results developed TB after KT, and 1 of the 87 patients with negative QFT results developed TB after KT. In both of these 2 cases, active TB developed despite isoniazid prophylaxis. Among 272 patients on the waiting list for KT, the tuberculin skin test and QFT were positive in 22.8% and 35.3%, respectively. The degree of agreement between the 2 tests was poor (κ = 0.352). CONCLUSIONS: The QFT test did not predict subsequent short-term TB development. Furthermore, a long-term and larger-scale study is needed to confirm our results.

The effects of photon flux on energy spectra and imaging characteristics in a photon-counting x-ray detector.

The purpose of this paper was to investigate the effect of photon flux on the recorded energy spectrum and images produced with a photon-counting detector. We used a photon-counting cadmium telluride (CdTe) x-ray detector (model PID350, Oy Ajat, Finland). The CdTe array was composed of 16 384 pixels, each 0.35 × 0.35 × 0.75 mm(3) in dimension. The photon flux is controlled by an additional aluminum filter (1, 10, 20, 30 and 40 mm). Images were acquired at three different tube voltages (50, 70 and 90 kVp) with various thicknesses of photon flux control (PFC) filters. The data acquisition time was changed to acquire an approximately equal number of counts within the selected energy window between different thicknesses of PFC filters at the same tube voltage. A phantom was manufactured to evaluate the photon flux effect on the image. The phantom was made from polymethyl methacrylate and four concentrations of iodine. The photon flux effect on the image was evaluated by the signal-difference-to-noise ratio (SDNR) between iodine and the background material. The changes of photon flux affected the recorded energy spectra and image. The thickness of the PFC filter that showed the maximum SDNR differed according to the tube voltage. The 10 mm PFC filter showed the highest SDNR at 50 and 70 kVp, while the 30 mm PFC filter exhibited the highest SDNR at 90 kVp. The SDNR was improved up to, on average, 30-fold in optimal photon flux conditions which acquired a spectrum including the lowest electronic noise with no pulse pile-up effect. The results of this study showed that the photon flux affected not only the acquired energy spectrum but also the image. Based on these results, the spectral distortion correction should be considered in connection with the image that is the ultimate purpose of medical imaging.

Radiological response predicts survival following transarterial chemoembolisation in patients with unresectable hepatocellular carcinoma.

BACKGROUND: It remains unclear whether initial compact lipiodol uptake after transarterial chemoembolisation (TACE) is associated with improved survival in patients with hepatocellular carcinoma (HCC). AIM: To reveal the clinical relevance of compact lipiodolisation after TACE. METHODS: We studied 490 patients with unresectable HCC who had first been treated with TACE. Compact lipiodolisation was defined as the absence of an arterial enhancing lesion, reflecting complete lipiodol uptake, as assessed by dynamic computed tomography (CT) 1 month after treatment. The rate of initial compact lipiodolisation was analysed according to multiplicity and size of tumour, and survival of patients who achieved compact lipiodolisation was compared to that of patients who did not. RESULTS: Of the 490 patients, 409 (83.5%) were in Child-Pugh class A and 81 (16.5%) in class B. The rate of initial compact lipiodolisation in single HCCs was higher than that in multinodular HCCs (33.7% vs. 14.6%, P < 0.001). Among single HCCs, the rate of compact lipiodolisation in tumours ≤5, 5-10 and >10 cm was 46.6%, 13.6%, and 0% respectively. The 1-, 3- and 5-year survival rates of patients with compact uptake were 92.7%, 70.7% and 52.4% compared to 60.8%, 28.0% and 16.9% in patients with noncompact lipiodolisation. Multivariate analysis revealed that Child-Pugh class, alpha-fetoprotein level, tumour node metastasis stage, portal vein thrombosis and initial compact lipiodolisation were independent predictors of survival. CONCLUSIONS: Initial compact lipiodol uptake after transarterial chemoembolisation is associated with improved survival in patients with unresectable hepatocellular carcinoma. Accordingly, initial complete lipiodolisation should be considered a relevant therapeutic target.

F-actin depolymerization accelerates clasmatodendrosis via activation of lysosome-derived autophagic astroglial death.

Clasmatodendrosis is an irreversible astroglial degenerative change, which includes extensive swelling and vacuolization of cell bodies and disintegrated and beaded processes. Since alteration in F-actin level influences on the formation of vacuoles/vesicles during exocytosis/endocytosis in astrocytes, we investigated whether F-actin polymerization involves clasmatodendrosis in the rat hippocampus following status epilepticus (SE). In the present study, vacuoles in clasmatodendrotic astrocytes showed LAMP-1 and LC3-II (a marker for autophagy) immunoreactivity. These findings reveal that clasmatodendrosis may be lysosome-derived autophagic astroglial death. Jasplakinolide (an F-actin stabilizer) infusion significantly decreased the size and the number of medium/large-sized vacuoles in each clasmatodendritic astrocyte accompanied by enhancement of phalloidin signals, as compared to vehicle-infusion. In contrast, latrunculin A (an F-actin-depolymerizing agent) infusion increased the size and the number of medium/large-sized vacuoles, which were dissociated adjacent to cell membrane. Therefore, our findings suggest that F-actin stabilization may inhibit lysosome-derived autophagic astroglial death during clasmatodendrosis.

ReLA/P65-serine 536 nuclear factor-kappa B phosphorylation is related to vulnerability to status epilepticus in the rat hippocampus.

Although nuclear factor-kappa B (NF-κB) is essential for neuron survival and its activation may protect neuron against oxidative-stresses or ischemia-induced neurodegeneration, NF-κB activation can contribute to inflammatory reaction and apoptotic cell death after brain injury and stroke. However, there are little data concerning the specific pattern of NF-κB phosphorylations in neuronal damage/survival induced by status epilepticus (SE). In the present study, NF-κB phosphorylation showed the cellular specific pattern in responses to SE. p52-S865, p52-Ser869, p65-Ser276, p65-Ser311, p65-Ser468, and p65-Ser529 NF-κB phosphorylation was significantly decreased in the CA1 and CA3 pyramidal cells vulnerable to SE, although neuronal specific nuclear antigen immunoreactivity was strongly detected. In contrast, p65-Ser536 NF-κB phosphorylation was enhanced in these neurons accompanied by TUNEL- and Fluoro-Jade B 244signals. These findings serve as the first comprehensive description of the cellular specific distribution of NF-κB phosphorylation in response to pilocarpine-induced SE in the rat hippocampus, and suggest that enhancement in p65-Ser536 NF-κB phosphorylation may be closely relevant to neuronal vulnerability to SE, while others may be involved in neuronal survival.

The roles of fractalkine/CX3CR1 system in neuronal death following pilocarpine-induced status epilepticus.

Although fractalkine is one of chemokines involved in mediation of neuronal/microglial interaction, it is not known whether fractalkine/CX3CR1-mediated pathogenesis occurs in the rat brain following epileptogenic insults. In order to elucidate the roles of the fractalkine/CX3CR1 system in microglial activation and neurodegeneration induced by status epilepticus (SE), we investigated changes in fractalkine/CX3CR1 system within the rat hippocampus following SE. In non-SE induced animals, fractalkine and CX3CR1 immunoreactivity was detected in neurons and microglia, respectively. Following SE, fractalkine immunoreactivity was transiently increased in neurons and astrocytes. CX3CR1 immunoreactivity was also transiently detected in neurons (particularly in CA1 pyramidal cells). Intracerebroventricular infusions of recombinant rat fractalkine aggravated SE-induced neuronal damage, while fractalkine IgG or CX3CR1 IgG infusion alleviated it, compared to saline-infused animals. These findings suggest that fractalkine/CX3CR1 system may play an important role in SE-induced neuronal damages via neuron-microglial interactions.

The protective effects of interleukin-18 and interferon-γ on neuronal damages in the rat hippocampus following status epilepticus.

To elucidate whether interleukin-18 (IL-18) or interferon-γ (IFN-γ) participates in neurodegeneartion, we investigated the changes in IL-18 and IFN-γ systems within the rat hippocampus following status epilepticus (SE). In non-SE induced animals, IL-18, IL-18 receptor α (IL-18Rα), IFN-γ and IFN-γ receptor α (IFN-γRα) immunoreactivity was not detected in the hippocampus. Following SE, IL-18 immunoreactivity was increased in CA1-3 pyramidal cells as well as dentate granule cells. IL-18 immunoreactivity was also up-regulated in astrocytes and microglia/macrophages. IL-18Rα immunoreactivity was detected in astrocytes and microglia/macrophages. IFN-γ immunoreactivity was detected only in astrocytes within all regions of the hippocampus. IFN-γRα immunoreactivity was increased in neurons as well as astrocytes. Intracerebroventricular infusions of recombinant rat IL-18 or IFN-γ alleviated SE-induced neuronal damages, while neutralization of IL-18, IFN-γ or their receptors aggravated them, as compared to saline-infused animals. These findings suggest that astroglial-mediated IFN-γ pathway in response to IL-18 induction may play an important role in alleviation of SE-induced neuronal damages.

Differential expressions of aquaporin subtypes in astroglia in the hippocampus of chronic epileptic rats.

In order to elucidate the roles of aquaporins (AQPs) in astroglial responses, we investigated AQP expressions in the experimental epileptic hippocampus. In control animals, AQP1 protein expression was restricted to the ventricular-facing surface of the choroid plexus. AQP4 was expressed in astrocyte foot processes near blood vessels and in ependymal and pial surfaces in contact with cerebrospinal fluid. AQP9 protein has been detected in cells lining the cerebral ventricles, and in astrocytes. Six to eight weeks after status epilepticus (SE), AQP1 expression was mainly, but not all, detected in vacuolized astrocytes, which were localized in the stratum radiatum of the CA1 region. AQP4 was negligible in vacuolized CA1 astrocytes, although AQP4 immunoreactivity in non-vacuolized astrocytes was increased as compared to control level. AQP9 expression was shown to be mainly induced in non-vacuolized CA1 astrocytes. Therefore, our findings suggest that AQP subunits may play differential roles in various astroglial responses (including astroglial swelling and astroglial loss) in the chronic epileptic hippocampus.