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Jeju Haenyeo have been playing a crucial role in Jeju economy for a long time. However, the number of Jeju Haenye has decreased since the 1970s, despite the efforts from the government and Jeju Provincial Office including a variety of welfare and benefits. In order to understand the unique culture of Jeju Haenyeo, and to provide a good program to help transfer their muljil skills, a qualitative research including in-depth interviews and participant observation in combination of an ethnographic method was performed. For the qualitative research, the interview preparation was reviewed, the language and culture of local communities were understood, and the location of the researcher was determined. Then, the following procedures were carried out; selecting informants, gaining their confidence, forming a rapport with them, and collecting data. For a preliminary survey, The first author visited Jeju alone for 10 days from late June to early July in 2015. The first author walked around the area and observed the dialects and life of local people from the viewpoint of an outsider. For interviews, four still active and three former Jeju Haenyeo were selected from skilled workers with diving experience of at least 20 to 60 years. The transfer of Jeju Haenyeo’s muljil skills, and their education and training vary, depending on the community culture of each village. As a result, the transfer of Jeju Haenyeo’s muljil skills is carried out not just at the level of maternal succession, but it is also performed by the village community that participate in co-childcare and joint training of diving skills.

Mitochondrial dysfunction caused by oxidative stress appears at early stages of aging and age-related diseases. Plasma membrane redox enzymes act in a compensatory manner to decrease oxidative stress and supply reductive capacity to ensure cell survival. Plasma membrane redox enzymes transfer electrons from NAD(P)H to oxidized ubiquinone and α-tocopherol, resulting in inhibition of further oxidative damage. Plasma membrane redox enzymes and their partners are affected by aging, leading to progression of neurodegenerative disease pathogenesis. Up-regulating plasma membrane redox enzymes via calorie restriction and phytochemicals make cells more resistant to oxidative damage under stress conditions by maintaining redox homeostasis and improving mitochondrial function. Investigation into plasma membrane redox enzymes can provide mechanistic details underlying the relationships between plasma membrane redox enzymes and mitochondrial complexes and provide a good therapeutic target for prevention and delay of neurodegenerative disorders.

Modest levels of reactive oxygen species (ROS) are necessary for intracellular signaling, cell division, and enzyme activation. These ROS are later eliminated by the body’s antioxidant defense system. High amounts of ROS cause carcinogenesis by altering the signaling pathways associated with metabolism, proliferation, metastasis, and cell survival. Cancer cells exhibit enhanced ATP production and high ROS levels, which allow them to maintain elevated proliferation through metabolic reprograming. In order to prevent further ROS generation, cancer cells rely on more glycolysis to produce ATP and on the pentose phosphate pathway to provide NADPH. Pro-oxidant therapy can induce more ROS generation beyond the physiologic thresholds in cancer cells. Alternatively, antioxidant therapy can protect normal cells by activating cell survival signaling cascades, such as the nuclear factor erythroid 2-related factor 2 (Nrf2)-Kelch-like ECH-associated protein 1 (Keap1) pathway, in response to radio- and chemotherapeutic drugs. Nrf2 is a key regulator that protects cells from oxidative stress. Under normal conditions, Nrf2 is tightly bound to Keap1 and is ubiquitinated and degraded by the proteasome. However, under oxidative stress, or when treated with Nrf2 activators, Nrf2 is liberated from the Nrf2-Keap1 complex, translocated into the nucleus, and bound to the antioxidant response element in association with other factors. This cascade results in the expression of detoxifying enzymes, including NADH-quinone oxidoreductase 1 (NQO1) and heme oxygenase 1. NQO1 and cytochrome b5 reductase can neutralize ROS in the plasma membrane and induce a high NAD+/NADH ratio, which then activates SIRT1 and mitochondrial bioenergetics. NQO1 can also stabilize the tumor suppressor p53. Given their roles in cancer pathogenesis, redox homeostasis and the metabolic shift from glycolysis to oxidative phosphorylation (through activation of Nrf2 and NQO1) seem to be good targets for cancer therapy. Therefore, Nrf2 modulation and NQO1 stimulation could be important therapeutic targets for cancer prevention and treatment.

Inhibition of Notch signalling has shown anti-inflammatory properties in vivo and in vitro models of rheumatoid arthritis (RA). The objective of this study was to determine whether Notch1 might play a role in regulating T-regulatory cells (Tregs) in animal models of RA. Methods: Collagen-induced arthritis (CIA) and collagen antibody-induced arthritis (CAIA) were induced in C57BL/6, Notch1 antisense transgenic (NAS) or DBA1/J mice. We examined whether pharmacological inhibitors of γ-secretase (an enzyme required for Notch1 activation) and antisense-mediated knockdown of Notch1 could attenuate the severity of inflammatory arthritis in CIA and CAIA mice. Proportions of CD4+CD25+Foxp3+ Treg cells were measured by flow cytometry. To assess the suppressive capacity of Treg toward responder cells, CFSE-based suppression assay of Treg was performed. Results: γ-secretase inhibitors and antisense-mediated knockdown of Notch1 reduced the severity of inflammatory arthritis in both CIA and CAIA mice. Pharmacological and genetic inhibition of Notch1 signalling induced significant elevation of Treg cell population in CIA and CAIA mice. We also demonstrated that inhibition of Notch signalling suppressed the progression of inflammatory arthritis through modulating the expansion and suppressive function of regulatory T (Treg) cells. Conclusion: Pharmacological and genetic inhibition of Notch1 signalling suppresses the progression of inflammatory arthritis through modulating the population and suppressive function of Treg cells in animal models of RA.

The exit surface of a lens is designed using a three-dimensional free-form expression in order to easily modify a curved surface. This enables the design of numerical values and mathematical things using three-dimensional free-form expression, and enhances precision because it can be fine-tuned via numerical control. The standard of “Classification of Luminaire Light Distribution” for outdoor lighting fixtures by IESNA is adopted in order to examine the correlation between three-dimensional free-form surface expression and lighting performance. The variation of light distribution type and range is analyzed using the values of maximum light intensity and 50% light intensity. The actual tolerance occurs owing to parameters such as the thickness of the lens, the distance between LEDs, and the movement of the center of the incident surface; the effects of changes in these parameters on the performance are compared and analyzed.

Lipid-soluble ginseng extracts (LSGE) is known to inhibit many types of cancer cells through arresting cell cycle and inducing apoptosis. Usually, normal cells are can also be damaged by anti-tumor reagents. The plasma membrane redox system (PMRS) is enhanced to compensate mitochondrial dysfunction and impaired energy metabolism. NADH-quinone oxidoreductase 1 (NQO1), a plasma membrane redox enzyme, is known to be induced by panaxytriol, one of components of lipid-soluble ginseng extracts (LSGE). The objective of this study was determine the mechanisms of NQO1 involved in neuroprotection in response to cytotoxicity induced by LSGE. Exposure of control SH-SY5Y cells to LSGE resulted in dramatic loss of cell viability in a dose-dependent manner. The loss of cell viability was significantly recovered in cells transfected with NQO1. LSGE-induced cell death occurred through apoptosis such as cell shrinkage, chromatin condensation and cleavage of poly (ADP-ribose) polymerase. These apoptotic features were significantly attenuated by overexpression of NQO1. Levels of oxidative/nitrative damage were highly elevated by LSGE in a dose-dependent manner. However, these elevated levels were greatly reduced by overexpression of NQO1. In addition, overexpression of NQO1 attenuated the decrease in mitochondrial complex I activity caused by LSGE. Taken together, these findings suggest that overexpressed NQO1 can protect cells against LSGE-induced cytotoxicity through lowering oxidative/nitrative damage and delaying apoptosis, supporting that stimulation of NQO1 activity could be a therapeutic targets in neurodegeration.

The purpose of this paper is to analyze the effect of tube length in calibration instrumentation on dew point measurement of dew point sensors (DPS) and evaluation of measurement uncertainty. When measuring dew point temperature, various tube lengths between dew point generator and dew point sensor (DPS) cause a significant error due to moisture absorption of inner tube. The measurement is carried out to analyze the variation on measured dew point temperature for four cases of tube lengths with 300 mm, 1200 mm, 2500 mm and 5000 mm. The dew point temperature measurements were performed in the range from-60 °C to 10 °C by using calibrated standard chilled mirror hygrometer as reference standard. In order to investigate contribution to the standard uncertainty for the tube length variation as an uncertainty source, expanded uncertainties were evaluated for the cases including the effect of tube length variation as an uncertainty source and excluding it at each measurement point. The measurement was conducted according to standard calibration procedure of Korea Testing Laboratory which assures suitability and traceable results. It is also based on international standards.

Article history: In this paper, the band structural design that is typically in a line was arranged in a ring shape, so as to configure the high power LED lighting in such a way as to form a concentrated light distribution angle of less than 15 degrees. The parabolic aluminized reflector PAR38 that facilitates design using area and the area of the optical system to the same extent, applied a multiple light-source condenser lens optical system for the control of integration. The LED used here implemented a single linear light source using ans LED module with ans LED, flip-chip chip-scale package. The optical system was designed based on the energy star standard.

In this paper, the performance of a system was analyzed according to the design parameters of a LED secondary lens that can be applied at a very close range, e.g., for direct lighting or display systems. We designed the secondary lens of the very-close-range LED using an aspheric equation and analyzed its performance-particularly the angle of the beam spread, central luminous intensity, and light uniformity-with respect to the thickness of lens, radius, conic constant, and asphericity (4th). Our analysis shows that four parameters affect the performance. The simulation results indicate an optimal thickness of 1 mm and show that a larger radius yields higher performance. The optimal range for the conic constant was determined as -1.21 to -1.25, the optimal range for the asphericity was determined as 0.0047xx to 0.0049xx (4th).

Article history: We have investigated anamorphic prism lenses with distortions of 0.3-0.5%. We designed the plastic triangular lens and confirmed the minimum resolution using MTF graphs. Also we confirmed that the SVGA optical system can realize a resolution of 864 × 648 56 megapixels. A distortion of about 0.5% aberration appears in the maximum field, and a finite beam aberration of about 15 μm is confirmed. We made a mold based on the design data and completed the prism lens through exodus molding. We confirmed the shape error ( 40 nm) of the three sides. We made the videoinformation-display prototype glasses using prism lens by measuring the performance, we determined the distortion aberration (0.3%) and SVGA resolution. Our approach will enable fabrication of a portable large-screen display device for glasses and sunglasses for the domestic market and, after 2015, for the world market. Received 4 November 2014 Revised 7 December 2014 Accepted 10 December 2014

The purpose of this paper is to study the effect of purging rate on calibration or test of the dew point sensors and estimation of measurement uncertainty. The measurement is carried out to analyze the variation on measured dew point temperatures for the sample dew point sensors (DPS) due to various durations of purge by using calibrated standard chilled mirror hygrometer. To set up measurement condition, the whole measurement system were kept in the state of purging for 3 hours, 15 hours, 65 hours, 140 hours, 200 hours. The dew point temperatures were measured in the range from-50 °C to 10 °C. In order to investigate the effect of purging rate as an uncertainty source on the measurement uncertainty, the contributions to the standard uncertainty for purging rate were also estimated due to reference dew point temperatures. The measurement was conducted according to standard calibration procedure of Korea Testing Laboratory which assures suitability and traceable results. It is also based on international standards.

In this study, we researched a pendant-type aspherical optical system, which could be applied to street lighting and security lighting in Europe. The goal of this research was eco-friendly artificial lighting that could be used for the one-to-one replacement of ordinary lighting. LED lighting was miniaturized by using one COB LED Module and one aspherical optical system, which could control the luminosity of the LED. Through the aspherical optical system, the light distribution angle could be controlled in a range of for the X-axis and for the Y-axis. This means that this optical system is appropriate for catenary-type lighting, which is widely used in Europe on both narrow and broad roads. The performance was determined using a lighting simulation program. This lighting system simulation showed that road rates M4 and M5 could be satisfied, with the condition of a 13-m height and 50-m distance (U0 and TI). The simulation program estimated that light pollution, which disturbs sleep, could beeliminated in the European streetlight case. Determining methods for the light distribution control, performance, and optimal lighting setup conditions is very important to prevent light pollution. Moreover, the initial step of developing the lighting system design and post management will require an effort with much analysis.

In this study, we demonstrate that activation of AMP-activated protein kinase (AMPK) with glabridin alleviates adiposity and hyperlipidemia in obesity. In several obese rodent models, glabridin decreased body weight and adiposity with a concomitant reduction in fat cell size. Further, glabridin ameliorated fatty liver and plasma levels of triglyceride and cholesterol. In accordance with these findings, glabridin suppressed the expression of lipogenic genes such as sterol regulatory element binding transcription factor (SREBP)-1c, fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and stearoyl-CoA desaturase (SCD)-1 in white adipose tissues and liver, whereas it elevated the expression of fatty acid oxidation genes such as carnitine palmitoyl transferase (CPT)1, acyl-CoA oxidase (ACO), and peroxisome proliferator-activated receptor (PPAR)α in muscle. Moreover, glabridin enhanced phosphorylation of AMPK in muscle and liver and promoted fatty acid oxidation by modulating mitochondrial activity. Together, these data suggest that glabridin is a novel AMPK activator that would exert therapeutic effects in obesity-related metabolic disorders.

In this study we researched a spotlight in LED lighting. Ordinary LED spotlight was manufactured with characterized property of traveling straightness of LED light source, but multiple use of shell type LED, a yellow band has formed caused by light source interference between the LED. Also, there was a high miscellaneous light efficiency with losing light source homogeneity and efficiency due to light source control uneasiness. The study uses aspheric reflector and aspheric lens, so we can control the light source of LED spotlight with effectively and we reached surface light source by using COB/COM for LED module. Furthermore it can change its use by a reduced scale of light system. It has been designed to make its various application from low power consumption of bicycle lamp, up to high power consumption of automobile lamps and lighthouse.

The cause of elevated level of amyloid β-peptide (Aβ42) in common late-onset sporadic (AD) has not been established. Here we show that the membrane lipid peroxidation product 4-hydroxynonenal (HNE) is associated with amyloid and neurodegenerative pathologies in AD, and that it enhances γ-secretase activity and Aβ42 production in neurons. The γ-secretase substrate receptor, nicastrin was found to be modified by HNE in cultured neurons and in brain specimens from AD patients, in which HNE-nicastrin levels were found to be correlated with increased γ-secretase activity and Aβ plaque burden. Furthermore, HNE modification of nicastrin enhanced its binding to the γ-secretase substrate, amyloid precursor protein (APP) C99. In addition, the stimulation of γ-secretase activity and Aβ42 production by HNE were blocked by an HNE-scavenging histidine analog in a 3xTgAD mouse model of AD. These findings suggest a specific molecular mechanism by which oxidative stress increases Aβ42 production in AD, and identify HNE as a novel therapeutic target upstream of the γ-secretase cleavage of APP.

A number of epidemiological studies have demonstrated a strong association between the incidence of neurodegenerative disease and pesticide exposure. Fluazinam (FZN) is a preventative fungicide from the pyridinamine group that was introduced in the 1990s and that quickly established itself as a new standard for the control of blight caused by Phytophthora infestans in potatoes. We used human neuroblastoma SH-SY5Y cells to investigate mechanisms of neuronal cell death in response to FZN and showed that FZN was cytotoxic to SH-SY5Y cells in a concentration- and time-dependent manner. Additionally, we showed that FZN treatment significantly decreased the neuron numbers including dopaminergic neurons and mitochondrial complex I activity. The cytotoxic effects of FZN were associated with an increase in reactive oxygen species (ROS) generation because pretreatment with N-acetyl cysteine, an anti-oxidant, reduced cell death. We showed that neuronal cell death in response to FZN was due to apoptosis because FZN increased cytochrome C release into the cytosol and activated caspase-3 through the accumulation of p53. FZN also reduced the levels of Bcl-2 protein but increased the levels of Bax. Our results provide insight into the molecular mechanisms of FZN-induced apoptosis in neuronal cells.

The nature of mitochondrial dysfunction in dopaminergic neurons in familial Parkinson's disease (PD) is unknown. We characterized the pathophenotypes of dopaminergic neuronal cells that were deficient in PINK1 or DJ-1, genes with mutations linked to familial PD. Both PINK1- and DJ-1-deficient dopaminergic neurons had the increased production of ROS, severe mitochondrial structural damages and complex I deficits. A striking decrease in complex IV activity was also prominent by the PINK1-deficiency. The complex I deficits were relatively PD-specific and were significantly improved by an antioxidant Trolox. These data suggest that mitochondrial deficits are severe in dopaminergic neurons in familial PD and antioxidant-mediated functional recovery is feasible.

Background/Objectives: Artificial light has developed with both sides of light pollution. International organizations recognize the seriousness of light pollution and are offering ways to make restrictions light pollution.Methods/Statistical analysis: It padded an additional surface on the back of the lens to convert the light to the House side into a street side. The slope of the additional surface was determined by the angle of the light that emerged from the LED.As a result, it implemented B1 rating of security light on BUG Rating defined by IESNA.Findings: The total internal reflection of the lens was used to control the posterior light. The inner surface was set to totally reflect the light directed toward the house side inside the lens, and the inclination of the outer surface was set so that the light refracted from the outer surface and directed forward when the light exits. As a result of controlling the backlight in this way, the B1 light distribution classified by the BUG rating was implemented. It also made the ratio of light from Street side to House side about 8:2.Improvements/Applications: When applying the expression proposed in this paper to the streetlight optical system, it can complement the light pollution problem.

Increased cell mass is one of the characteristics of senescent cells, but this event has not been clearly defined. When subcellular organellar mass was estimated with organelle-specific fluorescence dyes, we observed that most membranous organelles progressively increase in mass during cell senescence. This increase was accompanied by an increase in membrane lipids and augmented expression of lipogenic enzymes, such as fatty acid synthase (FAS), ATP citrate lyase, and acetyl-CoA carboxylase. The mature form of sterol regulatory element-binding protein (SREBP)-1 was also elevated. Increased expression of these lipogenic effectors was further observed in the liver tissues of aging Fischer 344 rats. Ectopic expression of mature form of SREBP-1 in both Chang cells and primary young human diploid fibroblasts was enough to induce senescence. Blocking lipogenesis with FAS inhibitors (cerulenin and C75) and via siRNA-mediated silencing of SREBP-1 and ATP citrate lyase significantly attenuated H(2)O(2)-induced senescence. Finally, old human diploid fibroblasts were effectively reversed to young-like cells by challenging with FAS inhibitors. Our results suggest that enhanced lipogenesis is not only a common event, but also critically involved in senescence via SREBP-1 induction, thereby contributing to the increase in organelle mass (as a part of cell mass), a novel indicator of senescence.

Beta-secretase (BACE1), an enzyme responsible for the production of amyloid beta-peptide (Abeta), is increased by oxidative stress and is elevated in the brains of patients with sporadic Alzheimer's disease (AD). Here, we show that oxidative stress fails to induce BACE1 expression in presenilin-1 (gamma-secretase)-deficient cells and in normal cells treated with gamma-secretase inhibitors. Oxidative stress-induced beta-secretase activity and sAPPbeta levels were suppressed by gamma-secretase inhibitors. Levels of gamma- and beta-secretase activities were greater in brain tissue samples from AD patients compared to non-demented control subjects, and the elevated BACE1 level in the brains of 3xTgAD mice was reduced by treatment with a gamma-secretase inhibitor. Our findings suggest that gamma-secretase mediates oxidative stress-induced expression of BACE1 resulting in excessive Abeta production in AD.

In the present work, a second gene encoding protein disulfide isomerase (PDI2) was cloned and characterized from Schizosaccharomyces pombe, and its regulation was studied. The structural gene encoding PDI2 was amplified from the genomic DNA using PCR, and ligated into the E. coli-yeast shuttle vector pRS316 to generate the recombinant plasmid pYPDI2. The determined DNA sequence carries 2,578 bp and is able to encode a protein of 726 amino acid sequence with CGAC at the putative active site. The fission yeast cells harboring pYPDI2 contained 1.62- and 2.73-fold higher PDI activity than the control yeast cells in exponential and stationary phases, respectively, indicating that the cloned gene is in vivo functioning. The PDI2 mRNA levels in both vector control and pYPDI2-containing yeast cells were found to be significantly higher in the stationary phase than in the exponential phase, suggesting that expression of the PDI2 gene is under stationary control. The yeast cells harboring pYPDI2 showed enhanced survival on minimal media plates containing nitric oxide (NO)-generating sodium nitroprusside (SNP) and no nitrogen. The synthesis of β-galactosidase from the PDI2-lacZ fusion gene was markedly enhanced in the Pap1-positive KP1 cells by SNP and nitrogen starvation. However, the enhancement in the synthesis of β-galactosidase from the PDI2-lacZ fusion gene by SNP and nitrogen starvation appeared to be relatively reduced in the Pap1-negative TP108-3C cells than in the Pap1-positive KP1 cells. The PDI2 mRNA level was elevated by SNP and nitrogen starvation in the Pap1-positive cells but not in the Pap1-negative cells. In brief, the S. pombe PDI2 plays a protective role against nitrosative and nutritional stresses, and is positively regulated by NO and nitrogen starvation in a Pap1-dependent manner.

The objective of the present study was to examine the role of selenium in the metabolism of Aβ and in Aβ-induced neuronal death. Selenium treatment significantly reduced Aβ40, Aβ42, and sAPPβ production by reducing Aβ producing β-secretase and γ-secretase activities. The lipid peroxidation product 4-Hydroxynonenal (HNE)-induced transcription of β-secretase (BACE1) was blocked by selenium. Finally, our data show that selenium protects against HNE and Aβ-mediated toxicity in primary cultured neurons. The present study suggests that selenium may be able to salvage the neuronal degeneration of Alzheimer's disease, thereby limiting β-amyloid production and neuronal death.

The plasma membrane redox system (PMRS) containing NADH-dependent reductases is known to be involved in the maintenance of redox state and bioenergetics. Neuronal cells are very vulnerable to oxidative stress and altered energy metabolism linked to mitochondrial dysfunction. However, the role of the PMRS in these pathways is far from clear. In this study, in order to investigate how cytochrome b5 reductase (b5R), one of the PM redox enzymes, regulates cellular response under stressed conditions, human neuroblastoma cells transfected with b5R were used for viability and mitochondrial functional assays. Cells transfected with b5R exhibited significantly higher levels of the NAD(+)/NADH ratio, consistent with increased levels of b5R activity. Overexpression of b5R made cells more resistant to H2O2 (oxidative stress), 2-deoxyglucose (metabolic stress), rotenone and antimycin A (energetic stress), and lactacystin (proteotoxic stress), but did not protect cells against H2O2 and serum withdrawal. Overexpression of b5R induced higher mitochondrial functions such as ATP production rate, oxygen consumption rate, and activities of complexes I and II, without formation of further reactive oxygen species, consistent with lower levels of oxidative/nitrative damage and resistance to apoptotic cell death. In conclusion, higher NAD(+)/NADH ratio and consequent more efficient mitochondrial functions are induced by the PMRS, enabling them to maintain redox state and energy metabolism under conditions of some energetic stresses. This suggests that b5R can be a target for therapeutic intervention for aging and neurodegenerative diseases.

The plasma membrane (PM) contains redox enzymes that provide electrons for energy metabolism and recycling of antioxidants such as coenzyme Q and α-tocopherol. Brain aging and neurodegenerative disorders involve impaired energy metabolism and oxidative damage, but the involvement of the PM redox system (PMRS) in these processes is unknown. Caloric restriction (CR), a manipulation that protects the brain against aging and disease, increased activities of PMRS enzymes (NADH-ascorbate free radical reductase, NADH-quinone oxidoreductase 1, NADH-ferrocyanide reductase, NADH-coenzyme Q10 reductase, and NADH-cytochrome c reductase) and antioxidant levels (α-tocopherol and coenzyme Q10) in brain PM during aging. Age-related increases in PM lipid peroxidation, protein carbonyls, and nitrotyrosine were attenuated by CR, levels of PMRS enzyme activities were higher, and markers of oxidative stress were lower in cultured neuronal cells treated with CR serum compared with those treated with ad libitum serum. These findings suggest important roles for the PMRS in protecting brain cells against age-related increases in oxidative and metabolic stress.

Oxidative stress over time leads to the accumulation of damaged macromolecules and to profound physiological changes that are associated with several age-related diseases. The plasma membrane redox system (PMRS) appears to attenuate oxidative stress acting as a compensatory mechanism during the aging process. The PMRS appears to play a protective role during mitochondrial dysfunction to provide cells with a survival mechanism by lowering oxidative stress. The PMRS accomplishes this by producing more NAD(+) for glycolytic ATP production via transfer of electrons from intracellular reducing equivalents to extracelluar acceptors. Ubiquinone and alpha-tocopherol are key antioxidant molecules in the plasma membrane that are affected by aging and can be up-regulated by dietary interventions such as calorie restriction (CR). Up-regulation of PMRS activity leads to cell survival and membrane homeostasis under stress conditions and during calorie restriction. Further studies of the PMRS may provide not only additional information on the mechanisms involved in aging and CR, but may provide therapeutic targets for the prevention and treatment of age-related diseases.

Optical properties of normal spinel MxCo3−xO4(M=CrandCu) films grown by sol-gel method have been investigated by the spectroscopic ellipsometry (SE) in the 1.5–4eV region. For x

Mutations in Cu,Zn-superoxide dismutase (SOD-1) are associated with some familial cases of amyotrophic lateral sclerosis (ALS), but it is not known how they result in cell death. We examined effects of overexpression of wild-type SOD-1 or the G37R or G85R mutations on the accumulation of ubiquitinated and nitrated proteins, and on loss of cell viability induced by the proteasome inhibitor, lactacystin. Wild-type SOD-1 had no effect on proteasomal activity, but the mutants decreased it somewhat. Treatment with lactacystin (1 micro m) caused only limited cell viability loss, even though it induced a marked inhibition of proteasomal activities. However, viability loss due to apoptosis was substantial in response to lactacystin when cells were overexpressing a mutant SOD-1. The frequency of cells showing immunoreactivity against ubiquitinated- or nitrated-proteins was enhanced when wild-type and mutant SOD-1 s were overexpressed. Ubiquitinated or nitrated alpha-tubulin, SOD-1, alpha-synuclein and 68K neurofilaments were observed in the aggregates. Similar aggregates were observed in cells overexpressing mutant parkin (Del3-5, T240R and Q311'X). The nitric oxide synthase inhibitor, l-NAME, decreased viability loss and aggregation, suggesting that nitration of proteins may play an important role in aggregation and in the cell death accompanying it.