bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hypoxic survival strategies in two fishes: extreme anoxia tolerance in the North European crucian carp and natural hypoxic preconditioning in a coral-reef shark
Authors: Nilsson Göran E. , Renshaw Gillian M. C. 
Published: August 2004

SUMMARYEspecially in aquatic habitats, hypoxia can be an important evolutionary driving force resulting in both convergent and divergent physiological strategies for hypoxic survival. Examining adaptations to anoxic/hypoxic survival in hypoxia-tolerant animals may offer fresh ideas for the treatment of hypoxia-related diseases. Here, we summarise our present knowledge of two fishes that have evolved to survive hypoxia under very different circumstances.The crucian carp (Carassius carassius) is of particular interest because of its extreme anoxia tolerance. During the long North European winter, it survives for months in completely oxygen-deprived freshwater habitats. The crucian carp also tolerates a few days of anoxia at room temperature and, unlike anoxia-tolerant freshwater turtles, it is still physically active in anoxia. Moreover, the crucian carp does not appear to reduce neuronal ion permeability during anoxia and may primarily rely on more subtle neuromodulatory mechanisms for anoxic metabolic depression.The epaulette shark (Hemiscyllium ocellatum) is a tropical marine vertebrate. It lives on shallow reef platforms that repeatedly become cut off from the ocean during periods of low tides. During nocturnal low tides, the water [O2] can fall by 80% due to respiration of the coral and associated organisms. Since the tides become lower and lower over a period of a few days, the hypoxic exposure during subsequent low tides will become progressively longer and more severe. Thus, this shark is under a natural hypoxic preconditioning regimen. Interestingly, hypoxic preconditioning lowers its metabolic rate and its critical PO2. Moreover, repeated anoxia appears to stimulate metabolic depression in an adenosine-dependent way.
Oxidants, antioxidants and the ischemic brain
Authors: Warner David S. , Sheng Huaxin , Batinić-Haberle Ines 
Published: August 2004

SUMMARYDespite numerous defenses, the brain is vulnerable to oxidative stress resulting from ischemia/reperfusion. Excitotoxic stimulation of superoxide and nitric oxide production leads to formation of highly reactive products,including peroxynitrite and hydroxyl radical, which are capable of damaging lipids, proteins and DNA. Use of transgenic mutants and selective pharmacological antioxidants has greatly increased understanding of the complex interplay between substrate deprivation and ischemic outcome. Recent evidence that reactive oxygen/nitrogen species play a critical role in initiation of apoptosis, mitochondrial permeability transition and poly(ADP-ribose) polymerase activation provides additional mechanisms for oxidative damage and new targets for post-ischemic therapeutic intervention. Because oxidative stress involves multiple post-ischemic cascades leading to cell death, effective prevention/treatment of ischemic brain injury is likely to require intervention at multiple effect sites.
Chaperones, protein aggregation, and brain protection from hypoxic/ischemic injury
Authors: Giffard Rona G. , Xu Lijun , Zhao Heng , Carrico Whitney , Ouyang Yibing , Qiao Yanli , Sapolsky Robert , Steinberg Gary , Hu Bingren , Yenari Midori A. 
Published: August 2004

SUMMARY
Chaperones, especially the stress inducible Hsp70, have been studied for their potential to protect the brain from ischemic injury. While they protect from both global and focal ischemia in vivo and cell culture models of ischemia/reperfusion injury in vitro, the mechanism of protection is not well understood. Protein aggregation is part of the etiology of chronic neurodegenerative diseases such as Huntington's and Alzheimer's, and recent data demonstrate protein aggregates in animal models of stroke. We now demonstrate that overexpression of Hsp70 in hippocampal CA1 neurons reduces evidence of protein aggregation under conditions where neuronal survival is increased. We have also demonstrated protection by the cochaperone Hdj-2 in vitro and demonstrated that this is associated with reduced protein aggregation identified by ubiquitin immunostaining. Hdj-2 can prevent protein aggregate formation by itself, but can only facilitate protein folding in conjunction with Hsp70. Pharmacological induction of Hsp70 was found to reduce both apoptotic and necrotic astrocyte death induced by glucose deprivation or oxygen glucose deprivation. Protection from ischemia and ischemia-like injury by chaperones thus involves at least anti-apoptotic,anti-necrotic and anti-protein aggregation mechanisms.
Negotiating brain anoxia survival in the turtle
Authors: Lutz Peter L. , Milton Sarah L. 
Published: August 2004

SUMMARYThe turtle brain's extraordinary ability to tolerate anoxia is based on constitutive and expressed factors. Constitutive factors that predispose for anoxia tolerance include enhanced levels of glycogen stores, increased densities of protective receptors, elevated antioxidant capacities and elevated heat shock protein. However, to survive an anoxic insult, three distinct phases must be negotiated successfully. (1) A coordinated downregulation of ATP demand processes to basal levels. This phase, which takes 1–2 h, includes a reduction in voltage-gated K+ (Kv)channel transcription and a substantial increase in Hsp72 and Hsc73 levels. During this period, adenosine and KATP channels mediate several key events including channel arrest initiation and a reduction in the release of excitatory amino acids (EAAs). (2) Long-term survival (days) at basal levels of ATP expenditure. Neuronal network integrity is preserved through the continued operation of core activities. These include periodic electrical activity, an increased release of GABA and a continued release of glutamate and dopamine. Adenosine and GABA modulate the glutamate release. There is a further increase in Hsc73, indicating a `housekeeping' role for this protein during this period. (3) A rapid upregulation of neuronal processes when oxygen becomes available to restore full function, together with the activation of protection mechanisms against reperfusion-generated reactive oxygen species.
Hypoxia–ischemia in the immature brain
Authors: Vannucci Susan J. , Hagberg Henrik 
Published: August 2004

SUMMARYThe immature brain has long been considered to be resistant to the damaging effects of hypoxia and hypoxia–ischemia (H/I). However, it is now appreciated that there are specific periods of increased vulnerability, which relate to the developmental stage at the time of the insult. Although much of our knowledge of the pathophysiology of cerebral H/I is based on extensive experimental studies in adult animal models, it is important to appreciate the major differences in the immature brain that impact on its response to, and recovery from, H/I. Normal maturation of the mammalian brain is characterized by periods of limitations in glucose transport capacity and increased use of alternative cerebral metabolic fuels such as lactate and ketone bodies, all of which are important during H/I and influence the development of energy failure. Cell death following H/I is mediated by glutamate excitotoxicity and oxidative stress, as well as other events that lead to delayed apoptotic death. The immature brain differs from the adult in its sensitivity to all of these processes. Finally, the ultimate outcome of H/I in the immature brain is determined by the impact on the ensuing cerebral maturation. A hypoxic–ischemic insult of insufficient severity to result in rapid cell death and infarction can lead to prolonged evolution of tissue damage.
Protective role of neuronal KATP channels in brain hypoxia
Authors: Ballanyi Klaus 
Published: August 2004

SUMMARYDuring severe arterial hypoxia leading to brain anoxia, most mammalian neurons undergo a massive depolarisation terminating in cell death. However,some neurons of the adult brain and most immature nervous structures tolerate extended periods of hypoxia–anoxia. An understanding of the mechanisms underlying this tolerance to oxygen depletion is pivotal for developing strategies to protect the brain from consequences of hypoxic-ischemic insults. ATP-sensitive K+ (KATP) channels are good subjects for this study as they are activated by processes associated with energy deprivation and can counteract the terminal anoxic-ischemic neuronal depolarisation. This review summarises in vitro analyses on the role of KATP channels in hypoxia–anoxia in three distinct neuronal systems of rodents. In dorsal vagal neurons, blockade of KATPchannels with sulfonylureas abolishes the hypoxic-anoxic hyperpolarisation. However, this does not affect the extreme tolerance of these neurons to oxygen depletion as evidenced by a moderate and sustained increase of intracellular Ca2+ (Cai). By contrast, a sulfonylurea-induced block of KATP channels shortens the delay of occurrence of a major Cai rise in cerebellar Purkinje neurons. In neurons of the neonatal medullary respiratory network, KATP channel blockers reverse the anoxic hyperpolarisation associated with slowing of respiratory frequency. This may constitute an adaptive mechanism for energy preservation. These studies demonstrate that KATP channels are an ubiquituous feature of mammalian neurons and may, indeed, play a protective role in brain hypoxia.
A unique pathway of cardiac myocyte death caused by hypoxia–acidosis
Authors: Graham Regina M. , Frazier Donna P. , Thompson John W. , Haliko Shannon , Li Huifang , Wasserlauf Bernard J. , Spiga Maria-Grazia , Bishopric Nanette H. , Webster Keith A. 
Published: August 2004

SUMMARY
Chronic hypoxia in the presence of high glucose leads to progressive acidosis of cardiac myocytes in culture. The condition parallels myocardial ischemia in vivo, where ischemic tissue becomes rapidly hypoxic and acidotic. Cardiac myocytes are resistant to chronic hypoxia at neutral pH but undergo extensive death when the extracellular pH (pH[o]) drops below 6.5. A microarray analysis of 20 000 genes (cDNAs and expressed sequence tags)screened with cDNAs from aerobic and hypoxic cardiac myocytes identified&gt;100 genes that were induced by &gt;2-fold and ∼20 genes that were induced by &gt;5-fold. One of the most strongly induced transcripts was identified as the gene encoding the pro-apoptotic Bcl-2 family member BNIP3. Northern and western blot analyses confirmed that BNIP3 was induced by 12-fold(mRNA) and 6-fold (protein) during 24 h of hypoxia. BNIP3 protein, but not the mRNA, accumulated 3.5-fold more rapidly under hypoxia–acidosis. Cell fractionation experiments indicated that BNIP3 was loosely bound to mitochondria under conditions of neutral hypoxia but was translocated into the membrane when the myocytes were acidotic. Translocation of BNIP3 coincided with opening of the mitochondrial permeability pore (MPTP). Paradoxically,mitochondrial pore opening did not promote caspase activation, and broad-range caspase inhibitors do not block this cell death pathway. The pathway was blocked by antisense BNIP3 oligonucleotides and MPTP inhibitors. Therefore,cardiac myocyte death during hypoxia–acidosis involves two distinct steps: (1) hypoxia activates transcription of the death-promoting BNIP3 gene through a hypoxia-inducible factor-1 (HIF-1) site in the promoter and (2) acidosis activates BNIP3 by promoting membrane translocation. This is an atypical programmed death pathway involving a combination of the features of apoptosis and necrosis. In this article, we will review the evidence for this unique pathway of cell death and discuss its relevance to ischemic heart disease. The article also contains new evidence that chronic hypoxia at neutral pH does not promote apoptosis or activate caspases in neonatal cardiac myocytes.
Role of trehalose phosphate synthase and trehalose during hypoxia: from flies to mammals
Authors: Chen Qiaofang , Haddad Gabriel G. 
Published: August 2004

SUMMARY
Trehalose is a nonreducing disaccharide in which the two glucose units are linked in an α,α-1,1-glycosidic linkage. The best known and most widely distributed pathway of trehalose synthesis involves the transfer of glucose from UDP-glucose to glucose 6-phosphate to form trehalose-6-phosphate and UDP via the trehalose-6-phosphate synthase (TPS1). Trehalose-6-phosphate phosphatase (TPS2) then converts trehalose-6-phosphate to free trehalose. This sugar is present in a wide variety of organisms,including bacteria, yeast, fungi, insects, invertebrates and plants, and because of its particular physical features, trehalose is able to protect the integrity of cells against a variety of environmental stresses such as desiccation, dehydration, heat, cold and oxidation. Our current studies described here indicate that trehalose protects Drosophila and mammalian cells from hypoxic and anoxic injury. The mechanism of this protection is probably related to a decrease in protein denaturation through protein–trehalose interactions.
Synthesis and Structures of Highly Conducting Charge-Transfer Salts of Selenium Containing TTM-TTP Derivatives
Authors: Ashizawa Minoru , Akutsu Akane , Noda Bunpei , Nii Hirofumi , Kawamoto Tadashi , Mori Takehiko , Nakayashiki Takashi , Misaki Yohji , Tanaka Kazuyoshi , Takimiya Kazuo , Otsubo Tetsuo 
Published: August 2004

Abstract
Selenium-substituted TTM-TTP (2,5-bis[4,5-bis(methylthio)-1,3-dithiol-2-ylidene]-1,3,4,6-tetrathiapentalene) derivatives (1a–1d), in which several 1,3-dithiole rings of the bis-fused TTF framework are replaced by 1,3-diselenole rings, have been prepared. In particular, we have accomplished the first selenium substitution of the inner TTP part (1a). The 1:1 composition iodine salt, (1a)I3, is an insulator constructed of the donor trimers. The 1:1 GaCl4 salt, (1a)GaCl4, has a uniform column isostructural to the sulfur analog, (TTM-TTP)FeBr1.8Cl2.2; it exhibits metallic conduction down to about 60 K, the lowest metal–insulator (M–I) transition temperature in 1:1 salts. The donors 1c and 1d give the iodine salts isostructural to the sulfur analog, (TTM-TTP)(I3)5/3. By the selenium substitution, the M–I transition of (1d)(I3)5/3 is entirely suppressed.
Effects of Cyclodextrins on the Fluorescence of 2-Methylnaphth[2,3-d]oxazole in Aqueous Solution
Authors: Hamai Sanyo 
Published: August 2004

Abstract
In organic solvents, 2-methylnaphth[2,3-d]oxazole (MNO) exhibits a single emission, whereas it exhibits dual emissions (the 350-nm band fluorescence and the longer-wavelength fluorescence) in water (pH 6.1). In acidic aqueous solution, the 350-nm band fluorescence alone is observed with a disappearance of the longer-wavelength fluorescence. In pH 6.1 buffers, α-CD has been found to form a 2:1 inclusion complex with MNO. Upon the addition of α-CD to MNO solution, the longer-wavelength fluorescence is significantly reduced in intensity, relative to the 350-nm band fluorescence. The incorporation of an MNO molecule into the α-CD cavities obstructs the generation of the excited state responsible for the longer-wavelength fluorescence. The longer-wavelength fluorescence is most likely due to the intramolecular charge transfer (ICT) state of MNO, which is induced by water molecules of high polarity. MNO forms a 1:1 inclusion complex with β-CD. In the presence of β-CD, the intensity ratio of the longer-wavelength fluorescence to the 350-nm band fluorescence is decreased. When 1-propanol is added to MNO solution containing β-CD, a ternary inclusion complex is formed among β-CD, MNO, and 1-propanol. In β-CD solution containing 1-propanol, the intensity ratio of the longer-wavelength fluorescence to the 350-nm band fluorescence is slightly reduced. These findings support the conclusion that the longer-wavelength fluorescence of MNO is due to the ICT state, whose generation is promoted by the water environment.
Ternary Complexes from Cu(II)–Oligopeptide and N-Acetyl-l-histidine, as Studied by Circular Dichroism Spectroscopy
Authors: Hanaki Akira , Ueda Jun-ichi , Ikota Nobuo 
Published: August 2004

Abstract
The Cu(II) complexes of oligopeptides, Cu(H−iL); i = 1, 2, or 3, reacted with N-acetyl-l-histidine (AHis) to form ternary complexes, Cu(H−jL)(AHis); j = 1 or 2. The Cu(H−1L) species formed Cu(H−1L)(AHis), which was either dimerized to [Cu(H−1L)]2(AHis−) or converted stepwise to Cu(AHis)n; n = 3, 4. The reaction of the Cu(H−2L) or Cu(H−3L) species with AHis led to the formation of Cu(H−2L)(AHis), and the formation constants of the ternary complexes were small, on the magnitude of 10−1–101 M−1.
19F NMR Study on the Heme Electronic Structure in Oxy and Carbonmonoxy Reconstituted Myoglobins
Authors: Hirai Yueki , Nagao Satoshi , Mita Hajime , Suzuki Akihiro , Yamamoto Yasuhiko 
Published: August 2004

Abstract
A 19F NMR study on myoglobin reconstituted with a ring-fluorinated C2 symmetric heme, 13,17-bis(2-carboxylatoethyl)-2,8,12,18-tetramethyl-3,7-difluoroporphyrinatoiron(II), demonstrated that the porphyrin π system is affected by the bent orientation of the Fe–O–O unit relative to the heme in oxy myoglobin and Fe dπ → CO π* back-donation in carbonmonoxy myoglobin.
The Synthesis of Difluoro and Dimethyl Derivatives of 2,6-Bis(dicyanomethylene)-2,6-dihydro-4H-cyclopenta[2,1-b:3,4-b′]dithiophen-4-one (CPDT-TCNQ) and the Conducting Properties of the Metallic Salts Based on the Dimethyl Derivative
Authors: Chonan Takehiro , Takahashi Kazuko 
Published: August 2004

Abstract
In order to investigate how the sheet-like network along the side-by-side direction constructed by the strong inter-column S···N and O···H atom–atom contacts influences the stability of the metallic state of novel one-dimensional metallic anion radical salts of 2,6-bis(dicyanomethylene)-2,6-dihydro-4H-cyclopenta[2,1-b:3,4-b′]dithiophen-4-one (CPDT-TCNQ), the 3,5-difluoro (F2CPDT-TCNQ) and 3,5-dimethyl (Me2CPDT-TCNQ) derivatives of CPDT-TCNQ, not possessing hydrogen atoms at the 3,5-positions to construct the inter-column O···H contacts, have been synthesized. The anion radical salts, Me4X(Me2CPDT-TCNQ)2 (X = P and As), showed a metallic temperature dependence of the resistivity from room temperature down to around 240 K and 200 K, respectively, whereas Me4X(Me2CPDT-TCNQ)2 (X = N and Sb) were semiconducting. The metal–insulator transition temperatures (TMI) of Me4X(Me2CPDT-TCNQ)2 (X = P and As) are significantly higher than those of MX4(CPDT-TCNQ)2 (X = P and As). Moreover, the extent of destabilization of the metallic state is much more significant in Me4N(Me2CPDT-TCNQ)2, since MeN4(CPDT-TCNQ)2 is metallic down to 130 K. Although electric conduction can not occur along the side-by-side direction in either salt of CPDT-TCNQ and Me2CPDT-TCNQ, these facts suggest that the two-dimensional sheet-like molecular network along the a-axis may contribute to stabilize the one-dimensional metallic states of the anion radical salts of CPDT-TCNQ.
Origin of the Endo/Exo Stereoselectivity and Syn/Anti Face-Selectivity in Diels–Alder Reactions, Determined by Transition State Energy Partitioning
Authors: Kiri Shingo , Odo Yuka , Omar Huda Izzat , Shimo Tetsuro , Somekawa Kenichi 
Published: August 2004

Abstract
The origins of stereo- and face-selective Diels–Alder reactions of 5-substituted 1,3-cyclopentadienes (CP) with some dienophiles were elucidated by means of semiempirical PM5, DFT(B3LYP), and ab initio RHF methods. The activation energies by the improved PM5 and B3LYP/6-31+G(d) methods were in good agreement with the experimental results. We partitioned the activation energy (ΔEact) into diene deformation (ΔEdf-dien) and dienophile deformation (ΔEdf-dphil), and the diene–dienophile interaction (Eint) energies, in addition to the new intrinsic reaction coordinate (IRC) energy (ΔEirc) partitioning. Such analysis revealed the major factors in the determining endo/exo and syn/anti selectivities of the reactions of 5-substituted CP. The syn-selectivity of the 5-F-CP is explained by the lower ΔEact (2–3 kcal/mol) caused by relatively smaller ΔEdf-dien, which leads to slighter repulsion between the reactants. This low activation energy is inferred to be caused by the better second orbital interaction or intramolecular orbital interactions between the diene π and fluoro-substituent n orbital moieties, as well as by better intermolecular π–π orbital interactions between the diene-π and dienenophile-π moieties. On the other hand, the anti-selectivity of the methyl substituted CP mainly appears from bigger Edf-dien in the syn-isomer. A novel economical method of IRC energy partitioning to the reactants, TS intermediates and products is also introduced in order to verify the energy balance of other calculation methods and other reactions.
A Novel Short-Step Synthesis of Functionalized 4-Hydroxy-2-quinolones Using a 1-Hydroxybenzotriazole Methodology
Authors: Zikou Lamprini , Athanasellis Giorgos , Detsi Anastasia , Zografos Alexandros , Mitsos Christos , Igglessi-Markopoulou Olga 
Published: August 2004

Abstract
A novel method for the synthesis of 3-substituted 4-hydroxy-1-methyl- and 1-phenyl-2-quinolones is presented. The compounds are produced in a one-step reaction in very good yields (51–76%). The major advantage of the methodology is the short time for the synthesis in contrast to previous methodologies requiring several steps and harsh conditions for the synthesis of quinolone derivatives.
The Photoinduced Hydrogen Atom Transfer and trans–cis Isomerization of the C=C Double Bond in 1-(1-Hydroxy-2-naphthyl)-3-(1-naphthyl)-2-propen-1-one and Related Compounds Studied Using Nanosecond Time-Resolved Infrared Spectroscopy
Authors: Kaneda Kaoru , Sato Shin , Hamaguchi Hiro-o , Arai Tatsuo 
Published: August 2004

Abstract
The mechanism and intermediates of photoinduced hydrogen atom transfer and photoisomerization in 1-(1-hydroxy-2-naphthyl)-3-(1-naphthyl)-2-propen-1-one (1) and 1-(1-methoxy-2-naphthyl)-3-(1-naphthyl)-2-propen-1-one (2) have been investigated using nanosecond time-resolved infrared spectroscopy. For compound 1, a bleach signal was observed at 1575 cm−1 just after the laser excitation and recovered within 2 ms. The transient absorption at 1500 cm−1 decayed with two components of 1 μs and 2 ms, which are due to the triplet state and the ground state tautomer, respectively. On the basis of these results, the potential energy surface of hydrogen atom transfer in compound 1 was deciphered. Upon laser excitation of compound 2, the transient absorption signals at 1528 cm−1 and 1392 cm−1 assigned to the triplet state were observed in addition to the bleach signals at 1664 cm−1 and 1600 cm−1. The bleach signal at 1600 cm−1 remained as a permanent bleaching after the fast recovery with the 1.2 μs time constant. This result indicates that compound 2 underwent trans-to-cis isomerization upon laser excitation. By utilizing the data obtained in stationary and transient IR spectroscopy, we have directly determined the quantum yield of trans-to-cis isomerization to be 0.23 ± 0.01 from the difference in the IR signals.