bluuebunny/crossref_metadata_2025_split huggingface dataset:
Standardized extract of Bacopa monniera (BESEB CDRI‐08) attenuates contextual associative learning deficits in the aging rat's brain induced by D‐galactose
Authors: Prisila Dulcy Charles , Singh Hemant K. , Preethi Jayakumar , Emmanuvel Rajan Koilmani 
Published: June 2012

AbstractIn this study, we examined the neuroprotective effect of standardized Bacopa monniera extract (BME: BESEB CDRI‐08) against the D‐galactose (D‐gal)‐induced brain aging in rats. Experimental groups were subjected to contextual‐associative learning task. We found that the administration of BME in the D‐gal‐treated group attenuated contextual‐associative learning deficits; the individuals showed more correct responses and retrieved the reward with less latency. Subsequent analysis showed that the BME administration significantly decreased advance glycation end product (AGE) in serum and increased the activity of antioxidant response element (ARE) and the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and nuclear transcription factor NF‐E2‐related factor 2 (Nrf2), accompanied by a reduction in the level of serotonin (5‐HT) in the hippocampus. The BME treatment also reversed D‐gal‐induced brain aging by upregulating the levels of the presynaptic proteins synaptotagmin I (SYT1) and synaptophysin (SYP) and the postsynaptic proteins Ca2+/calmodulin dependent protein kinase II (αCaMKII) and postsynaptic density protein‐95 (PSD‐95) in the hippocampus during synaptic plasticity. A significant finding is that the D‐gal‐ + BME‐treated rats exhibited more correct responses in contextual‐associative learning than D‐gal alone‐treated rats. Our findings suggest that BME treatment attenuates D‐gal‐induced brain aging and regulates the level of antioxidant enzymes, Nrf2 expression, and the level of 5‐HT, which was accompanied by concomitantly increased levels of synaptic proteins SYT1, SYP, αCaMKII, p‐αCaMKII, and PSD‐95. © 2012 Wiley Periodicals, Inc.
Transforming growth factor‐β stimulates β amyloid uptake by microglia through Smad3‐dependent mechanisms
Authors: Tichauer Juan E. , von Bernhardi Rommy 
Published: June 2012

AbstractInflammatory cytokines and β amyloid (Aβ) induce activation of glial cells, leading to both protective and deleterious changes that are relevant for the pathogenesis of Alzheimer disease (AD). We have shown that astrocytes downregulate microglial cell cytotoxic activation through secretion of transforming growth factor‐β (TGFβ1), and there is evidence that TGFβ1 modifies Aβ removal through the modulation of microglia. However, inflammatory activation of microglia is increased and Aβ clearance is reduced in AD patients, regardless of the fact that TGFβ1 is increased in their nervous system. We propose that changes in TGFβ Smad3 signal transduction could modify the regulation mediated by TGFβ1. Here we evaluated the participation of the TGFβ Smad3 pathway in regulation of the expression pattern of scavenger receptors (SR) and activation of microglia through nitric oxide (NO·) secretion and phagocytosis of Aβ. We found that TGFβ1 increased SR‐A by 2.4‐fold and decreased SR‐BI expression by 79% at 48 hr, whereas it did not change SR‐MARCO or CD36 expression. In addition, we observed a 51% increase of Aβ uptake and an 83% decrease of NO· production induced by lipopolysaccharide in microglial cell cultures. Increased expression of SR‐A, phagocytosis, and downregulation of NO· by TGFβ1 were prevented by the inhibition of the TGFβ Smad3 pathway. Our results indicate that the modulation of microglial cell activation by TGFβ1, leading to increased clearance of Aβ and reduced cytotoxicity, is at least partially mediated by the Smad pathway. © 2012 Wiley Periodicals, Inc.
Altered global and regional brain mean diffusivity in patients with obstructive sleep apnea
Authors: Kumar Rajesh , Chavez Alexa S. , Macey Paul M. , Woo Mary A. , Yan‐Go Frisca L. , Harper Ronald M. 
Published: June 2012

AbstractObstructive sleep apnea (OSA) is a common and progressive disorder accompanied by severe cardiovascular and neuropsychological sequelae, presumably induced by brain injury resulting from the intermittent hypoxia and cardiovascular processes accompanying the syndrome. However, whether the predominant brain tissue pathology is acute or chronic in newly‐diagnosed, untreated OSA subjects is unclear; this assessment is essential for revealing pathological processes. Diffusion tensor imaging (DTI)‐based mean diffusivity (MD) procedures can detect and differentiate acute from chronic pathology and may be useful to reveal processes in the condition. We collected four DTI series from 23 newly‐diagnosed, treatment‐naïve OSA and 23 control subjects, using a 3.0‐Tesla magnetic resonance imaging scanner. Mean diffusivity maps were calculated from each series, realigned, averaged, normalized to a common space, and smoothed. Global brain MD values for each subject were calculated using normalized MD maps and a global brain mask. Mean global brain MD values and smoothed MD maps were compared between groups by using analysis of covariance (covariate: age). Mean global brain MD values were significantly reduced in OSA compared with controls (P = 0.01). Multiple brain sites in OSA, including medullary, cerebellar, basal ganglia, prefrontal and frontal, limbic, insular, cingulum bundle, external capsule, corpus callosum, temporal, occipital, and corona radiata regions showed reduced regional MD values compared with controls. The results suggest that global brain MD values are significantly reduced in OSA, with certain regional sites especially affected, presumably a consequence of axonal, glial, and other cell changes in those areas. The findings likely represent acute pathological processes in newly‐diagnosed OSA subjects. © 2012 Wiley Periodicals, Inc.
Signalling routes and developmental regulation of group I metabotropic glutamate receptors in rat auditory midbrain neurons
Authors: Martinez‐Galan Juan R. , Perez‐Martinez Francisco C. , Juiz Jose M. 
Published: June 2012

AbstractGroup I metabotropic glutamate receptors (mGluRs) are linked to intracellular Ca2+ signalling and play important roles related to synaptic plasticity and development. In neurons from the central nucleus of the inferior colliculus (CIC), the activation of these receptors evokes large [Ca2+]i responses. By using optical imaging of the fluorescent Ca2+‐sensitive dye Fura‐2, we have explored which [Ca2+]i routes are triggered by group I mGluR activation in young CIC neurons and whether mGluR‐induced [Ca2+]i responses are regulated during postnatal development. In addition, real‐time quantitative RT‐PCR was used to study the developmental expression of both group I mGluR subtypes, mGluR1 and mGluR5. Application of DHPG, a specific agonist of group I mGluRs, was used on CIC slices from young rats to elicit [Ca2+]i responses. A majority of responses consisted of an initial thapsigargin‐sensitive Ca2+ peak, related to store depletion, followed by a plateau phase, sensitive to the store‐operated Ca2+ entry blocker 2‐APB. During postnatal development, from P6 to P17, DHPG‐induced [Ca2+]i responses changed. The largest Ca2+ responses were reached at P6, whereas lower peak and plateau responses were found after hearing onset, at P13–P14 and P17. qRT‐PCR analysis also revealed important differences in the expression of both mGluR1 and mGluR5 subtypes during development, with the highest levels of both subtypes at P7 and a developmental decrease of both transcripts. Our results suggest both intra‐ and extracellular routes for [Ca2+]i increases linked to group I mGluRs in CIC neurons and a regulation of group I mGluR activity and expression during auditory development. © 2012 Wiley Periodicals, Inc.
Hypoactivity of the central dopaminergic system and autistic‐like behavior induced by a single early prenatal exposure to lipopolysaccharide
Authors: Kirsten Thiago B. , Chaves‐Kirsten Gabriela P. , Chaible Lucas M. , Silva Ana C. , Martins Daniel O. , Britto Luiz R.G. , Dagli Maria L.Z. , Torrão Andrea S. , Palermo‐Neto João , Bernardi Maria M. 
Published: June 2012

AbstractThe aim of the present study was to evaluate the behavioral patterns associated with autism and the prevalence of these behaviors in males and females, to verify whether our model of lipopolysaccharide (LPS) administration represents an experimental model of autism. For this, we prenatally exposed Wistar rats to LPS (100 μg/kg, intraperitoneally, on gestational day 9.5), which mimics infection by gram‐negative bacteria. Furthermore, because the exact mechanisms by which autism develops are still unknown, we investigated the neurological mechanisms that might underlie the behavioral alterations that were observed. Because we previously had demonstrated that prenatal LPS decreases striatal dopamine (DA) and metabolite levels, the striatal dopaminergic system (tyrosine hydroxylase [TH] and DA receptors D1a and D2) and glial cells (astrocytes and microglia) were analyzed by using immunohistochemistry, immunoblotting, and real‐time PCR. Our results show that prenatal LPS exposure impaired communication (ultrasonic vocalizations) in male pups and learning and memory (T‐maze spontaneous alternation) in male adults, as well as inducing repetitive/restricted behavior, but did not change social interactions in either infancy (play behavior) or adulthood in females. Moreover, although the expression of DA receptors was unchanged, the experimental animals exhibited reduced striatal TH levels, indicating that reduced DA synthesis impaired the striatal dopaminergic system. The expression of glial cell markers was not increased, which suggests that prenatal LPS did not induce permanent neuroinflammation in the striatum. Together with our previous finding of social impairments in males, the present findings demonstrate that prenatal LPS induced autism‐like effects and also a hypoactivation of the dopaminergic system. © 2012 Wiley Periodicals, Inc.
Deficiency of ganglioside GM1 correlates with Parkinson's disease in mice and humans
Authors: Wu Gusheng , Lu Zi‐Hua , Kulkarni Neil , Ledeen Robert W. 
Published: June 2012

AbstractSeveral studies have successfully employed GM1 ganglioside to treat animal models of Parkinson's disease (PD), suggesting involvement of this ganglioside in PD etiology. We recently demonstrated that genetically engineered mice (B4galnt1−/−) devoid of GM1 acquire characteristic symptoms of this disorder, including motor impairment, depletion of striatal dopamine, selective loss of tyrosine hydroxylase‐expressing neurons, and aggregation of α‐synuclein. The present study demonstrates similar symptoms in heterozygous mice (HTs) that express only partial GM1 deficiency. Symptoms were alleviated by administration of L‐dopa or LIGA‐20, a membrane‐permeable analog of GM1 that penetrates the blood–brain barrier and accesses intracellular compartments. Immunohistochemical analysis of paraffin sections from PD patients revealed significant GM1 deficiency in nigral dopaminergic neurons compared with age‐matched controls. This was comparable to the GM1 deficiency of HT mice and suggests that GM1 deficiency may be a contributing factor to idiopathic PD. We propose that HT mice with partial GM1 deficiency constitute an especially useful model for PD, reflecting the actual pathophysiology of this disorder. The results point to membrane‐permeable analogs of GM1 as holding promise as a form of GM1 replacement therapy. © 2012 Wiley Periodicals, Inc.
Immunohistochemical study of semicarbazide‐sensitive amine oxidase/vascular adhesion protein‐1 in the hippocampal vasculature: Pathological synergy of Alzheimer's disease and diabetes mellitus
Authors: Valente Tony , Gella Alejandro , Solé Montse , Durany Núria , Unzeta Mercedes 
Published: June 2012

AbstractSemicarbazide‐sensitive amine oxidase/vascular adhesion protein‐1 (SSAO/VAP‐1) is involved in vascular endothelial damage as well as in the vascular degeneration underlying diabetes mellitus and Alzheimer's disease (AD). Recent evidence suggests that classic pathological features of AD are more pronounced in diabetic mellitus patients. To investigate the expression and distribution of SSAO/VAP‐1 in the two pathologies, we have performed an immunohistochemical study in human hippocampal vessels of AD, AD with diabetic mellitus (ADD), diabetic mellitus (DM), and nondemented (ND) patients. The present results demonstrate major vessel accumulation of both SSAO/VAP‐1 and amyloid‐β immunolabeling intensity in ADD compared with AD patients. Interestingly, nearly damaged vessels with high levels of SSAO/VAP‐1 also showed increased oxidative damage markers (AGE, RAGE, and SOD‐1) and glial activation (GFAP and HLA). Overall, this work suggests that high vascular SSAO/VAP‐1 levels in human hippocampus may contribute to vascular degeneration, which can explain the severe progression in patients with both pathologies. © 2012 Wiley Periodicals, Inc.
Calpain inhibition attenuated morphological and molecular changes in skeletal muscle of experimental allergic encephalomyelitis rats
Authors: Park Sookyoung , Nozaki Kenkichi , Guyton M. Kelly , Smith Joshua A. , Ray Swapan K. , Banik Naren L. 
Published: June 2012

AbstractMuscle weakness and atrophy are important manifestations of multiple sclerosis (MS). To investigate the pathophysiological mechanisms of skeletal muscle change in MS, we induced experimental autoimmune encephalomyelitis (EAE) in Lewis male rats and examined morphological and molecular changes in skeletal muscle. We also treated EAE rats with calpepetin, a calpain inhibitor, to examine its beneficial effects on skeletal muscle damage. Morphological changes in muscle tissue of EAE rats included smaller and irregularly shaped muscle fibers and fibrosis. Western blot analysis demonstrated increased calpain:calpastatin ratio, inflammation‐related transcription factors (nuclear factor‐κB:inhibitor of κB α ratio), and proinflammatory enzymes (cyclooxygenase‐2). TUNEL‐positive myonuclei in skeletal muscle cells of EAE rats indicated cell death. In addition, markers of apoptotic cell death (Bax:Bcl‐2 ratio and caspase‐12 protein levels) were elevated. Expression of muscle‐specific ubiquitin ligases (muscle atrophy F‐box and muscle ring finger protein 1), was upregulated in muscle tissue of EAE‐vehicle animals. Both prophylactic and therapeutic treatment with calpeptin partially attenuated muscle changes noted in EAE animals. These results indicate that morphological and molecular changes including apoptotic cell death and protein breakdown develop in skeletal muscle of EAE animals and that these changes can be reversed by calpain inhibition. © 2012 Wiley Periodicals, Inc.
The effect of induced yellowing on the physicochemical properties of specialty rice
Authors: Bryant Rolfe J , Yeater Kathleen M , Belefant‐Miller Helen 
Published: June 2012

AbstractBACKGROUND: Postharvest yellowing (PHY) of rice kernels can be a major problem in the rice industry. This is especially true with high‐valued specialty rice, because profit loss will be greater. The objective of this work was to determine whether a significant change occurs in the physicochemical properties (apparent amylose and protein concentrations, viscosity profile and gelatinisation temperature) as a result of induced PHY.RESULTS: In this study, four specialty rices (Basmati, Jasmine, Arborio and Sushi) were yellowed using a laboratory method. PHY increased apparent amylose concentration. It also significantly increased onset and peak gelatinisation temperatures. However, peak, breakdown and setback Rapid ViscoAnalyzer viscosities were decreased by PHY. Trough viscosity for Basmati and Jasmine decreased, whereas it increased for Arborio. Moisture and protein concentrations were unchanged by the yellowing process. Attempts to rehydrate the kernels after induced PHY caused them to fracture, thus making them unsuitable for their intended purpose.CONCLUSION: This study indicates that rice that has been subjected to PHY shows a reduction not only in appearance but also in cooking and processing quality, decreasing its value. However, the changes differed for each rice type, with Jasmine being affected the least. Published 2012 by John Wiley & Sons, Ltd.
Selenium increases chlorogenic acid, chlorophyll and carotenoids of Lycium chinense leaves
Authors: Dong Jing Z , Wang Ying , Wang Shu H , Yin Ling P , Xu Guan J , Zheng Cheng , Lei Can , Zhang Ming Z 
Published: June 2012

AbstractBACKGROUND: Leaves of Lycium chinense L. are widely used in traditional Chinese medicine and as functional food in China and south‐east Asia. Polyphenols are important active compounds in leaves of L. chinense L, but their compositions are still not very clear. Selenium has been reported to increase some components of plants. In this study, the composition of polyphenols of L. chinense leaves were analysed, and the effects of selenium on the polyphenols and other components were studied.RESULTS: The main polyphenols were identified as rutin, chlorogenic acid, quercetin, kaempferol and apigenin‐7‐O‐(6′‐O‐acetyl) glucose‐rhamnose. Chlorogenic acid showed the highest average content of 78.36 g kg−1. Rutin, quercetin and kaempferol were determined at low contents from 3.85 g kg−1 to 7.08 g kg−1. Correlation coefficients between selenium and chlorogenic acid, chlorophyll a, chlorophyll b and carotenoids were: R2 = 0.963 (P = 0.002), 0.943 (P = 0.005), 0.957 (P = 0.003) and 0.943 (P = 0.005), respectively. Selenium (0.01–0.05 g kg−1) significantly increased chlorogenic acid, chlorophyll and carotenoids by 200–400% and reduced rutin by 400–900%.CONCLUSION: L. chinense can be an alternative source of chlorogenic acid. Selenium significantly increased chlorogenic acid, chlorophyll a, chlorophyll b and carotenoids, hence increasing the medicinal value of L. chinense leaves. Rutin, quercetin, kaempferol and apigenin‐7‐O‐(6′‐O‐acetyl) glucose‐rhamnose proved to be not significantly influenced by selenium. Copyright © 2012 Society of Chemical Industry
Radionuclide therapy of adrenal tumors
Authors: Carrasquillo Jorge A. , Pandit‐Taskar Neeta , Chen Clara C. 
Published: June 2012

AbstractAdrenal tumors arising from chromaffin cells will often accumulate radiolabeled metaiodobenzylguanidine (MIBG) and thus are amenable to therapy with I‐131 MIBG. More recently, therapy studies have targeted the somatostatin receptors using Lu‐177 or Y‐90 radiolabeled somatostatin analogs. Because pheochromocytoma (PHEO)/paraganglioma (PGL) and neuroblastoma (NB), which often arise from the adrenals, express these receptors, clinical trials have been performed with these reagents. We will review the experience using radionuclide therapy for targeting PHEO/PGL and NBs. J. Surg. Oncol. 2012; 106:632–642. © 2012 Wiley Periodicals, Inc.
A second superior gluteal artery perforator flap with previous liposuction to the same breast after resection of initial SGAP breast reconstruction due to cancer recurrence
Authors: Avashia Yash J. , Desrosiers Arthur E. , Flores Jaime I. 
Published: June 2012

AbstractFree superior gluteal artery perforator (SGAP) flaps are a reliable option for breast reconstruction in patients with insufficient abdominal tissue or abdominal scarring. Liposuction in a donor site is a relative contraindication for harvesting a free flap, despite current case reports challenging this tenet. We describe a case of a 36‐year‐old woman who underwent unilateral breast reconstruction with free SGAP flap. She underwent liposuction of the contralateral buttock for symmetry. Approximately, one year post‐operatively, she developed local recurrence of the breast cancer. Previously liposculpted buttock was used as donor site for a second free SGAP flap anastomosed to internal mammary artery. © 2012 Wiley Periodicals, Inc. Microsurgery, 2012.
The intestinal bioavailability of vaccenic acid and activation of peroxisome proliferator‐activated receptor‐α and ‐γ in a rodent model of dyslipidemia and the metabolic syndrome
Authors: Wang Ye , Jacome‐Sosa Maria M. , Ruth Megan R. , Lu Yan , Shen Jianheng , Reaney Martin J. , Scott Shannon L. , Dugan Michael E. R. , Anderson Hope D. , Field Catherine J. , Proctor Spencer D. , Vine Donna F. 
Published: June 2012

ScopeEvidence suggests a neutral to beneficial role of certain trans fatty acids (TFA) from natural ruminant sources. Trans11–18:1 (vaccenic acid, VA), the most predominant ruminant TFA and a precursor to conjugated linoleic acid, has been shown to improve atherogenic dyslipidemia and symptoms of hepatic steatosis in animal models. The objective of this study was to assess the intestinal bioavailability of various VA sources including synthetic free fatty acid (FFA) and natural ruminant triglyceride forms, as well as the mechanistic pathways that mediate VA's bioactivity.Methods and resultsVA acts as a partial agonist to both peroxisome proliferator‐activated receptors (PPAR)‐α and PPAR‐γ in vitro, with similar affinity compared to commonly known PPAR agonists. It was further confirmed that VA at 30 and 100 μM concentrations suppressed cardiomyocyte hypertrophy vitro in a PPAR‐α‐ and PPAR‐γ‐dependent manner. In vivo, feeding of VA (1%, w/w) resulted in increased mRNA and protein expression of PPAR‐γ in the mucosa of JCR:LA‐cp rats, a model of the metabolic syndrome (p < 0.01 and p < 0.05, respectively) compared to control. In addition, VA from a triglyceride source had greater intestinal bioavailability in vivo compared to VA provided in an FFA form (p < 0.01).ConclusionThe activation of PPAR‐α‐ and PPAR‐γ‐dependent pathways provides a mechanistic explanation of how VA improves blood lipids and related metabolic disorders during conditions of hyperlipidemia. This report also supports the consideration of differential reporting of industrially produced versus natural TFA on food nutrient labels.
Resveratrol ameliorates diabetes‐related metabolic changes via activation of AMP‐activated protein kinase and its downstream targets in db/db mice
Authors: Do Gyeong‐Min , Jung Un Ju , Park Hae‐Jin , Kwon Eun‐Young , Jeon Seon‐Min , McGregor Robin A , Choi Myung‐Sook 
Published: June 2012

ScopeThis study investigated the effects of resveratrol (RV) on diabetes‐related metabolic changes in a spontaneous model of type 2 diabetes, as well as activation of AMP‐activated protein kinase (AMPK) and downstream targets.Methods and resultsC57BL/KsJ‐db/db mice were fed a normal diet with RV (0.005% and 0.02%, w/w) or rosiglitazone (RG, 0.001%, w/w) for 6 weeks. Both doses of RV significantly decreased blood glucose, plasma free fatty acid, triglyceride, apo B/apo AІ levels and increased plasma adiponectin levels. RV activated AMPK and downstream targets leading to decreased blood HbA1c levels, hepatic gluconeogenic enzyme activity, and hepatic glycogen, while plasma insulin levels, pancreatic insulin protein, and skeletal muscle GLUT4 protein were higher after RV supplementation. The high RV dose also significantly increased hepatic glycolytic gene expression and enzyme activity, along with skeletal muscle glycogen synthase protein expression, similar to RG. Furthermore, RV dose dependently decreased hepatic triglyceride content and phosphorylated I kappa B kinase (p‐IKK) protein expression, while hepatic uncoupling protein (UCP) and skeletal muscle UCP expression were increased.ConclusionRV potentiates improving glycemic control, glucose uptake, and dyslipidemia, as well as protecting against pancreatic β‐cell failure in a spontaneous type 2 diabetes model. Dietary RV has potential as an antidiabetic agent via activation of AMPK and its downstream targets.