LEADER 01090nam0-22003491i-450- 001 990006965040403321 005 20050125103803.0 035 $a000696504 035 $aFED01000696504 035 $a(Aleph)000696504FED01 035 $a000696504 100 $a20011002d1962----km-y0itay50------ba 101 0 $aeng 102 $aNL 105 $aa-------001yy 200 1 $a<>study in econometrics$ethe demand for electricity in the United States$fby Franklin M. Fisher$gin association with Carl Kaysen 210 $aAmsterdam$cNorth-Holland Publishing Company$d1962 215 $aIX, 190 p.$d22 cm 225 1 $aContributions to Economic Analysis$v27 610 0 $aConsumi$aStati Uniti 676 $a330.015.195$v20$zita 700 1$aFisher,$bFranklin M.$f<1934 >$0101762 702 1$aKaysen,$bCarl$f<1920-2010> 801 0$aIT$bUNINA$gRICA$2UNIMARC 901 $aBK 912 $a990006965040403321 952 $aXV C 45 (27)$b68853$fFGBC 952 $aL/2.33 FIS$b021161$fSES 959 $aFGBC 959 $aSES 996 $aStudy in econometrics$9699848 997 $aUNINA LEADER 01063cam0 22003011 450 001 SOBE00045573 005 20210623085856.0 010 $a2906462047 100 $a20150112d1993 |||||ita|0103 ba 101 $afre 102 $aFR 200 1 $aEsclave à Alger$erécit de captivité de João Mascarenhas (1621-1626)$ftraduit du portugais, annoté & presénté par Paul Teyssier 210 $aParis$cChandeigne$d1993 215 $a244 p.$cill.$d22 cm 225 2 $aMagellane 300 $aDossier historique, glossaire & bibliographie, gravures & carte 410 1$1001LAEC00028141$12001 $a*Magellane 700 1$aMascarenhas$b, João$3SOBA00010664$4070$0773648 702 1$aTeyssier, Paul$3SOBA00010665$4070 801 0$aIT$bUNISOB$c20210623$gRICA 850 $aUNISOB 852 $aUNISOB$j869$m83114 912 $aSOBE00045573 940 $aM 102 Monografia moderna SBN 941 $aM 957 $a869$b000027$gSI$d83114$tN$1menle$2UNISOB$3UNISOB$420150112094321.0$520210623085847.0$6Alfano 996 $aEsclave à Alger$91710856 997 $aUNISOB LEADER 01180nam a22002891i 4500 001 991000245959707536 005 20040731180728.0 008 040920s1997 xxu eng 020 $a9780691043012 035 $ab1319527x-39ule_inst 035 $aARCHE-114151$9ExL 040 $aSet. Economia$bita$cA.t.i. Arché s.c.r.l. Pandora Sicilia s.r.l. 082 04$a332.0724 100 1 $aCampbell, John Y$0117380 245 14$aThe econometrics of financial markets /$cJohn Y. Campbell, Andrew W. Lo, A. Craig MacKinlay 260 $aPrinceton :$bPrinceton university,$cc1997 300 $aXVIII, 611 p. ;$c24 cm 650 4$aEconomia$xMatematica 650 4$aMercati finanziari$xModelli econometrici 700 1 $aLo, Andrew W$eauthor$4http://id.loc.gov/vocabulary/relators/aut$0117381 700 1 $aMacKinlay, Archie Craig 907 $a.b1319527x$b19-03-19$c23-09-04 912 $a991000245959707536 945 $aLE025 ECO 332 CAM01.01$g1$i2025000174795$lle025$nCatalogato 2019$o-$pE0.00$q-$rl$s- $t0$u1$v0$w1$x0$y.i13849098$z23-09-04 996 $aEconometrics of financial markets$9416558 997 $aUNISALENTO 998 $ale025$b23-09-04$cm$da $e-$feng$gxxu$h4$i1 LEADER 00944cam a22002414i 4500 001 991001466899707536 008 111107s2011 it b bq 001 0 ita d 020 $a9788874968008 035 $ab14019097-39ule_inst 040 $aDip.to Studi Storici$bita 082 04$a398.094575 100 1 $aPacoda, Pierfrancesco$0468782 245 10$aSalento, amore mio :$bviaggio nella musica, nei luoghi e tra i protagonisti del rinascimento salentino /$cPierfrancesco Pacoda 260 $aMilano :$bKowalski,$c[2011] 300 $a184 p. ;$c21 cm. 651 4$aSalento$xUsi e costumi 651 4$aSalento$xVita artistica e culturale 907 $a.b14019097$b28-01-14$c07-11-11 912 $a991001466899707536 945 $aLE023 398.094 PAP 1 1 $g1$i2023000131251$lle023$o-$pE13.00$q-$rn$so $t0$u5$v2$w5$x0$y.i15343753$z09-11-11 996 $aSalento, amore mio$9243002 997 $aUNISALENTO 998 $ale023$b14-11-11$cm$da $e-$fita$git $h0$i0 LEADER 09083nam 2200457z- 450 001 9910220056703321 005 20210212 035 $a(CKB)3800000000216211 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/58592 035 $a(oapen)doab58592 035 $a(EXLCZ)993800000000216211 100 $a20202102d2017 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aThe Role of Mitochondria, Oxidative Stress and Altered Calcium Homeostasis in Amyotrophic Lateral Sclerosis: From Current Developments in the Laboratory to Clinical Treatments 210 $cFrontiers Media SA$d2017 215 $a1 online resource (336 p.) 225 1 $aFrontiers Research Topics 311 08$a2-88945-146-1 330 $aAmyotrophic lateral sclerosis (ALS) is a rapidly progressive, devastating and fatal disease characterized by selective loss of upper and lower motor neurons of the cerebral cortex, brainstem, spinal cord and muscle atrophy. In spite of many years of research, the pathogenesis of ALS is still not well understood. ALS is a multifaceted genetic disease, in which genetic susceptibility to motor neuron death interacts with environmental factors and there is still no cure for this deleterious disease. At present, there is only one FDA approved drug, Riluzole which according to past studies only modestly slows the progression of the disease, and improves survival by up to three months. The suffering of the ALS patients, and their families is enormous and the economic burden is colossal. There is therefore a pressing need for new therapies. Different molecular pathways and pathological mechanisms have been implicated in ALS. According to past studies, altered calcium homeostasis, abnormal mitochondrial function, protein misfolding, axonal transport defects, excessive production of extracellular superoxide radicals, glutamate-mediated excitotoxicity, inflammatory events, and activation of oxidative stress pathways within the mitochondria and endoplasmic reticulum can act as major contributor that eventually leads to loss of connection between muscle and nerve ultimately resulting to ALS. However, the detailed molecular and cellular pathophysiological mechanisms and origin and temporal progression of the disease still remained elusive. Ongoing research and future advances will likely advance our improve understanding about various involved pathological mechanism ultimately leading to discoveries of new therapeutic cures. Importantly, clinical biomarkers of disease onset and progression are thus also urgently needed to support the development of the new therapeutic agents and novel preventive and curative strategies. Effective translation from pre-clinical to clinical studies will further require extensive knowledge regarding drug activity, bioavailability and efficacy in both the pre-clinical and clinical setting, and proof of biological activity in the target tissue. During the last decades, the development of new therapeutic molecules, advance neuroimaging tools, patient derived induced stem cells and new precision medicine approaches to study ALS has significantly improved our understanding of disease. In particular, new genetic tools, neuroimaging methods, cellular probes, biomarker study and molecular techniques that achieve high spatiotemporal resolution have revealed new details about the disease onset and its progression. In our effort to provide the interested reader, clinician and researchers a comprehensive summaries and new findings in this field of ALS research, hereby we have created this electronic book which comprises of twenty seven chapters having various reviews, perspective and original research articles. All these chapters and articles in this book not only summarize the cutting-edge techniques, approaches, cell and animal models to study ALS but also provide unprecedented coverage of the current developments and new hypothesis emerging in ALS research. Some examples are novel genetic and cell culture based models, mitochondria-mediated therapy, oxidative stress and ROS mechanism, development of stem cells and mechanism-based therapies as well as novel biomarkers for designing and testing effective therapeutic strategies that can benefit ALS patients who are at the earlier stages in the disease. I am extremely grateful to all the contributors to this book and want to thank them for their phenomenal efforts. Amyotrophic lateral sclerosis (ALS) is a rapidly progressive, devastating and fatal disease characterized by selective loss of upper and lower motor neurons of the cerebral cortex, brainstem, spinal cord and muscle atrophy. In spite of many years of research, the pathogenesis of ALS is still not well understood. ALS is a multifaceted genetic disease, in which genetic susceptibility to motor neuron death interacts with environmental factors and there is still no cure for this deleterious disease. At present, there is only one FDA approved drug, Riluzole which according to past studies only modestly slows the progression of the disease, and improves survival by up to three months. The suffering of the ALS patients, and their families is enormous and the economic burden is colossal. There is therefore a pressing need for new therapies. Different molecular pathways and pathological mechanisms have been implicated in ALS. According to past studies, altered calcium homeostasis, abnormal mitochondrial function, protein misfolding, axonal transport defects, excessive production of extracellular superoxide radicals, glutamate-mediated excitotoxicity, inflammatory events, and activation of oxidative stress pathways within the mitochondria and endoplasmic reticulum can act as major contributor that eventually leads to loss of connection between muscle and nerve ultimately resulting to ALS. However, the detailed molecular and cellular pathophysiological mechanisms and origin and temporal progression of the disease still remained elusive. Ongoing research and future advances will likely advance our improve understanding about various involved pathological mechanism ultimately leading to discoveries of new therapeutic cures. Importantly, clinical biomarkers of disease onset and progression are thus also urgently needed to support the development of the new therapeutic agents and novel preventive and curative strategies. Effective translation from pre-clinical to clinical studies will further require extensive knowledge regarding drug activity, bioavailability and efficacy in both the pre-clinical and clinical setting, and proof of biological activity in the target tissue. During the last decades, the development of new therapeutic molecules, advance neuroimaging tools, patient derived induced stem cells and new precision medicine approaches to study ALS has significantly improved our understanding of disease. In particular, new genetic tools, neuroimaging methods, cellular probes, biomarker study and molecular techniques that achieve high spatiotemporal resolution have revealed new details about the disease onset and its progression. In our effort to provide the interested reader, clinician and researchers a comprehensive summaries and new findings in this field of ALS research, hereby we have created this electronic book which comprises of twenty seven chapters having various reviews, perspective and original research articles. All these chapters and articles in this book not only summarize the cutting-edge techniques, approaches, cell and animal models to study ALS but also provide unprecedented coverage of the current developments and new hypothesis emerging in ALS research. Some examples are novel genetic and cell culture based models, mitochondria-mediated therapy, oxidative stress and ROS mechanism, development of stem cells and mechanism-based therapies as well as novel biomarkers for designing and testing effective therapeutic strategies that can benefit ALS patients who are at the earlier stages in the disease. I am extremely grateful to all the contributors to this book and want to thank them for their phenomenal efforts. 517 $aRole of Mitochondria, Oxidative Stress and Altered Calcium Homeostasis in Amyotrophic Lateral Sclerosis 606 $aNeurosciences$2bicssc 610 $aAmyotrophic lateral sclerosis (ALS) 610 $aCa2+ signaling 610 $aexcitotoxicity 610 $aMitochondria 610 $aMotor neuron disease (MND) 610 $amultidrug therapy 610 $amultifactorial disease 610 $aneurodegenerative disease 610 $aRiluzole 610 $aSuperoxide dismutase 1 (SOD1) 615 7$aNeurosciences 700 $aManoj Kumar Jaiswal$4auth$01332395 906 $aBOOK 912 $a9910220056703321 996 $aThe Role of Mitochondria, Oxidative Stress and Altered Calcium Homeostasis in Amyotrophic Lateral Sclerosis: From Current Developments in the Laboratory to Clinical Treatments$93040936 997 $aUNINA