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Quercetin is a bioactive flavonoid which abundantly exists in vegetables and fruits. Quercetin exerts a neuroprotective effect against cerebral ischemia. Thioredoxin acts as antioxidant by regulating redox signaling. This study investigated whether quercetin regulates thioredoxin expression in focal cerebral ischemia and glutamate-induced neuronal cell death. Male Sprague Dawley rats (210–230 g) were intraperitoneally injected with vehicle or quercetin (10 mg/kg) 1 h prior to middle cerebral artery occlusion (MCAO). Cerebral cortex was collected 24 h after MCAO. MCAO led to neurological movement deficits, brain edema, and serious histopathological damages in cerebral cortex, and quercetin alleviated these damages following MCAO. We observed the change of thioredoxin expression in MCAO animals with quercetin using proteomic approach, reverse-transcription PCR, and Western blot analyses. Thioredoxin expression decreased in vehicle-treated MCAO animals, while quercetin attenuated this decrease. Moreover, quercetin treatment alleviated the decrease in the number of thioredoxin-positive cells in cerebral cortex of MCAO animals. Furthermore, immunoprecipitation analysis demonstrated that interaction of apoptosis signal-regulating kinase 1 (ASK1) and thioredoxin was decreased in MCAO animals with vehicle, while quercetin prevented MCAO-induced decrease in these binding. In addition, quercetin also alleviated the reduction of cell viability and the decrease in thioredoxin expression in glutamate-treated hippocampal cell line and primary cultures of cortical neurons. However in thioredoxin-silenced cortical neuron, anti-apoptotic effect of quercetin was decreased. Thus, changes of thioredoxin expression by quercetin may contribute to the neuroprotective effect of quercetin in focal cerebral ischemia. Our findings suggest that quercetin mediates its neuroprotective function by regulation of thioredoxin expression and maintenance of interaction between ASK1 and thioredoxin.

Cerebral ischemia is a neurological disorder that leads to cognitive decline and high mortality. Retinoic acid is a metabolite of vitamin A that has anti-inflammatory and anti-apoptotic effects. This study investigated whether retinoic acid prevents neuronal cell damage on focal cerebral ischemia through modulating apoptosis signaling pathway. Middle cerebral artery occlusion (MCAO) was performed to induce focal cerebral ischemia in adult male rats. Retinoic acid (5 mg/kg) or vehicle was injected intraperitoneally for 4 days prior to MCAO. Neurological behavior deficit tests were performed 24 h after MCAO. Brain edema and infarct volume were measured, and TUNEL histochemistry was carried out. We also investigated the changes in apoptosis-related proteins including bcl-2 family proteins and caspases. MCAO injury induced severe neurological behavior deficits and brain edema. It also increased infarct volume, histopathological damages, and the number of TUNEL-positive cells in cerebral cortex. However, retinoic acid pretreatment attenuated MCAO-induced neurological behavior deficits, brain edema, and infarction. It also alleviated histopathological lesion and decreased the number of TUNEL-positive cells. Bcl-2 and bax proteins are representative bcl-2 family proteins. MCAO injury induced a decrease in bcl-2 expression and an increase in bax expression, and retinoic acid pretreatment alleviated these changes. MCAO injury caused a decrease in bcl-2/bax expression ratio in cerebral cortex, while retinoic acid restored this decrease by MCAO. Moreover, our result showed increases in caspase-9, caspase-3, PARP protein levels in MCAO-operated animals. Retinoic acid pretreatment prevented these increases. We identified the changes in cleaved forms of these proteins, similar to the changes in full-length protein. Activation of caspases and PARP proteins are considered to be representative apoptosis indicators. This study showed that retinoic acid regulates bcl-2 family proteins and caspase proteins in focal cerebral ischemia. Thus, our findings demonstrate that retinoic acid exhibits a neuroprotective effect against ischemic damage by modulating apoptosis signaling pathway.

Glutamate induces neuronal damage by generating oxidative stress and neurotoxicities. The neurological damage caused by glutamate is more severe during brain development in newborns than in adults. Resveratrol is naturally present in a variety of fruits and medicinal plants and exerts a neuroprotective effect against brain damage. The goal of this study was to evaluate the neuroprotective effects of resveratrol and to identify changed proteins in response to resveratrol treatment during glutamate-induced neonatal cortical damage. Sprague-Dawley rat pups (7 days old) were randomly divided into vehicle, resveratrol, glutamate, and glutamate and resveratrol groups. The animals were intraperitoneally injected with glutamate (10 mg/kg) and/or resveratrol (20 mg/kg) and their brain tissue was collected 4 hr after drug administration. Glutamate exposure caused severe histopathological changes, while resveratrol attenuated this damage. We identified regulated proteins by resveratrol in glutamate-induced cortical damaged tissue using two-dimensional gel electrophoresis and mass spectrometry. Among identified proteins, we focused on eukaryotic initiation factor 4A2, γ-enolase, protein phosphatase 2A subunit B, and isocitrate dehydrogenase. These proteins decreased in the glutamate-treated group, whereas the combination treatment of glutamate and resveratrol attenuated these protein reductions. These proteins are anti-oxidant proteins and anti-apoptotic proteins. These results suggest that glutamate induces brain cortical damage in newborns; resveratrol exerts a neuroprotective effect by controlling expression of various proteins with anti-oxidant and anti-apoptotic functions.

Background Calcium is a critical factor involved in modulation of essential cellular functions. Parvalbumin is a calcium buffering protein that regulates intracellular calcium concentrations. It prevents rises in calcium concentrations and inhibits apoptotic processes during ischemic injury. Quercetin exerts potent antioxidant and anti-apoptotic effects during brain ischemia. We investigated whether quercetin can regulate parvalbumin expression in cerebral ischemia and glutamate toxicity-induced neuronal cell death. Adult male rats were treated with vehicle or quercetin (10 mg/kg) 30 min prior to middle cerebral artery occlusion (MCAO) and cerebral cortical tissues were collected 24 h after MCAO. We used various techniques including Western blot, reverse transcription-PCR, and immunohistochemical staining to elucidate the changes of parvalbumin expression. Results Quercetin ameliorated MCAO-induced neurological deficits and behavioral changes. Moreover, quercetin prevented MCAO-induced a decrease in parvalbumin expression. Conclusions These findings suggest that quercetin exerts a neuroprotective effect through regulation of parvalbumin expression.

Cerebral ischemia is a neurological disorder that causes permanent disability and is sometimes fatal. Epigallocatechin gallate (EGCG) is a natural polyphenol that exerts beneficial antioxidant and anti-inflammatory effects. The aim of this study was to investigate the neuroprotective effects of EGCG against cerebral ischemia. Middle cerebral artery occlusion was surgically initiated to induce focal cerebral ischemia in adult male rats. EGCG (50 mg/kg) or vehicle was intraperitoneally injected just prior to middle cerebral artery occlusion (MCAO) induction. Neuronal behavior tests were performed 24 hr after MCAO. Brain tissues were isolated to evaluate infarct volume, histological changes, apoptotic cell death, and caspase-3 and poly ADP-ribose polymerase (PARP) levels. MCAO injury led to serious functional neurological deficits and increased infarct volume. Moreover, it induced histopathological lesions and increased the numbers of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells in the cerebral cortex. However, EGCG improved MCAO-induced neurological deficits and reduced infarct volume, alleviated histopathological changes, and decreased TUNEL-positive cells in the cerebral cortex of MCAO rats. Western blot analysis showed increases of caspase-3 and PARP expression levels in MCAO rats with vehicle, whereas EGCG administration alleviated these increases after MCAO injury. These results demonstrate that EGCG exerts a neuroprotective effect by regulating caspase-3 and PARP proteins during cerebral ischemia. In conclusion, we suggest that EGCG acts as a potent neuroprotective agent by modulating the apoptotic signaling pathway.

Cerebral ischemia is a neurological disorder with high mortality. Quercetin is a flavonoid compound that is abundant in vegetables and fruits. It exerts anti-inflammatory and anti-apoptotic effects. This study investigated the neuroprotective effects of quercetin in focal cerebral ischemia. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) to induce focal cerebral ischemia. Quercetin or vehicle was injected 30 min before the onset of ischemia. A neurological function test, brain edema measurement, and 2,3,5-triphenyltetrazolium chloride staining were performed to elucidate the neuroprotective effects of quercetin. Western blot analysis was performed to observe caspase-3 and poly ADP-ribose polymerase (PARP) protein expression. MCAO leads to severe neuronal deficits and increases brain edema and infarct volume. However, quercetin administration attenuated the MCAO-induced neuronal deficits and neuronal degeneration. We observed increases in caspase-3 and PARP protein levels in MCAO-operated animals injected with vehicle, whereas quercetin administration attenuated these increases in MCAO injury. This study reveals the neuroprotective effect of quercetin in an MCAO-induced animal model and demonstrates the regulation of caspase-3 and PARP expression by quercetin treatment. These results suggest that quercetin exerts a neuroprotective effect through preventing the MCAO-induced activation of apoptotic pathways affecting caspase-3 and PARP expression.

Hyperglycemia is a major risk factor for stroke and increases brain damage during ischemic stroke. Hyperglycemia increases the intracellular calcium concentration after ischemic injury, thereby triggering neuronal cell death. Calcium binding proteins, including hippocalcin and parvalbumin, are critical regulators of intracellular calcium levels. This study aimed to investigate whether hyperglycemic conditions affect hippocalcin and parvalbumin expression during ischemic brain injury. Male adult rats were treated intraperitoneally with streptozotocin (40 mg/kg) to induce hyperglycemia. Four weeks later, cerebral ischemic injury was induced via surgical middle cerebral artery occlusion (MCAO). Cerebral cortex samples were collected 24 h after MCAO. A proteomic approach showed that the protein levels of hippocalcin and parvalbumin were significantly decreased in streptozotocin-treated animals with MCAO injury compared to streptozotocin-treated animals and animals that underwent MCAO alone. Reverse transcription-PCR and Western blot analyses clearly confirmed the decreased levels of these proteins. These decreases indicate dysregulation of the intracellular calcium balance and induction of cell death. Thus, these results suggest that significantly decreased levels of hippocalcin and parvalbumin exacerbate neuronal cell death in diabetic animals with ischemic brain injury.

Ischemic stroke is one of the leading causes of adult disability and death. Hyperglycemia is associated with an increased risk of stroke and poor outcomes after brain injury. Dynamin-like protein I (DLP-1) regulates mitochondrial fission and promotes mitochondrial dynamics. Neurodegenerative diseases are associated with mitochondrial dysfunction, and the downregulation of DLP-1 has been previously identified in a stroke animal model. Here, we investigated the changes in DLP-1 protein expression in an animal model of focal cerebral ischemia with induced hyperglycemia. Streptozotocin (40 mg/kg) was intraperitoneally injected into male rats to induce hyperglycemia, and middle cerebral artery occlusion (MCAO) was surgically induced 4 weeks after streptozotocin treatment. Brain tissue was isolated 24 hours after MCAO, and cerebral cortex samples were used for this study. Proteomics revealed a decrease in DLP-1 expression in MCAO animals when compared with controls, and this downregulation was more prominent in MCAO animals with hyperglycemia. Reverse-transcription polymerase chain reaction and Western blot analyses confirmed that DLP-1 was significantly downregulated in MCAO-injured animals with hyperglycemia compared to those without hyperglycemia. The decrease in DLP-1 indicates mitochondrial morphological changes and dysfunction. Together, these results suggest that the severe decrease of DLP-1 seen after brain injury under hyperglycemic conditions may exacerbate the damage to the brain.

Diabetes is a metabolic disorder that worsens clinical outcome following cerebral ischemia. Protein phosphatase 2A (PP2A) is a conserved, heterotrimeric, serine/threonine phosphatase with various cellular functions. PP2A subunit B is abundant in brain tissue and modulates PP2A function. The aim of this study was to investigate PP2A subunit B protein expression in the cerebral cortex of non-diabetic and diabetic animals with middle cerebral artery occlusion (MCAO) injury. Sprague-Dawley rats were injected with streptozotocin (40 mg/kg, i.p.) to induce diabetic conditions. After 4 weeks of streptozotocin treatment, the rats underwent MCAO to induce focal cerebral ischemia. The cerebral cortex tissue was collected 24 hr after MCAO. Body weight and blood glucose were measured, and Western blot analysis was performed to elucidate the expression of PP2A subunit B. We confirmed decreased body weight and increased blood glucose in diabetic animals. Reverse transcription-PCR and Western blot analyses showed decreased PP2A subunit B expression in the cerebral cortices of MCAO-injured animals. Moreover, diabetic animals with MCAO showed more severe decreases in PP2A subunit B protein levels than non-diabetic animals following MCAO. The decline of PP2A subunit B indicates degradation of neuronal function. These findings suggest that conspicuous decreases in PP2A subunit B may exacerbate cerebral ischemia under diabetic conditions following MCAO.

Baicalin is a plant-derived flavonoid that has anti-inflammatory and anti-oxidative effects. We investigated an anti-inflammatory effect of baicalin against lipopolysaccharide (LPS)-induced damage in cerebral cortex. Adult mice were divided into control, LPS-treated, and LPS and baicalin co-treated animals. LPS (250 µg/kg/day) and baicalin (10 mg/kg/day) were intraperitoneally injected for 7 days. LPS treatment induced histopathological changes in cerebral cortex, whereas baicalin protected neuronal cells against LPS toxicity. Moreover, baicalin treatment attenuated LPS-induced increases of reactive oxygen species and oxidative stress in cerebral cortices. Ionized calcium binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) are known as markers of activated microglia and astrocyte, respectively. Results of Western blot and immunofluorescence staining showed that LPS exposure induces increases of Iba-1 and GFAP expressions, whereas baicalin alleviates LPS-induced increases of these proteins. Baicalin also prevented LPS-induced increase of nuclear factor kappa B (NF-κB). LPS treatment led to increases of pro-inflammatory factors including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Increases of these pro-inflammatory mediators were attenuated in baicalin co-treated animals. These results demonstrated that baicalin regulates neuroglia activation and modulates inflammatory factors in LPS-induced neuronal injury. Thus, our findings suggest that baicalin exerts a neuroinflammatory effect against LPS-induced toxicity through decreasing oxidative stress and inhibiting NF-κB mediated inflammatory factors, such as IL-1β and TNF-α.

Cerebral ischemia is a major cause of neurodegenerative disease. It induces neuronal vulnerability and susceptibility, and leads to neuronal cell death. Resveratrol is a polyphenolic compound that acts as an anti-oxidant. It exerts a neuroprotective effect against focal cerebral ischemic injury. Akt signaling pathway is accepted as a representative cell survival pathway, including proliferation, growth, and glycogen synthesis. This study investigated whether resveratrol regulates Akt/glycogen synthase kinase-3β (GSK-3β) pathway in a middle cerebral artery occlusion (MCAO)-induced ischemic brain injury. Adult male rats were intraperitoneally injected with vehicle or resveratrol (30 mg/kg) and cerebral cortices were isolated 24 h after MCAO. Neurological behavior test, corner test, brain edema measurment, and 2,3,5-triphenyltetrazolium chloride staining were performed to elucidate the neuroprotective effects of resveratrol. Phospho-Akt and phospho-GSK-3β expression levels were measured using Western blot analysis. MCAO injury led to severe neurobehavioral deficit, infraction, and histopathological changes in cerebral cortex. However, resveratrol treatment alleviated these changes caused by MCAO injury. Moreover, MCAO injury induced decreases in phospho-Akt and phospho-GSK-3β protein levels, whereas resveratrol attenuated these decreases. Phosphorylations of Akt and GSK-3β act as a critical role for the suppression of apoptotic cell death. Thus, our finding suggests that resveratrol attenuates neuronal cell death in MCAO-induced cerebral ischemia and Akt/GSK-3β signaling pathway contributes to the neuroprotective effect of resveratrol.

Calcium acts as a second messenger that mediates physiologic functions, such as metabolism, cell proliferation, and apoptosis. Hippocalcin is a neuronal calcium sensor protein that regulates intracellular calcium concentration. Moreover, it prevents neuronal cell death from oxidative stress. Quercetin has excellent antioxidant properties and preventative effects. We studied modulation of hippocalcin expression by quercetin treatment in cerebral ischemic injury and glutamate-induced neuronal cell damage. Focal cerebral ischemia was induced by permanent middle cerebral artery occlusion (pMCAO). Male Sprague-Dawley rats were injected with vehicle or quercetin (10 mg/kg) 1 h prior to pMCAO, and cerebral cortical tissues were isolated 24 h after pMCAO. Quercetin improved pMCAO-induced neuronal movement deficit and infarction. pMCAO induced a decrease in hippocalcin expression in the cerebral cortex. However, quercetin treatment attenuated this pMCAO-induced decrease. In cultured hippocampal cells, glutamate excitotoxicity dramatically increased the intracellular calcium concentration, whereas quercetin alleviated intracellular calcium overload. Moreover, Western blot and immunocytochemical studies showed reduction of hippocalcin expression in glutamate-exposed cells. Quercetin prevented this glutamate-induced decrease. Furthermore, caspase-3 expression in hippocalcin siRNA transfection conditions is higher than caspase-3 expression in un-transfection conditions. Quercetin treatment attenuated the increase of caspase-3. Taken together, these results suggest that quercetin exerts a preventative effect through attenuation of intracellular calcium overload and restoration of down-regulated hippocalcin expression during ischemic injury.

Lipopolysaccharide (LPS) acts as an endotoxin, releases inflammatory cytokines, and promotes an inflammatory response in various tissues. This study investigated whether LPS modulates neuroglia activation and nuclear factor kappa B (NF-κB)-mediated inflammatory factors in the cerebral cortex. Adult male mice were divided into control animals and LPS-treated animals. The mice received LPS (250 μg/kg) or vehicle via an intraperitoneal injection for 5 days. We confirmed a reduction of body weight in LPS-treated animals and observed severe histopathological changes in the cerebral cortex. Moreover, we elucidated increases of reactive oxygen species and oxidative stress levels in LPS-treated animals. LPS administration led to increases of ionized calcium-binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) expression. Iba-1 and GFAP are well accepted as markers of activated microglia and astrocytes, respectively. Moreover, LPS exposure induced increases of NF-κB and pro-inflammatory factors, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Increases of these inflammatory mediators by LPS exposure indicate that LPS leads to inflammatory responses and tissue damage. These results demonstrated that LPS activates neuroglial cells and increases NF-κB-mediated inflammatory factors in the cerebral cortex. Thus, these findings suggest that LPS induces neurotoxicity by increasing oxidative stress and activating neuroglia and inflammatory factors in the cerebral cortex.

Quercetin is a plant flavonoid that has anti-oxidant, anti-inflammatory, anti-cancer, and anti-ischemic properties. Moreover, quercetin exerts neuroprotective effects against focal cerebral ischemia. Protein phosphatase 2A (PP2A) is a form of serine/threonine phosphatase that modulates various biological functions. Among PP2A subunit types, subunit B exists abundantly in brain tissue and plays an essential function in nervous system. We previously reported the decrease of PP2A subunit B in focal cerebral animal model. This study explored the change of PP2A subunit B expression by quercetin treatment in cerebral ischemic animal model and glutamate-treated hippocampal-derived (HT22) cell culture. Quercetin (10 mg/kg) or vehicle was injected intraperitoneally into male rats before 30 min of middle cerebral artery occlusion (MCAO), and cerebral cortices were isolated 24 hr after MCAO. MCAO induced the neurological behavioral deficit and increased infarct volume. However, quercetin treatment attenuated the increase of neurological deficit and infarction. We detected the alleviation of MCAO-induced the decrease in PP2A subunit B by quercetin treatment using a proteomic approach. Reverse-transcription PCR and Western blot analyses confirmed lower PP2A subunit B expression levels in MCAO group with vehicle. However, quercetin treatment attenuated MCAO-induced this reduction. We also observed the neuroprotective effect of quercetin and the change of PP2A subunit B expression in glutamate-exposed HT22 cells. Glutamate exposure dramatically reduced cell viability and PP2A subunit B expression, and quercetin treatment significantly improved these decreases. We clearly showed that quercetin performs a neuroprotective function and modulates down-regulation of PP2A subunit B against MCAO injury and glutamate toxicity. Thus, our finding suggests that the regulation of PP2A subunit B by quercetin contributes to neuroprotective function in ischemic brain injury.

Cerebral ischemia leads to neuronal cell death, causes neurological disorder and permanent disability. Chlorogenic acid has antioxidant, anti-inflammatory, and anti-apoptotic properties. This study investigated the neuroprotective effects of chlorogenic acid against cerebral ischemia. Focal cerebral ischemia was induced in male adult rats via middle cerebral artery occlusion (MCAO). Chlorogenic acid (30 mg/kg) or vehicle was injected in the intraperitoneal cavity 2 h after MCAO operation. Neurological behavior tests were performed 24 h after MCAO, brain edema and infarction were measured. Oxidative stress was assessed by investigating the levels of reactive oxygen species (ROS) and lipid peroxidation (LPO) levels. MCAO damage leaded to severe neurobehavioral deficits, increased ROS and LPO levels, and induced brain edema and infarction. MCAO damage caused histopathological damages and increased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells in the cerebral cortex. However, chlorogenic acid treatment improved neurological behavioral deficits caused by MCAO and attenuated the increase in ROS and LPO levels. It also alleviated MCAO-induced brain edema, infarction, and histopathological lesion. Chlorogenic acid treatment attenuated the increase in the number of TUNEL-positive cells in the cerebral cortex of MCAO animals. We also investigated caspase proteins expression to elucidate the neuroprotective mechanism of chlorogenic acid. Caspase-3, caspase-7, and poly ADP-ribose polymerase expression levels were increased in the MCAO damaged cortex, while chlorogenic acid mitigated these increases. These results showed that MCAO injury leads to severe neurological damages and chlorogenic acid exerts neuroprotective effects by regulating oxidative stress and caspase proteins expressions. Thus, our findings suggest that chlorogenic acid acts as a potent neuroprotective agent by modulating the apoptotic-related proteins.

The molecular epidemiology of norovirus infections was studied in food handlers without any symptoms from January to December 2015 in Busan city, Korea. A total of 2,174 fecal specimens from asymptomatic food handlers were analyzed, and 2.3% (49/2,174) were norovirus-positive. Fourteen of 335 samples (4.2%) were positive in January; fifteen of 299 samples (5.0%) in February, and seven of 189 samples (3.7%) in December. However, norovirus was rarely detected in other months. From sequencing analysis, 11 genotypes (five GI and six GII genotypes) were detected. Among the 42 capid gene sequences identified, 14 were from the GI genogroup, while 28 were from the GII genogroup. The most commonly detected genotype was GII.17, comprising 15 (35.7%) of positive samples. From January 2012 to December 2015, 5,138 samples were collected from gastroenteritis patients and outbreaks in Busan. The most detected genotype in 2012, 2013, and 2014 was GII.4 (121, 24, and 12 cases, respectively), but in 2015, GII.17 (25 cases) was the most common. The GII.4 genotype was the major cause of acute gastroenteritis from 2012 to 2014, but the GII.17 genotype became the most prevalent cause in 2015. Continued epidemiological surveillance of GII.17 is needed, together with assessment of the risk of norovirus infection.

Background: Many studies have recently reported that vitamin D deficiency may be associated with obesity. However, the relationship between vitamin D deficiency and obesity in Korean adolescents has yet to be sufficiently studied. Therefore, this study aims to reveal the relationship between vitamin D levels and obesity (or body mass index, BMI) in Korean adolescents. Methods: Among those who participated in the Korean National Health and Nutrition Examination Survey (2012–2014), we selected 1,238 adolescents aged 12 to 19 who underwent tests for determining 25-hydroxyvitamin D (25(OH)D) levels. The odds ratio of obesity according to 25(OH)D concentration was calculated using logistic regression analysis. The odds ratio of obesity in the vitamin D deficiency group compared with the vitamin D sufficiency group was calculated in the same way. The influence of 25(OH)D concentration on BMI was analyzed using regression analysis. All results were adjusted for variables, such as biologic sex, age, household income level, area of residence, physical activity, stress perception, sleeping hours, alcohol drinking, and smoking. Results: The mean 25(OH)D concentration of subjects was lower than the 20 ng/mL. In both male and female subjects, 25(OH)D concentration did not have any influence on obesity. Furthermore, no difference in obesity was found between the vitamin D deficiency and sufficiency groups. However, when 25(OH)D concentration was increased by 1 ng/mL, BMI was decreased by 0.043 kg/m 2 . Conclusion: In Korean adolescents, the vitamin D level increased as the BMI decreased.

Cerebral ischemia is a major cause of death and neurological disability. It also leads to severe brain tissue damage by excessive generation of oxidative stress. Quercetin is a bioflavonoid substance that acts an antioxidant agent and exerts a neuroprotective effect against cerebral ischemia. The aim of this study was to detect specific proteins that are differentially expressed in response to quercetin treatment in focal cerebral ischemia. Adult male rats were intraperitoneally injected with vehicle or quercetin (10 mg/kg) 30 min prior to right middle cerebral artery occlusion (MCAO). Brain tissues were collected 24 h after MCAO surgery and right cerebral cortices proteins were identified by two-dimensional gel electrophoresis and mass spectrometry. MCAO leads to neurological behavior disorders, infarction, and histopathological change. However, quercetin treatment alleviated MCAO-induced neuronal deficits and damages. We identified specific proteins differentially expressed between vehicle- and quercetin-treated animals. Among these detected proteins, isocitrate dehydrogenase [NAD+], adenosylhomocysteinase, pyruvate kinase, and ubiquitin carboxy terminal hydrolase L1 were decreased in vehicle-treated animals, while quercetin administration alleviated the MCAO-induced decreases in these proteins. However, 60 kDa heat shock protein and collapsin response mediator protein 2 were increased in the vehicle-treated animals, and quercetin treatment attenuated increases in these proteins. The expression changes in these proteins were confirmed by Western blot and reverse transcription-PCR analyses. These proteins are associated with cellular differentiation, metabolism, and oxidative stress related proteins. These results suggest that quercetin reduces ischemic injury by modulating the expression of various proteins in focal cerebral ischemia.

A new manipulation strategy has been proposed to grasp various objects stably using a dual-arm robotic system in the ROS environment. The grasping pose of the dual-arm has been determined depending upon the shape of the objects which is identified by the pan/tilt camera. For the stable grasping of the object, an operability index of the dual-arm robot (OPIND) has been defined by using the current values applied to the motors for the given grasping pose. When analyzing the motion of a manipulator, the manipulability index of both arms has been derived from the Jacobian to represent the relationship between the joint velocity vector and the workspace velocity vector, which has an elliptical range representing easiness to work with. Through the experiments, the OPIND applied state and the non — applied state of the dual-arm robotic system have been compared to each to other.

Human respiratory syncytial virus (HRSV) is known as the leading cause of respiratory tract illness in infancy and elderly children worldwide. We investigate the prevalence pattern and genetic characteristics in the second variable region G protein gene of HRSV during 5 consecutive seasons from 2010 to 2015. A total of 4,793 specimens (throat swabs) were collected from patients with acute respiratory tract. HRSV were evaluated and classified as HRSV A (n=111) or HRSV B (n=64) by real-time RT-PCR or RT-PCR. In general HRSV were detected in winter season. Coughing, fever, rhinorrhea and sputum were confirmed main symptoms in patients with HRSV. There were no significant differences in clinical characteristics or severity according to the HRSV subgroup infections. Out of 175 HRSV positive samples, 94 samples were successfully sequenced using G gene. Phylogenetic analysis revealed that 62 HRSV-A strains clustered into genotypes ON1 (n=54, 87.1%), NA1 (n=7), NA2 (n=1) and 32 HRSV-B strains clustered into three genotypes: BA4 (n=28, 87.5%), BA5 (n=2), BA6 (n=2). These results provide a better understanding of HRSV prevalence pattern and genetic characteristics.

SummaryAlthough Aβ peptides are causative agents in Alzheimer's disease (AD), the underlying mechanisms are still elusive. We report that Aβ42 induces a translational block by activating AMPK, thereby inhibiting the mTOR pathway. This translational block leads to widespread ER stress, which activates JNK3. JNK3 in turn phosphorylates APP at T668, thereby facilitating its endocytosis and subsequent processing. In support, pharmacologically blocking translation results in a significant increase in Aβ42 in a JNK3-dependent manner. Thus, JNK3 activation, which is increased in human AD cases and a familial AD (FAD) mouse model, is integral to perpetuating Aβ42 production. Concomitantly, deletion of JNK3 from FAD mice results in a dramatic reduction in Aβ42 levels and overall plaque loads and increased neuronal number and improved cognition. This reveals AD as a metabolic disease that is under tight control by JNK3.