Z-scheme WO3/PANI heterojunctions with enhanced photocatalytic activity under visible light: A depth experimental and DFT studies.

A WO3@PANI heterojunction photocatalyst with a various mass ratio of polyaniline to WO3 was obtained via the in situ oxidative deposition polymerization of aniline monomer in the presence of WO3 powder. The characterization of WO3@PANI composites was carried via X-ray diffraction (XRD), scanning electron microscopy (SEM-EDS), transmission electron microscopy (TEM), Fourier transform infrared spectroscopy (FT-IR), ultraviolet-visible diffuse reflection spectroscopy (DRS), X-ray photoelectron spectroscopy (XPS) and photoluminescence spectroscopy (PL). The photocatalytic efficiency of WO3@PANI photocatalysts was assessed by following the decomposition of the Rhodamine B (RhB) dye under visible light irradiation (λ >420 nm). The results evidenced the high efficiency of the WO3@PANI (0.5 wt %) nanocomposite in the photocatalytic degradation of RhB (90% within 120 min) under visible light irradiation 3.6 times compared to pure WO3. The synergistic effect between PANI and WO3 is the reason for the increased photogenerated carrier separation. The superior photocatalytic performance of the WO3@PANI catalyst was ascribed to the increased visible light in the visible range and the efficient charge carrier separation. Furthermore, the Density Functional Theory study (DFT) of WO3@PANI was performed at the molecular level, to find its internal nature for the tuning of photocatalytic efficiency. The DFT results indicated that the chemical bonds connected the solid-solid contact interfaces between WO3 and PANI. Finally, a plausible photocatalytic mechanism of WO3@PANI (0.5 wt %) performance under visible light illumination is suggested to guide additional photocatalytic activity development.

FUS immunoreactivity of neuronal and glial intranuclear inclusions in intranuclear inclusion body disease.

AIMS: Recent studies have shown that fused-in-sarcoma (FUS) protein is a component of 'neuronal' intranuclear inclusion bodies (INIBs) in the brains of patients with intranuclear inclusion body disease (INIBD). However, the extent and frequency of FUS-immunoreactive structures in INIBD are uncertain. METHODS: We immunohistochemically examined the brain, spinal cord and peripheral ganglia from five patients with INIBD and five control subjects, using anti-FUS antibodies. RESULTS: In controls, the nuclei of both neurones and glial cells were intensely immunolabelled with anti-FUS and neuronal cytoplasm was weakly positive for FUS. In INIBD, neuronal and glial INIBs in the brain and spinal cord were positive for FUS. FUS-positive INIBs were also found in the peripheral ganglia. The proportion of FUS-positive neuronal INIBs relative to the total number of inclusion-bearing neurones ranged from 55.6% to 83.3% (average 73.2%) and that of FUS-positive glial INIBs ranged from 45.9% to 85.7% (average 62.7%). The nucleus and cytoplasm of inclusion-bearing neurones and glial cells showed no FUS immunoreactivity. CONCLUSIONS: These findings suggest that FUS is incorporated into INIBs in both neurones and glial cells and that loss of normal FUS immunoreactivity may result from reduced protein expression and/or sequestration within inclusions.

Relationship between Bunina bodies and TDP-43 inclusions in spinal anterior horn in amyotrophic lateral sclerosis.

AIMS: Amyotrophic lateral sclerosis (ALS) is characterized by upper and lower motor neurone involvement with Bunina bodies (BBs) and TDP-43 inclusions. To elucidate the relationship between BBs and TDP-43 inclusions, we examined the spinal cord from 18 patients with ALS. METHODS: Five serial sections from lumbar cord were first stained with haematoxylin and eosin to detect BBs and subsequently immunostained with anti-TDP-43 antibody. Immunoelectron microscopy was performed on vibratome sections from two cases of ALS. RESULTS: BBs were found in 15 out of 18 cases. TDP-43 inclusions were found in all the cases. The average incidence of anterior horn cells with BBs and TDP-43 inclusions relative to the total number of neurones was 17.1% and 46.4%, respectively. The concurrence of both inclusions in the same neurones was found in 15 cases. The incidence of co-localization of BBs and TDP-43 inclusions was 15.7% of total neurones. The frequency of TDP-43 inclusions was significantly higher in neurones with BBs than in those without. Ultrastructurally, TDP-43-immunoreactive filamentous structures were intermingled with early-stage BBs, but not associated with advanced-stage BBs. CONCLUSION: These findings suggest that there is a close relationship in the occurrence between BBs and TDP-43 inclusions.

NUB1, an interferon-inducible protein, mediates anti-proliferative actions and apoptosis in renal cell carcinoma cells through cell-cycle regulation.

BACKGROUND: NEDD8 ultimate buster 1 (NUB1) is an interferon (IFN)-inducible protein that downregulates NEDD8 expression and its conjugation system. Although overexpression of NUB1 induces a growth-inhibitory effect in cells, the mechanisms underlying the anti-mitogenic actions of NUB1 in cancer cells remain uncertain. We investigated the anti-cancer effects of NUB1 in human renal cell carcinoma (RCC) cells. METHODS: Nine human RCC cells were used for this study. The proliferation of RCC cells exposed to IFN-alpha was measured by water-soluble tetrazolium salt assay. The expression level of NUB1 in cells was measured by quantitative reverse transcriptase PCR or western blot analysis. Apoptosis and cell-cycle analysis were performed by flow cytometry. Silencing of NUB1 was performed using a small interfering RNA. RESULTS: Both NUB1 messenger RNA and protein were significantly induced by IFN-alpha in seven out of nine selected RCC cell lines, and the NUB1 expressions induced by IFN-alpha correlated positively with cell growth inhibition. Overexpression of NUB1 remarkably induced S-phase transition during cell cycle and apoptosis in IFN-alpha-resistant A498 cells, in which NUB1 is not induced by IFN-alpha. The expression levels of two cell-cycle regulator proteins, cyclin E and p27, were increased under the aforementioned conditions. The knockdown of NUB1 enhanced cell proliferation of IFN-alpha-resistant A498 cells and suppressed IFN-alpha-induced growth inhibition in IFN-alpha-sensitive 4TUHR cells. CONCLUSION: NUB1 may be a key factor involved not only in cell growth inhibition by IFN-alpha in RCC cells but also in the anti-cancer effect against IFN-alpha-resistant RCC cells.

Chemical status of selenium in evaporation basins for disposal of agricultural drainage.

Evaporation basins (or ponds) are the most commonly used facilities for disposal of selenium-laden saline agricultural drainage in the closed hydrologic basin portion of the San Joaquin Valley, California. However concerns remain for potential risk from selenium (Se) toxicity to water fowl in these evaporation basins. In this study, we examined the chemical status of Se in both waters and sediments in two currently operating evaporation pond facilities in the Tulare Lake Drainage District. Some of the saline ponds have been colonized by brine-shrimp (Artemia), which have been harvested since 2001. We evaluated Se concentration and speciation, including selenate [Se(VI)], selenite [Se(IV)], and organic Se [org-Se or Se(-II)] in waters and sediment extracts, and fractionation (soluble, adsorbed, organic matter (OM)-associated, and Se(0) and other resistant forms) in sediments and organic-rich surface detrital layers from the decay of algal blooms. Selenium in ponds without vascular plants exhibited similar behavior to wetlands with vascular plant present, indicating that similar Se transformation processes and mechanisms had resulted in Se immobilization and an increase of reduced Se species [Se(IV), org-Se, and Se(0)] from Se(VI)-dominated input waters. Selenium concentrations in most pond waters were significantly lower than the influent drainage water. This decrease of dissolved Se concentration was accompanied by the increase of reduced Se species. Selenium accumulated preferentially in sediments of the initial pond cell receiving drainage water. Brine-shrimp harvesting activities did not affect Se speciation but may have reduced Se accumulation in surface detrital and sediments.

Arsenic speciation and accumulation in evapoconcentrating waters of agricultural evaporation basins.

To sustain agricultural productivity, evaporation basins (or ponds) have been widely used for the disposal of agricultural drainage in areas requiring subsurface drainage in the San Joaquin Valley of California, USA. The drainage water contains elevated concentration of trace elements including selenium (Se) and arsenic (As). Unlike Se, little information is available about As, a potentially high risk element. The objective of this study was to characterize the chemical behavior of As and acquire data for better understanding of biogeochemical processes and conditions affecting As fate in evaporation ponds. The study site was a 726 ha evaporation basin facility (containing 10 cells with water flowing in series) in the hydrologically closed Tulare Basin of California. We examined water chemistry, As concentration and speciation along the water flow path between cells as well as within the cells. Arsenic concentrations in the water increased linearly with Cl(-), a conservative ion from evapoconcentration. Reduced As species as arsenite [As(III)] and organic arsenic (org-As) also increased with increases in Cl(-) and salinity. Water samples with elevated EC (i.e., towards the end of flow path) had high dissolved organic matter, low dissolved oxygen, and elevated sulfide concentrations, indicating the development of reducing conditions. We hypothesize that such changes could facilitate the reduction of arsenate [As(V)] to As(III) and org-As. Elevated As in sediment profiles indicate a solid phase sink mechanism, but not significant enough to remove and reduce As concentrations in the water columns. These findings help us better define the processes that affect As in drainage facilities and contribute to our understanding of how As behaves in other regions of the world that have similar climatic and hydrogeochemical conditions.

Detection and localization of HIV-1 DNA in renal tissues by in situ polymerase chain reaction.

The localization of HIV-1 DNA in renal tissues is critically important for understanding pathogenesis of HIV-associated nephropathy (HIVAN), but the clarification has been technically challenging. We applied in situ polymerase chain reaction (IS-PCR) to human renal tissues to demonstrate viral entry into the renal epithelial cells in vivo. To test the specificity of this method and to determine the cell types infected, we used IS-PCR followed by in situ hybridization (ISH) and IS-PCR followed by immunohistochemistry and histochemical counterstains. Brief 2 hour fixation in 4% paraformaldehyde had 92.9% sensitivity and 100% specificity for detection of viral DNA in renal biopsies of HIVAN patients, compared to 70.8% sensitivity and 66.7% specificity in renal biopsies fixed overnight in 10% formalin. Under optimized conditions, the only signals detectable in HIV-1 seronegative cases were false positives attributable to renal tubular apoptosis. In HIVAN cases, positive signal was observed in podocytes, parietal cells, renal tubular cells, and interstitial leukocytes. Immunohistochemical co-labeling for pan-T cell and macrophage markers revealed that the interstitial leukocytes with positivity for HIV-1 DNA included both T cells and macrophages. Application of ISH after IS-PCR showed the same distribution of signal as observed using IS-PCR alone, confirming the specificity of the technique. IS-PCR is a powerful technique to detect viral DNA in human tissue sections, but requires proper use of negative controls to set optimal fixation, protein digestion, and amplification conditions.

Formant interaction as a cue to vowel perception: a case report.

Accumulating evidence indicates that cerebral processing of consonants and vowels is separable. It has been shown that disordered temporal acuity leads to disturbed consonant perception in cases with pure word deafness. In contrast, there has been no clear explanation of how vowel perception is impaired. We examined a patient with auditory agnosia, who showed a differential ability to identify the five Japanese vowels after bilateral cerebral lesions. He correctly identified the vowel [a] in more than 70% of auditory presentations, whereas he identified [i] in only about 30% of presentations. The difference between the first and second formant frequencies "F2-F1" and an artificially defined value "F1-(F2-F1)" for each vowel correlated significantly with the percentage of correct identifications. These findings support the hypothesis that vowel perception is based on formant interactions.

Selenium removal and mass balance in a constructed flow-through wetland system.

A field study on the removal of Se from agricultural subsurface drainage was conducted from May 1997 to February 2001 in the Tulare Lake Drainage District (TLDD) of San Joaquin Valley, California. A flow-through wetland system was constructed consisting of ten 15- x 76-m unlined cells that were continuously flooded and planted with either a monotype or combination of plants, including sturdy bulrush [Schoenoplectus robustus (Pursh) M.T. Strong], baltic rush (Juncus balticus Willd.), smooth cordgrass (Spartina alterniflora Loisel.), rabbitsfoot grass [Polypogon monspeliensis (L.) Desf.], salt-grass lDistichlis spicata (L.) Greene], cattail (Typha latifolia L.), tule [Schoenoplectus acutus (Muhl. ex Bigelow) A. Löve & D. Löve], and widgeon grass (Ruppia maritima L.). One cell had no vegetation planted. The objectives of this research were to evaluate Se removal efficiency of each wetland cell and to carry out a mass balance on Se. The inflow drainage water to the cells had average annual Se concentrations of 19 to 22 microg L(-1) dominated by selenate [Se(VI), 95%]. Average weekly water residence time varied from about 3 to 15 d for Cells 1 through 7 (target 7 d), 19 to 33 d for Cells 8 and 9 (target 21 d), and 13 to 18 d for Cell 10 (target 14 d). Average weekly Se concentration ratios of outflow to inflow ranged from 0.45 to 0.79 and mass ratio (concentration x water volume) from 0.24 to 0.52 for year 2000, that is, 21 to 55% reduction in Se concentration and 48 to 76% Se removal in mass by the wetland, respectively. The nonvegetated cell showed the least Se removal both in concentration and in mass. The global mass balance showed that on the average about 59% of the total inflow Se was retained within the cells and Se outputs were outflow (35%), seepage (4%), and volatilization (2%). Independent measurements of the Se retained in the cells totaled 53% of the total Se inflow: 33% in the surface (0-20 cm) sediment, 18% in the organic detrital layer above the sediment, 2% in the fallen litter, < 1% in the standing plants, and < 1% in the surface water. Thus, about 6% of the total Se inflow was unaccounted for in the internal compartments.

A case of frontal network amnesia.

A 63 year old man developed an amnesic syndrome coupled with an array of "frontal lobe" signs after bilateral small subcortical infarcts. His amnesia was characterised by severe difficulty in voluntary recall of recently memorised verbal and non-verbal materials, while his recognition for the same materials was less affected. The symptoms remained unimproved at a follow up evaluation eight months after onset. Magnetic resonance imaging showed two small circumscribed lesions, one in the dorsomedial nucleus of the left thalamus and the other in a region of the right globus pallidus and anterior limb of the right internal capsule. The mammillothalamic tracts and anterior nuclei of the thalami were clearly spared bilaterally. The left dorsomedial nucleus lesion disrupted the thalamofrontal circuit, while the anterior limb lesion of the right internal capsule disconnected the same circuit by damaging part of the anterior thalamic radiation. Thus the amnesia in this patient may have been caused by disruption of the bilateral thalamofrontal circuits. This type of amnesic pathology should be separated from more conventional types of amnesia that are produced by disruption of the so called Papez circuit or the Delay-Brion memory system.

Interleukin-1beta stimulates galectin-9 expression in human astrocytes.

Galectin-9 is an eosinophil chemoattractant produced by activated T lymphocytes. We have addressed expression of galectin-9 in normal human astrocytes in culture. Expression of galectin-9 mRNA and protein were examined by reverse transcription-polymerase chain reaction (RT-PCR), Western blotting, and immunofluorescent staining. Interleukin-1beta (IL-1beta) was found to enhance the galectin-9 expression in time- and concentration-dependent manners. Galectin-9 protein was detected in the membrane fraction, 105 000 x g precipitate, and immunofluorescent staining revealed diffuse cellular and perinuclear distributions. Dexamethasone pretreatment almost completely suppressed the production. We conclude that astrocytes produce galectin-9 in response to the stimulation with IL-1beta, and this may contribute to inflammatory reactions in the CNS.

Neuropathological features of mitochondrial disorders.

Genetic defects affecting the mitochondrial respiratory chain comprise an important cause of encephalomyopathies. Considering the structural complexity of the respiratory chain, its dual genetic control, and the numerous nuclear genes required for proper assembly of the enzyme complexes, the phenotypic heterogeneity is not surprising. From a neuropathological view point, application of in situ hybridization and immunohistochemistry to study the choroid plexus and brain-blood barrier in "prototypes" of mitochondrial encephalopathies have revealed alterations that we think are important in the pathogenesis of central nervous system dysfunction in these disorders. As the role of the blood-cerebrospinal fluid (CSF) and brain-blood barriers in mitochondrial encephalopathies is better understood, manipulation of their functions offers promises for therapeutic interventions.

Expression of beta-synuclein in normal human astrocytes.

Although alpha- and beta-synucleins are expressed predominantly in presynaptic nerve terminals, recent studies have demonstrated that alpha-synuclein is also expressed in cultured astrocytes and oligodendrocytes. We determined whether beta-synuclein might be expressed in astrocytes. Beta-synuclein mRNA and protein were detected in normal human astrocytes in culture, and immunofluorescent staining showed that beta-synuclein protein was expressed within the cytoplasm and nucleus. Furthermore, beta-synuclein immunoreactivity was present in astrocytes, but not in oligodendrocytes, in normal human brain tissues. Ultrastructurally, beta-synuclein immunoreactivity was found in the cytoplasm of astrocytes, in association with the plasma membrane, ribosomes, rough endoplasmic reticulum and the nuclear outer membrane. The novel expression of beta-synuclein in astrocytes may provide an important insight about the role of this protein.

Soluble interleukin-6 receptor alpha inhibits the cytokine-Induced fractalkine/CX3CL1 expression in human vascular endothelial cells in culture.

Soluble form of IL-6 receptor alpha (sIL-6R) is known to serve as an agonist, without exogenous IL-6, on endothelial cells which do not express IL-6R but have only IL-6 receptor beta chain, gp130. We investigated the effect of sIL-6R on fractalkine expression in human umbilical vein endothelial cells (HUVECs) in culture. sIL-6R markedly inhibited HUVEC fractalkine/CX3CL1 expression induced by interleukin (IL)-1alpha, tumor necrosis factor (TNF)-alpha, or interferon (IFN)-gamma. IL-1alpha-induced fractalkine expression was inhibited by sIL-6R in time- and concentration-dependent manners. The experiment using actinomycin D indicated that sIL-6R lowered the stability of fractalkine mRNA. The inhibitory effect of sIL-6R was reversed by anti-gp130 neutralizing antibody. sIL-6R inhibited adhesion of mononuclear cells (MNCs) to HUVEC monolayers stimulated with IFN-gamma, but it did not inhibit the adhesion to monolayers stimulated with IL-1alpha. MNC chemotactic activity of conditioned medium of HUVEC stimulated with IL-1alpha or IFN-gamma was inhibited by co-treatment with sIL-6R. sIL-6R may play a regulatory role in immune responses by modulating the interaction between leukocytes and the vascular endothelium.

Adefovir nephrotoxicity: possible role of mitochondrial DNA depletion.

This report investigates the pathomechanism of acute renal failure caused by toxic acute tubular necrosis after treatment with the antiretroviral agent adefovir. A 38-year-old white homosexual man with human immunodeficiency virus infection and no history of opportunistic infections was maintained on highly active antiretroviral therapy (HAART), including hydroxyurea, stavudine, indinavir, ritonavir, and adefovir dipivoxil. Histologic examination of the renal biopsy showed severe acute tubular degenerative changes primarily affecting the proximal tubules. On ultrastructural examination, proximal tubular mitochondria were extremely enlarged and dysmorphic with loss and disorientation of their cristae. Functional histochemical stains for mitochondrial enzymes revealed focal tubular deficiency of cytochrome C oxidase (COX), a respiratory chain enzyme partially encoded by mitochondrial DNA (mtDNA), with preservation of succinate dehydrogenase, a respiratory chain enzyme entirely encoded by nuclear DNA (nDNA). Immunoreactivity for COX subunit I (encoded by mtDNA) was weak to undetectable in most tubular epithelial cells, although immunoreactivities for COX subunit IV and iron sulfur subunit of respiratory complex III (both encoded by nDNA) were well preserved in all renal tubular cells. Single-renal tubule polymerase chain reaction revealed marked reduction of mtDNA in COX-immunodeficient renal tubules. We conclude that adefovir-induced nephrotoxicity is mediated by depletion of mtDNA from proximal tubular cells through inhibition of mtDNA replication. This novel form of nephrotoxicity may serve as a prototype for other forms of renal toxicity caused by reverse transcriptase inhibitors.

Expression of alpha-synuclein in a human glioma cell line and its up-regulation by interleukin-1beta.

Although alpha-synuclein is expressed primarily in neurons, it is a major component of oligodendroglial and astrocytic inclusions in several neurodegenerative diseases. Recent study has further demonstrated that alpha-synuclein is expressed in cultured rat oligodendrocytes. We determined whether alpha-synuclein might be expressed in astrocytic cells. alpha-Synuclein mRNA and protein were detected in U251 human astrocytic glioma cells and normal human astrocytes, and the levels were increased in the former, but not in the latter, by stimulation with interleukin-1beta in a time- and concentration-dependent manner. Serum deprivation also led to an increase of alpha-synuclein mRNA and protein in U251 cells. Immunofluorescent staining confirmed the cell-associated alpha-synuclein. These findings suggest that human astrocytes can produce alpha-synuclein in culture and that certain inflammatory cytokines and cell stress increase alpha-synuclein expression.

Myopathy with tubulin-reactive crystalline inclusions.

A 61-year-old man with muscle aches and persistently elevated serum creatine kinase had aggregates of randomly oriented, rhomboidal or rectangular protein crystalline inclusions in the sarcoplasm of type II fibers. Immunochemical studies showed strong reactivity of the inclusions to tubulin antibodies, suggesting that these unique crystalline inclusions may be a consequence of altered synthesis, processing, or degradation of tubulin.