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https://www.readbyqxmd.com/read/27935156/casp9-germline-mutation-in-a-family-with-multiple-brain-tumors
#1
Michael W Ronellenfitsch, Oh Ji Eun, Kaishi Satomi, Koichiro Sumi, Patrick N Harter, Joachim P Steinbach, Jörg Felsberg, David Capper, Catherine Voegele, Geoffroy Durand, James McKay, Florence Le Calvez-Kelm, Jens Schittenhelm, Barbara Klink, Michel Mittelbronn, Hiroko Ohgaki
We report a novel CASP9 germline mutation that may increase susceptibility to the development of brain tumors. We identified this mutation in a family in which three brain tumors had developed within three generations, including two anaplastic astrocytomas occurring in cousins. The cousins were diagnosed at similar ages (29 and 31 years), and their tumors showed similar histological features. Genetic analysis revealed somatic IDH1 and TP53 mutations in both tumors. However, no germline TP53 mutations were detected, despite the fact that this family fulfills the criteria of Li-Fraumeni-like syndrome...
December 9, 2016: Brain Pathology
https://www.readbyqxmd.com/read/27933294/branched-chain-amino-acid-levels-are-related-with-surrogates-of-disturbed-lipid-metabolism-among-older-men
#2
Urho M Kujala, Markku Peltonen, Merja K Laine, Jaakko Kaprio, Olli J Heinonen, Jouko Sundvall, Johan G Eriksson, Antti Jula, Seppo Sarna, Heikki Kainulainen
AIMS/HYPOTHESIS: Existing studies suggest that decreased branched-chain amino acid (BCAA) catabolism and thus elevated levels in blood are associated with metabolic disturbances. Based on such information, we have developed a hypothesis how BCAA degradation mechanistically connects to tricarboxylic acid cycle, intramyocellular lipid storage, and oxidation, thus allowing more efficient mitochondrial energy production from lipids as well as providing better metabolic health. We analyzed whether data from aged Finnish men are in line with our mechanistic hypothesis linking BCAA catabolism and metabolic disturbances...
2016: Frontiers in Medicine
https://www.readbyqxmd.com/read/27931027/anthracycline-induced-cardiotoxicity-in-young-cancer-patients-the-role-of-carnitine
#3
Saro H Armenian
While the increased rates of survival in childhood cancers have increased progressively in recent decades, many childhood cancer survivors will have at least one chronic health condition within 40 years of age. In this regard, cardiovascular complications have emerged as a leading cause of long-term morbidity and mortality in long-term survivors of childhood cancer, likely due to exposure to anthracycline chemotherapy, and outcomes in patients with anthracycline-related cardiomyopathy remain poor. Some progress has been made in understanding the mechanisms at the basis of anthracycline-related cardiomyopathy, which appear to involve generation of reactive oxygen species, leading to mitochondrial dysfunction, followed by myocyte apoptosis and maladaptive left ventricular remodeling...
December 9, 2016: Annals of Nutrition & Metabolism
https://www.readbyqxmd.com/read/27928778/previously-unreported-biallelic-mutation-in-dnajc19-are-sensorineural-hearing-loss-and-basal-ganglia-lesions-additional-features-of-dilated-cardiomyopathy-and-ataxia-dcma-syndrome
#4
Sema Kalkan Ucar, Johannes A Mayr, René G Feichtinger, Ebru Canda, Mahmut Çoker, Saskia B Wortmann
BACKGROUND: Dilated cardiomyopathy (DCM), non-progressive cerebellar ataxia (A), testicular dysgenesis, growth failure, and 3-methylglutaconic aciduria are the hallmarks of DNAJC19 defect (or DCMA syndrome) due to biallelic mutations in DNAJC19. To date DCMA syndrome has been reported in 19 patients from Canada and in two Finnish siblings. The underlying pathomechanism is unknown; however, DNAJC19 is presumed to be involved in mitochondrial membrane related processes (e.g., protein import and cardiolipin remodeling)...
December 8, 2016: JIMD Reports
https://www.readbyqxmd.com/read/27928512/extracellular-vesicle-associated-a%C3%AE-mediates-trans-neuronal-bioenergetic-and-ca-2-handling-deficits-in-alzheimer-s-disease-models
#5
Erez Eitan, Emmette R Hutchison, Krisztina Marosi, James Comotto, Maja Mustapic, Saket M Nigam, Caitlin Suire, Chinmoyee Maharana, Gregory A Jicha, Dong Liu, Vasiliki Machairaki, Kenneth W Witwer, Dimitrios Kapogiannis, Mark P Mattson
Alzheimer's Disease (AD) is an age-related neurodegenerative disorder in which aggregation-prone neurotoxic amyloid β-peptide (Aβ) accumulates in the brain. Extracellular vesicles (EVs) are small 50-150 nanometer membrane vesicles that have recently been implicated in the prion-like spread of self-aggregating proteins. Here we report that EVs isolated from AD patient CSF and plasma, from the plasma of two AD mouse models, and from the medium of neural cells expressing familial AD presenilin 1 mutations, destabilize neuronal Ca(2+) homeostasis, impair mitochondrial function, and sensitize neurons to excitotoxicity...
2016: NPJ Aging and Mechanisms of Disease
https://www.readbyqxmd.com/read/27927758/mitochondrial-aging-is-there-a-mitochondrial-clock
#6
Dmitry B Zorov, Vasily A Popkov, Ljubava D Zorova, Ivan A Vorobjev, Irina B Pevzner, Denis N Silachev, Savva D Zorov, Stanislovas S Jankauskas, Valentina A Babenko, Egor Y Plotnikov
Fragmentation (fission) of mitochondria, occurring in response to oxidative challenge, leads to heterogeneity in the mitochondrial population. It is assumed that fission provides a way to segregate mitochondrial content between the "young" and "old" phenotype, with the formation of mitochondrial "garbage," which later will be disposed. Fidelity of this process is the basis of mitochondrial homeostasis, which is disrupted in pathological conditions and aging. The asymmetry of the mitochondrial fission is similar to that of their evolutionary ancestors, bacteria, which also undergo an aging process...
December 7, 2016: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
https://www.readbyqxmd.com/read/27926738/corrigendum-mitochondrial-and-nuclear-dna-matching-shapes-metabolism-and-healthy-ageing
#7
Ana Latorre-Pellicer, Raquel Moreno-Loshuertos, Ana Victoria Lechuga-Vieco, Fátima Sánchez-Cabo, Carlos Torroja, Rebeca Acín-Pérez, Enrique Calvo, Esther Aix, Andrés González-Guerra, Angela Logan, María Luisa Bernad-Miana, Eduardo Romanos, Raquel Cruz, Sara Cogliati, Beatriz Sobrino, Ángel Carracedo, Acisclo Pérez-Martos, Patricio Fernández-Silva, Jesús Ruíz-Cabello, Michael P Murphy, Ignacio Flores, Jesús Vázquez, José Antonio Enríquez
No abstract text is available yet for this article.
December 7, 2016: Nature
https://www.readbyqxmd.com/read/27922823/slm35-links-mitochondrial-stress-response-and-longevity-through-tor-signaling-pathway
#8
Jose L Aguilar-Lopez, Raymond Laboy, Fabiola Jaimes-Miranda, Erika Garay, Alexander DeLuna, Soledad Funes
In most eukaryotic cells mitochondria are essential organelles involved in a great variety of cellular functions. One of the physiological processes linked to mitochondria is aging, a gradual process of damage accumulation that eventually promotes cell death. Aging depends on a balance between mitochondrial biogenesis, function and degradation. It has been previously shown that Tor1, Sch9 and Ras2 are activated in response to nutrient availability and regulate cell growth and division. A deficiency in any of these genes promotes lifespan extension and cell protection during oxidative and heat shock stress...
December 2, 2016: Aging
https://www.readbyqxmd.com/read/27919931/low-mt-co1-in-monocytes-and-microvesicles-is-associated-with-outcome-in-patients-with-coronary-artery-disease
#9
Paul Holvoet, Maarten Vanhaverbeke, Katarzyna Bloch, Pieter Baatsen, Peter Sinnaeve, Stefan Janssens
BACKGROUND: Cytochrome oxidase (COX) IV complex regulates energy production in mitochondria. Impaired COX gene expression is related to obesity and type 2 diabetes mellitus, but whether it is directly related to the incidence of cardiovascular events is unknown. We investigated whether COX gene expression in monocytes is predictive for cardiovascular events in coronary artery disease patients. To avoid monocyte isolation from fresh blood, we then aimed to validate our findings in monocyte-derived microvesicles isolated from plasma...
December 5, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27919855/uncoupling-protein-2-deficiency-reduces-proliferative-capacity-of-murine-pancreatic-stellate-cells
#10
Sarah Muller, Sandra Maria Klingbeil, Andreea Sandica, Robert Jaster
BACKGROUND: Uncoupling protein 2 (UCP2) has been suggested to inhibit mitochondrial production of reactive oxygen species (ROS) by decreasing the mitochondrial membrane potential. Experimental acute pancreatitis is associated with increased UCP2 expression, whereas UCP2 deficiency retards regeneration of aged mice from acute pancreatitis. Here, we have addressed biological and molecular functions of UCP2 in pancreatic stellate cells (PSCs), which are involved in pancreatic wound repair and fibrogenesis...
December 2016: Hepatobiliary & Pancreatic Diseases International: HBPD INT
https://www.readbyqxmd.com/read/27919679/regulation-of-protein-kinase-c-epsilon-and-its-age-dependence
#11
Chen Kang, Jingping Qin, Wil Osei, Keli Hu
Protein kinase C (PKC) is an important mediator in the cardioprotection of ischemic preconditioning and has been shown to translocate to mitochondria upon activation. However, little is known about the cellular signaling underlying the translocation of PKC isoforms to mitochondria and its age-dependence. The present study aimed to explore whether adenosine-induced translocation of PKCε to mitochondria is mediated by caveolin-3 and/or adenosine A2B receptor/PI3 kinase mediated signaling, and whether the mitochondrial targeting of PKCε is age-related...
December 2, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27916687/a-unique-combination-of-micronutrients-rejuvenates-cognitive-performance-in-aged-mice
#12
Sam D Perez, Kristy Du, Catarina Rendeiro, Lin Wang, Qian Wu, Stanislav S Rubakhin, Rema Vazhappilly, Jeffrey H Baxter, Jonathan V Sweedler, Justin S Rhodes
It is widely believed that diet can influence the onset and severity of cognitive aging, but the optimal combination of micronutrients and molecular and cellular mechanisms remain elusive. The purpose of this study was to compare the effects of eight distinct diets, consisting of various concentrations of selected micronutrients, on learning and memory as well as markers of neuronal plasticity, and metabolic and neuro-immune status of the aged hippocampus. Eighteen-month-old male and female C57BL/6J mice were fed the diets for 16 weeks, followed by learning and memory trials on the active avoidance task...
December 1, 2016: Behavioural Brain Research
https://www.readbyqxmd.com/read/27916650/cardiac-oxidative-stress-in-diabetes-mechanisms-and-therapeutic-potential
#13
REVIEW
Alyssa Faria, Shanta J Persaud
Macrovascular complications of diabetes, including diabetic cardiovascular disease (CVD), occur through a number of hyperglycaemia-induced mechanisms that include generation of oxidative stress, accumulation of advanced glycation end-products (AGE) and activation of protein kinase C (PKC). Cardiac oxidative stress is associated with increased cardiac fibrosis and hypertrophy, and reduced cardiac performance and contractility, leading to severe cardiac dysfunction and potentially fatal cardiac events. It occurs under conditions of excessive synthesis of reactive oxygen species (ROS)...
December 1, 2016: Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/27916530/enhanced-respiratory-chain-supercomplex-formation-in-response-to-exercise-in-human-skeletal-muscle
#14
Chiara Greggio, Pooja Jha, Sameer S Kulkarni, Sylviane Lagarrigue, Nicholas T Broskey, Marie Boutant, Xu Wang, Sonia Conde Alonso, Emmanuel Ofori, Johan Auwerx, Carles Cantó, Francesca Amati
Mitochondrial dysfunction is a hallmark of multiple metabolic complications. Physical activity is known to increase mitochondrial content in skeletal muscle, counteracting age-related decline in muscle function and protecting against metabolic and cardiovascular complications. Here, we investigated the effect of 4 months of exercise training on skeletal muscle mitochondria electron transport chain complexes and supercomplexes in 26 healthy, sedentary older adults. Exercise differentially modulated respiratory complexes...
November 28, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/27916526/the-mitochondrial-lon-protease-is-required-for-age-specific-and-sex-specific-adaptation-to-oxidative-stress
#15
Laura C D Pomatto, Caroline Carney, Brenda Shen, Sarah Wong, Kelly Halaszynski, Matthew P Salomon, Kelvin J A Davies, John Tower
Multiple human diseases involving chronic oxidative stress show a significant sex bias, including neurodegenerative diseases, cancer, immune dysfunction, diabetes, and cardiovascular disease. However, a possible molecular mechanism for the sex bias in physiological adaptation to oxidative stress remains unclear. Here, we report that Drosophila melanogaster females but not males adapt to hydrogen peroxide stress, whereas males but not females adapt to paraquat (superoxide) stress. Stress adaptation in each sex requires the conserved mitochondrial Lon protease and is associated with sex-specific expression of Lon protein isoforms and proteolytic activity...
November 23, 2016: Current Biology: CB
https://www.readbyqxmd.com/read/27915495/placental-respiratory-chain-complex-activities-in-high-risk-pregnancies
#16
Mojtaba Beyramzadeh, Zeliha Gunnur Dikmen, Nergiz K Erturk, Zafer Selcuk Tuncer, Filiz Akbiyik
OBJECTIVES: Mitochondrial oxidative phosphorylation is the key energy source for placental functions and fetal growth. The purpose of this study was to investigate the function of placenta in high risk pregnancies by measuring mitochondrial respiratory chain complex (RCC) activities, and to evaluate the correlation between double test risk ratio and RCC activities. METHODS: The placenta samples were collected from 50 pregnant women. The controls consisted of 20 normal uncomplicated pregnancies and the study group (n = 30) consisted of preeclampsia (PE), intrauterin growth restriction (IUGR), advanced maternal age (AMA), twins and preterm deliveries...
December 5, 2016: Journal of Maternal-fetal & Neonatal Medicine
https://www.readbyqxmd.com/read/27914941/therapeutic-role-of-sirtuins-in-neurodegenerative-disease-and-their-modulation-by-polyphenols
#17
REVIEW
Marjan Ajami, Hamidreza Pazoki-Toroudi, Hamed Amani, Seyed Fazel Nabavi, Nady Braidy, Rosa Anna Vacca, Atanas Georgiev Atanasov, Andrei Mocan, Seyed Mohammad Nabavi
Searching for effective therapeutic agents‏‎ to ‎‏prevent‏ ‏neurodegeneration ‎is a challenging task due ‎to ‎the growing list of neurodegenerative disorders associated with a multitude of inter-related pathways.‎ The induction and inhibition of several different signaling pathways has been shown to slow down and/or attenuate ‎neurodegeneration and decline in cognition and locomotor function. Among these signaling pathways, a new class of enzymes known as sirtuins or silent information regulators of gene transcription has been shown to play important regulatory roles in the ageing process...
November 30, 2016: Neuroscience and Biobehavioral Reviews
https://www.readbyqxmd.com/read/27913766/myocardial-cytochrome-oxidase-activity-increases-with-age-and-hypoxemia-in-patients-with-congenital-heart-disease
#18
Michael Onwugbufor, Richard J Levy, David Zurakowski, Richard A Jonas, Pranava Sinha
BACKGROUND: Myocardial tolerance to ischemia is influenced by age and preoperative cyanosis through unknown mechanisms and significantly affects postoperative outcomes. Cytochrome c oxidase (CcOx), the terminal enzyme of the mitochondrial electron transport chain, may play a role in the susceptibility to ischemic-reperfusion (IR) injury. Our study aimed at investigating changes in human myocardial CcOx activity based on age and preoperative oxygen saturation to understand its role in transition from neonatal to mature myocardium and hypoxic conditions...
December 1, 2016: Perfusion
https://www.readbyqxmd.com/read/27911443/transient-mitochondrial-dna-double-strand-breaks-in-mice-cause-accelerated-aging-phenotypes-in-a-ros-dependent-but-p53-p21-independent-manner
#19
Milena Pinto, Alicia M Pickrell, Xiao Wang, Sandra R Bacman, Aixin Yu, Aline Hida, Lloye M Dillon, Paul D Morton, Thomas R Malek, Siôn L Williams, Carlos T Moraes
We observed that the transient induction of mtDNA double strand breaks (DSBs) in cultured cells led to activation of cell cycle arrest proteins (p21/p53 pathway) and decreased cell growth, mediated through reactive oxygen species (ROS). To investigate this process in vivo we developed a mouse model where we could transiently induce mtDNA DSBs ubiquitously. This transient mtDNA damage in mice caused an accelerated aging phenotype, preferentially affecting proliferating tissues. One of the earliest phenotypes was accelerated thymus shrinkage by apoptosis and differentiation into adipose tissue, mimicking age-related thymic involution...
December 2, 2016: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27909728/calcineurin-nuclear-factor-%C3%AE%C2%BAb-signaling-mediates-isoflurane-induced-hippocampal-neuroinflammation-and-subsequent-cognitive-impairment-in-aged-rats
#20
Zhengqian Li, Cheng Ni, Chun Xia, Joey Jaw, Yujie Wang, Yiyun Cao, Mao Xu, Xiangyang Guo
It is known that inhaled anesthetics induce neuroinflammation and facilitate postoperative cognitive dysfunction (POCD) in aged individuals; however, the mechanisms by which they mediate these effects remain elusive. Inhalation of the isoflurane anesthetic leads to opening of the mitochondrial permeability transition pore and loss of mitochondrial membrane potential. Therefore, mitochondrial retrograde signaling, which is an adaptive mechanism that facilitates the transmission of signals from dysfunctional mitochondria to the nucleus to activate target gene expression, may be activated during isoflurane inhalation...
November 24, 2016: Molecular Medicine Reports
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