bluuebunny/crossref_metadata_2025_split huggingface dataset:
Metabolic Alterations and Shifts in Energy Allocations Are Corequisites for the Expression of Extended Longevity Genes in Drosophila
Authors: ARKING ROBERT , BUCK STEVEN , HWANGBO DAE‐SUNG , LANE MARK 
Published: July 2010

AbstractEvolutionary theories suggest that the expression of extended longevity depends on the organism's ability to shift energy from reproduction to somatic maintenance. New data led us to reexamine our older data and integrate the two into a larger picture of the genetic and metabolic alterations required if the animal is to live long. Our Ra normal‐lived control strain can express any one of three different extended longevity phenotypes, only one of which involves significant and proportional increases in both mean and maximum longevity and thus a delayed onset of senescence. This phenotype is dependent on the up‐regulation of the antioxidant defense system (ADS) genes and enzymes. Animals that express this phenotype typically have a pattern of altered specific activities in metabolically important enzymes, suggesting they are necessary to support the NAD+/NADP+ reducing system required for the continued high ADS enzyme activities. Fecundity data suggests that the energy required for this higher level of somatic maintenance initially came from a reduced egg production. This was only transient, however, for the females significantly increased their fecundity in later generations while still maintaining their longevity. The energy required for this enhanced fecundity was probably obtained from an increased metabolic efficiency, for the mitochondria of the La long‐lived strain are metabolically more efficient and have a lower leakage of reactive oxygen species (ROS) to the cytosol. Selection pressures that do not lead to these shifts in energy allocations result in extended longevity phenotypes characterized by increased early survival or increased late survival but not by a delayed onset of senescence.
Pharmacological Interventions in Aging and Age‐associated Disorders
Authors: KITANI KENICHI , MINAMI CHIYOKO , YAMAMOTO TAKAKO , KANAI SETSUKO , IVY GWEN O. , CARRILLO MARIA‐CRISTINA 
Published: July 2010

AbstractPast studies including our own have confirmed that chronic administration of deprenyl can prolong life spans of at least four different animal species. Pretreatment with the drug for several weeks increases activities of superoxide dismutase (SOD) and catalase (CAT) in selective brain regions. An up‐regulation of antioxidant enzyme activities can also be induced in organs such as the heart, kidney, spleen, and adrenal gland, and all are accompanied by an increase in mRNA levels for SODs in these organs. The effect of deprenyl on enzyme activities has a dose‐effect relationship of a typical inverted U shape. A similar inverted U shape also has emerged for the drug's effect on survival of animals. An apparent parallelism observed between these two effects of the drug seems to support our contention that the up‐regulation of antioxidant enzymes is at least partially responsible for the life‐prolonging effect on animals. Further, when a clinically applied dose of the drug for patients with Parkinson's disease was given to monkeys, SOD and CAT activities were increased in striatum of these monkeys, which suggests potential for the drug's applicability to humans. The drug was also found to increase concentrations of cytokines such as interleukin‐1β (IL‐1β) and tumor necrosis factor‐α (TNF‐α) in the above rat organs. Together with past reports demonstrating that deprenyl increases natural killer (NK) cell functions and interferon‐γ, and prevents the occurrence of malignant tumors in rodents and dogs, the mobilization of these humoral factors may therefore be included as possible mechanisms of action of deprenyl for its diverse antiaging and life‐prolonging effects. The potentials of propargylamines, (−)deprenyl in particular, for human use as antiaging drugs remain worthy of exploration in the future.
Oxidative Stress and Programmed Cell Death in Diabetic Neuropathy
Authors: VINCENT ANDREA M. , BROWNLEE MICHAEL , RUSSELL JAMES W. 
Published: July 2010

AbstractRecent evidence in both animal models and human sural nerve biopsies indicates an association with oxidative stress, mitochondrial (Mt) membrane depolarization (MMD), and induction of programmed cell death (PCD). In streptozotocin (STZ)‐treated diabetic rats, hyperglycemia induces typical apoptotic changes as well as swelling and disruption of the Mt cristae in diabetic dorsal root ganglion neurons (DRG) and Schwann cells (SC), but these changes are only rarely observed in control neurons. In human sural nerve biopsies, from patients with diabetic sensory neuropathy, there is transmission electromicrograph evidence of swelling and disruption of the Mt and cristae compared to patients without peripheral neuropathy. In human SH‐SY5Y neurons, rat sensory neurons, and SC, in vivo, there is an increase in reactive oxygen species (ROS) after exposure to 20 mM added glucose. In parallel, there is an initial Mt membrane hyperpolarization followed by depolarization (MMD). In turn, MMD is coupled with cleavage of caspases. Various strategies aimed at inhibiting the oxidative burst, or stabilizing the ΔΨM, block induction of PCD. First, growth factors such as NGF can block induction of ROS and/or stabilize the ΔΨM. This, in turn, is associated with inhibition of PCD. Second, reduction of ROS generation in neuronal Mt prevents neuronal PCD. Third, up‐regulation of uncoupling proteins (UCPs), which stabilize the ΔΨM, blocks induction of caspase cleavage. Collectively, these findings indicate that hyperglycemic conditions observed in diabetes mellitus are associated with oxidative stress‐induced neuronal and SC death, and targeted therapies aimed at regulating ROS may prove effective in therapy of diabetic neuropathy.
Oxidative Stress and Life Span Determination in the Nematode Caenorhabditis elegans
Authors: HONDA YOKO , HONDA SHUJI 
Published: July 2010

AbstractThe free radical theory of aging proposes that oxidative stress is one of the determinants of an organism's life span. In Caenorhabditis elegans, genetic or environmental changes have been shown to modulate life span. Here we discuss whether changes in the generation and destruction of free radicals are implicated in these life span modulations. Changes in culture oxygen concentrations that are considered to reflect free radical generation perturb the life span. The life spans under high and low oxygen concentrations were shorter and longer, respectively, than those under normoxic conditions. Short‐term exposure to high oxygen concentration lengthens the life span. This is considered to be the result of an increase in antioxidant defense induced by short‐term oxidative stress. Mutations in genes such as age‐1 and daf‐2 that compose the insulin‐like signaling network conferred oxidative stress resistance and an increase in Mn‐SOD gene expression as well as life span extension.
Mitochondrial Decay in the Aging Rat Heart
Authors: HAGEN TORY M. , MOREAU RÉGIS , SUH JUNG H. , VISIOLI FRANCESCO 
Published: July 2010

AbstractMitochondrial decay has been postulated to be a significant underlying part of the aging process. Decline in mitochondrial function may lead to cellular energy deficits, especially in times of greater energy demand, and compromise vital ATP‐dependent cellular operations, including detoxification, repair systems, DNA replication, and osmotic balance. Mitochondrial decay may also lead to enhanced oxidant production and thus render the cell more prone to oxidative insult. In particular, the heart may be especially susceptible to mitochondrial dysfunction due to myocardial dependency on β‐oxidation of fatty acids for energy and the postmitotic nature of cardiac myocytes, which would allow for greater accumulation of mitochondrial mutations and deletions. Thus, maintenance of mitochondrial function may be important to maintain overall myocardial function. Herein, we review the major age‐related changes that occur to mitochondria in the aging heart and the evidence that two such supplements, acetyl‐l‐carnitine (ALCAR) and (R)‐α‐lipoic acid, may improve myocardial bioenergetics and lower the increased oxidative stress associated with aging. We and others have shown that feeding old rats ALCAR reverses the age‐related decline in carnitine levels and improves mitochondrial β‐oxidation in a number of tissues studied. However, ALCAR supplementation does not appear to reverse the age‐related decline in cardiac antioxidant status and thus may not substantially alter indices of oxidative stress. Lipoic acid, a potent thiol antioxidant and mitochondrial metabolite, appears to increase low molecular weight antioxidant status and thereby decreases age‐associated oxidative insult. Thus, ALCAR along with lipoic acid may be effective supplemental regimens to maintain myocardial function.
The Competition Between Endogenous Dopamine and Radioligands for Specific Binding to Dopamine Receptors
Authors: CUMMING PAUL , WONG DEAN F. , DANNALS ROBERT F. , GILLINGS NIC , HILTON JOHN , SCHEFFEL URSULA , GJEDDE ALBERT 
Published: July 2010

Abstract:The ternary complex model of G‐protein‐linkage to receptors holds that agonists increase the affinity of the receptors for the G protein. Consequently, an agonist can exert the greatest inhibition of the binding of radioligands which are also agonists. We hypothesized that competition from endogenous dopamine in striatum of living mice should thus have a greater effect on the binding of the D2,3agonistN‐[3H]propylnorapomorphine ([3H]NPA), than on the binding of the D2,3antagonist [11C]raclopride in living brain. The binding potential (pB(0)), defined as the ratio of bound‐to‐unbound ligand after reserpine treatment, was measured in mouse striatum for [11C]raclopride,imageand for [3H]NPA.imageRelative to these baseline values after dopamine depletion, saline‐treatment decreased thepBof [3H]NPA by one‐half, while thepBof [11C]raclopride declined by only one‐third. Amphetamine decreased thepBof [3H]NPA to a greater extent than that of [11C]raclopride. The apparent inhibition constant of endogenous dopamine depended on the dopamine occupancy and declined to a value 1.66 times greater for [3H]NPA than for [11C]raclopride at its highest occupancies. Thus, the agonist binding was more sensitive than antagonist binding to competition from endogenous dopamine. Dopamine agonist ligands may be especially useful for PET studies of dopamine receptor occupancy by endogenous synaptic dopamine. Analysis of the effect of dopamine occupancy on the inhibition of agonist indicated a limited supply of G protein, with a maximum ternary complex fraction of 40% of maximum antagonist binding capacity.
Biochemical Changes during the Storage of High Hydrostatic Pressure Processed Avocado Paste
Authors: Jacobo‐Velázquez D.A. , Hernández‐Brenes C. 
Published: July 2010

Abstract:  High hydrostatic pressure (HHP) processing improves the shelf life of avocado paste without a significant impact on flavor; however, scarce information is available on biochemical modifications during its extended storage period. The present study focused on the changes in oxidative enzyme activities of pressurized avocado paste (600 MPa for 3 min) during refrigerated storage (45 d at 4 °C). Aerobic plate counts (APC), lactic acid bacteria counts (LAB), pH, and instrumental color were also evaluated during storage. Processing with HHP caused a decrease in polyphenol oxidase (PPO) and lipoxygenase (LOX) activities, resulting in residual enzyme levels of 50.72% and 55.16%, respectively. Although instrumental color values didn't change significantly during the evaluated storage period, both enzymes (PPO and LOX) recuperated their activities at 10 to 15 d of storage, reached the original values observed in the fresh paste, and then started a declining phase until the end of the storage period. Pulp pH presented a consistent decline during the first 20 d of storage. LAB counts were very low during storage, discarding lactic acid production as responsible for the observed pH decline. Enzyme reactivation, cell disruption, and a gradual migration of intracellular components such as organic acids are herein proposed as the main mechanisms for the deterioration of HHP treated avocado paste during its refrigerated storage.Practical Application:  At the present, HHP is the most effective commercial nonthermal technology to process avocado paste when compared to thermal and chemical alternatives. Although it has proven to be an excellent product‐technology match, little information is known on the biochemical changes that take place in the product during its refrigerated shelf life. Biochemical reactions during storage are important, since they can influence avocado paste nutritional and flavor qualities at the time of product consumption. The present study reports for the first time the re‐activation of PPO and LOX during storage of avocado paste under commercial and economically feasible processing conditions (600 MPa and 3 min). The reactivation of oxidative enzymes observed in the present study is relevant for future studies on the HHP stability of food systems in general, and it is considered an important finding for the food industry and researchers seeking to deliver products with superior nutritional and flavor characteristics.
Survival Analysis Applied to the Sensory Shelf‐Life Dating of High Hydrostatic Pressure Processed Avocado and Mango Pulps
Authors: Jacobo‐Velázquez D.A. , Ramos‐Parra P.A. , Hernández‐Brenes C. 
Published: July 2010

Abstract:  High hydrostatic pressure (HHP) pasteurized and refrigerated avocado and mango pulps contain lower microbial counts and thus are safer and acceptable for human consumption for a longer period of time, when compared to fresh unprocessed pulps. However, during their commercial shelf life, changes in their sensory characteristics take place and eventually produce the rejection of these products by consumers. Therefore, in the present study, the use of sensory evaluation was proposed for the shelf‐life determinations of HHP‐processed avocado and mango pulps. The study focused on evaluating the feasibility of applying survival analysis methodology to the data generated by consumers in order to determine the sensory shelf lives of both HHP‐treated pulps of avocado and mango. Survival analysis proved to be an effective methodology for the estimation of the sensory shelf life of avocado and mango pulps processed with HHP, with potential application for other pressurized products.Practical Application:  At present, HHP processing is one of the most effective alternatives for the commercial nonthermal pasteurization of fresh tropical fruits. HHP processing improves the microbial stability of the fruit pulps significantly; however, the products continue to deteriorate during their refrigerated storage mainly due to the action of residual detrimental enzymes. This article proposes the application of survival analysis methodology for the determination of the sensory shelf life of HHP‐treated avocado and mango pulps. Results demonstrated that the procedure appears to be simple and practical for the sensory shelf‐life determination of HHP‐treated foods when their main mode of failure is not caused by increases in microbiological counts that can affect human health.
Two Endogenous Substrates for Polyphenoloxidase in Pericarp Tissues of Postharvest Rambutan Fruit
Authors: Sun Jian , Su Weiqiang , Peng Hongxiang , Zhu Jianhua , Xu Liangxiong , Bruñá Nuria Martí 
Published: July 2010

Abstract:  The catalytic oxidation of phenolic substrates by polyphenoloxidase (PPO) causes pericarp browning of postharvest rambutan fruit. In the present study, PPO and its endogenous substrates were extracted from rambutan pericarp tissues (RPT). The substrate extracts were sequentially partitioned with ethyl acetate and n‐butanol. The analysis of total phenolic content showed that the most phenolic compounds were distributed in ethyl acetate fraction. By high‐performance liquid chromatography (HPLC), (−)‐epicatechin (EC) and proanthocyanidin A2 (PA2) were identified from this fraction. After reacting with rambutan PPO, EC turned brown rapidly within 10 min, indicating that it was a significant endogenous substrate. Although PA2 could also be oxidized by the PPO, it turned brown very slowly. In addition, because EC and PA2 were continually catalyzed into browning products by PPO during storage of the fruit at 4 and 25 °C, their contents in RPT gradually declined with the extended storage time. It was further observed that both substrate contents in rambutan fruit storing at 25 °C decreased more rapidly than that storing at 4 °C, suggesting that low temperature inhibited the catalytic oxidation of substrates so as to slow down pericarp browning.Practical Application:  Pericarp browning is a serious problem to storage and transport of harvested rambutan fruit. A generally accepted opinion on the browning mechanism is the oxidation of phenolic substrates by PPO. Ascertaining PPO substrates will effectively help us to control enzymatic reaction by chemical methods so as to delay or even prevent pericarp browning of harvested rambutan fruit.
High lenticular tolerance to ultraviolet radiation‐B by pigmented guinea‐pig; application of a safety limit strategy for UVR‐induced cataract
Authors: Mody Jr Vino C. , Kakar Manoj , Söderberg Per G. , Löfgren Stefan 
Published: July 2010

Abstract.Purpose:  The purpose of this study was to determine a threshold measure, maximum tolerable dose (MTD), for avoidance of UVR‐B‐induced cataract in the pigmented guinea‐pig.Methods:  Thirty pupil‐dilated anesthetized young female guinea‐pigs, divided into five equal groups, received between 0 and 84.9 kJ/m2 unilateral UVR‐B. Lens extraction and in vitro lens photography occurred 24 hr after exposure. Measurement of intensity of lens light scattering served as quantifying tool for the degree of cataract. Data analysis included regression, using a second order polynomial model. The applied MTD concept was based on the UVR‐B dose–response curve obtained for the pigmented guinea‐pig. A smaller number of pigmented guinea‐pigs, pigmented rats and albino rats underwent morphometric analysis of the anterior segment geometry.Results:  All eyes exposed to UVR‐B developed cataract in the anterior subcapsular region. MTD for avoidance of UVR‐B‐induced cataract was 69.0 kJ/m2 in the pigmented guinea‐pig. Iris was considerably thicker in the guinea‐pig than in the rats. Lens blockage by the dilated iris was lowest in the guinea‐pig.Conclusions:  Maximum tolerable dose for avoidance of UVR‐B‐induced cataract in the pigmented guinea‐pig was 69.0 kJ/m2, over 10‐fold higher than the threshold 5 kJ/m2 obtained by Pitts et al. in the pigmented rabbit. Maximum tolerable dose is an appropriate method for estimation of toxicity for UVR‐B‐induced cataract in the guinea‐pig. The pigmented guinea‐pig is significantly less sensitive to UVR‐B exposure than the pigmented rabbit and pigmented rat.
Selecting ribosomal protein genes for invertebrate phylogenetic inferences: how many genes to resolve the Mollusca?
Authors: Meyer Achim , Witek Alexander , Lieb Bernhard 
Published: July 2010

Summary1. Multi‐gene analyses are currently the gold standard in phylogenetics, despite limited taxon sampling. To facilitate broad taxon representation on an economically tolerable level, we optimize the gene selection for future PCR‐based sampling strategies.2. Highly expressed ribosomal proteins (RP) were sampled chiefly for molluscs, the second largest metazoan phylum with largely unknown internal relationships. Thirty‐two new sequences forLepidochitona cinerea(Polyplacophora) were integrated into a data‐matrix of 79 RP genes, comprising 16 mollusc species (five classes). The resulting maximum likelihood tree was used to evaluate each single‐gene tree according to its topological fit. Genes were sorted in ascending order, successively concatenated and then evaluated.3. The most efficient sub‐alignment consists of 18 selected genes. All analyses reveal the Mollusca as monophyletic. The phylogenetic utility of the selected and concatenated 18 ribosomal genes is comparable to results from phylogenomic analyses.4. This optimized data set can be assembled using PCR methods and will allow expanding the taxon coverage in deep molluscan phylogeny far beyond the current sampling.
Involvement of kappa opioid receptors in the formalin-induced inhibition of analgesic tolerance to morphine via suppression of conventional protein kinase C activation
Authors: Fujita-Hamabe Wakako , Nagae Ryuji , Nawa Ayaka , Harada Shinichi , Nakamoto Kazuo , Tokuyama Shogo 
Published: July 2010

AbstractObjectivesRepeated morphine treatment results in a decreased analgesic effect or the development of analgesic tolerance. However, we reported that some inflammatory chronic pain may inhibit morphine tolerance via kappa opioid receptor (KOR) activation. In this study, we further investigated the role of KOR in the inhibition of morphine tolerance in a chronic pain condition with a focus on the regulation of protein kinase C (PKC) activity.MethodsChronic pain was induced by formalin treatment into the dorsal part of the left hind paws of mice. The analgesic effect of morphine was measured by the tail flick method. We analysed the protein expression of PKC and its activity, and G-protein activity of mu opioid receptor (MOR) under repeated morphine treatment with or without formalin treatment.Key findingsWe found that conventional subtypes of PKC (cPKC) were up-regulated by repeated morphine treatment. Also, antisense oligonucleotide (AS-ODN) targeting cPKC completely suppressed the development of morphine tolerance. The disappearance of the repeated morphine-induced up-regulation of cPKC was completely reversed by treatment with AS-ODN targeting KOR. In addition, AS-ODN targeting KOR significantly reversed the chronic pain-induced down-regulation of PKC activity or up-regulation of MOR [35S]GTPγS binding activity after repeated morphine treatment.ConclusionsThese results indicate that KOR plays an important role in the inhibition of repeated morphine-induced cPKC up-regulation under chronic pain condition. Furthermore, this may result in the increase of MOR activity and in the inhibition of morphine tolerance under chronic pain condition.