bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Molecular Mechanism of Endoplasmic Reticulum Stress-Induced Apoptosis in PC-12 Neuronal Cells: The Protective Effect of Insulin-Like Growth Factor I
Authors: Zou Cheng-Gang , Cao Xiu-Zhen , Zhao Yue-Shui , Gao Shun-Yu , Li Shu-De , Liu Xian-Yong , Zhang Yan , Zhang Ke-Qin 
Published: September 2008

Endoplasmic reticulum (ER) stress has been implicated in several neurodegenerative diseases. Although CCAAT/enhancer-binding protein homologous protein (CHOP) has been shown to play a critical role in ER stress, the precise apoptosis cascade downstream of CHOP is unknown. In this report, we investigated the mechanism of ER stress-mediated apoptosis as well as the action of IGF-I in PC-12 neuronal cells. Our results demonstrated that tribbles-related protein 3 (TRB3), which is a target gene of CHOP, was responsible for tunicamycin (an ER stress inducer)-induced apoptosis. TRB3 could promote dephosphorylation of Akt in PC-12 cells. IGF-I inhibited ER stress-induced apoptosis by restoring the phosphorylation level of Akt. Both wortmannin (a phosphatidylinositide 3-kinase inhibitor) and SB 212090 (a p38 MAPK inhibitor) suppressed the protective effect of IGF-I on ER stress-induced apoptosis. Interestingly, IGF-I attenuated ER stress-mediated expression of TRB3 but not CHOP. This action of IGF-I was abolished by SB 212090 but not by wortmannin. Immunoprecipitation analysis revealed that IGF-I promoted the phosphorylation of CHOP by activating p38 MAPK, probably leading to a decrease in the transcriptional activity of CHOP. The dephosphorylation of Akt resulted in increased expression of a proapoptotic protein, p53 up-regulated modulator of apoptosis (PUMA), in a forkhead box O3a-dependent manner. Knockdown of PUMA by short hairpin RNA attenuated ER stress-mediated apoptosis. Thus, our current study indicates that both TRB3 and PUMA are critical molecules in ER stress-induced apoptosis. IGF-I effectively protects PC-12 neuronal cells against ER stress-induced apoptosis through the phosphatidylinositide 3-kinase/Akt and p38 MAPK pathways.
Endoplasmic reticulum (ER) stress causes neuronal apoptosis by inducing the expression of tribbles-related protein 3 and PUMA. IGF-1 prevents neuronal apoptosis against ER stress through phosphatidylinositide 3-kinase/Akt and p38 mitogen-activated protein kinase pathways.
High-Fat Diet Delays and Fasting Advances the Circadian Expression of Adiponectin Signaling Components in Mouse Liver
Authors: Barnea Maayan , Madar Zecharia , Froy Oren 
Published: September 2008

The circadian clock controls energy homeostasis by regulating circadian expression and/or activity of enzymes involved in metabolism. Disruption of circadian rhythms may lead to obesity and metabolic disorders. We tested whether the biological clock controls adiponectin signaling pathway in the liver and whether fasting and/or high-fat (HF) diet affects this control. Mice were fed low-fat or HF diet and fasted on the last day. The circadian expression of clock genes and components of adiponectin metabolic pathway in the liver was tested at the RNA, protein, or enzyme activity level. In addition, serum levels of glucose, adiponectin, and insulin were measured. Under low-fat diet, adiponectin signaling pathway components exhibited circadian rhythmicity. However, fasting and HF diet altered this circadian expression; fasting resulted in a phase advance, and HF diet caused a phase delay. In addition, adenosine monophosphate-activated protein kinase levels were high during fasting and low during HF diet. Changes in the phase and daily rhythm of clock genes and components of adiponectin signaling pathway as a result of HF diet may lead to obesity and may explain the disruption of other clock-controlled output systems, such as blood pressure and sleep/wake cycle, usually associated with metabolic disorders.Adiponectin signaling pathway components exhibit circadian rhythmicity under low-fat diet. Fasting and high-fat diet alter this circadian expression, leading to phase advance and delay, respectively.
Rhomboid-7 and HtrA2/Omi act in a common pathway with the Parkinson’s disease factors Pink1 and Parkin
Authors: Whitworth Alexander J. , Lee Jeffrey R. , Ho Venus M.-W. , Flick Robert , Chowdhury Ruhena , McQuibban G. Angus 
Published: September 2008

SUMMARYParkinson’s disease (PD) is a common neurodegenerative disorder caused by loss of midbrain dopaminergic neurons, the pathogenetic mechanisms of which remain unclear. Mitochondrial dysfunction, which has long been implicated in sporadic PD, has recently been highlighted as a key pathological cause, particularly with the identification of mutations in the PTEN-induced putative kinase (pink1), parkin and htrA2 (also known as omi) genes that are linked to PD. Studies in Drosophila melanogaster have shown that pink1 and parkin act in a common genetic pathway that maintains mitochondrial integrity, but other upstream or downstream components of this pathway are currently unknown. Using ectopic expression in the Drosophila eye as an assay, we have investigated the involvement of the mitochondrial protease encoded by omi in the Pink1/Parkin pathway and found that it acts genetically downstream of pink1 but functions independently of Parkin. Using the same approach, we also found that Rhomboid-7, a mitochondrial protease not previously implicated in PD, acts as an upstream component of this pathway, and showed that it is required to cleave the precursor forms of both Pink1 and Omi. These data further elucidate the composition of the Pink1 pathway and suggest that regulated intramembrane proteolysis is involved in its regulation.
Planarian PTEN homologs regulate stem cells and regeneration through TOR signaling
Authors: Oviedo Néstor J. , Pearson Bret J. , Levin Michael , Sánchez Alvarado Alejandro 
Published: September 2008

SUMMARY
We have identified two genes, Smed-PTEN-1 and Smed-PTEN-2, capable of regulating stem cell function in the planarian Schmidtea mediterranea. Both genes encode proteins homologous to the mammalian tumor suppressor, phosphatase and tensin homolog deleted on chromosome 10 (PTEN). Inactivation of Smed-PTEN-1 and -2 by RNA interference (RNAi) in planarians disrupts regeneration, and leads to abnormal outgrowths in both cut and uncut animals followed soon after by death (lysis). The resulting phenotype is characterized by hyperproliferation of neoblasts (planarian stem cells), tissue disorganization and a significant accumulation of postmitotic cells with impaired differentiation capacity. Further analyses revealed that rapamycin selectively prevented such accumulation without affecting the normal neoblast proliferation associated with physiological turnover and regeneration. In animals in which PTEN function is abrogated, we also detected a significant increase in the number of cells expressing the planarian Akt gene homolog (Smed-Akt). However, functional abrogation of Smed-Akt in Smed-PTEN RNAi-treated animals does not prevent cell overproliferation and lethality, indicating that functional abrogation of Smed-PTEN is sufficient to induce abnormal outgrowths. Altogether, our data reveal roles for PTEN in the regulation of planarian stem cells that are strikingly conserved to mammalian models. In addition, our results implicate this protein in the control of stem cell maintenance during the regeneration of complex structures in planarians.
Visualizing stromal cell dynamics in different tumor microenvironments by spinning disk confocal microscopy
Authors: Egeblad Mikala , Ewald Andrew J. , Askautrud Hanne A. , Truitt Morgan L. , Welm Bryan E. , Bainbridge Emma , Peeters George , Krummel Matthew F. , Werb Zena 
Published: September 2008

SUMMARYThe tumor microenvironment consists of stromal cells and extracellular factors that evolve in parallel with carcinoma cells. To gain insights into the activities of stromal cell populations, we developed and applied multicolor imaging techniques to analyze the behavior of these cells within different tumor microenvironments in the same live mouse. We found that regulatory T-lymphocytes (Tregs) migrated in proximity to blood vessels. Dendritic-like cells, myeloid cells and carcinoma-associated fibroblasts all exhibited higher motility in the microenvironment at the tumor periphery than within the tumor mass. Since oxygen levels differ between tumor microenvironments, we tested if acute hypoxia could account for the differences in cell migration. Direct visualization revealed that Tregs ceased migration under acute systemic hypoxia, whereas myeloid cells continued migrating. In the same mouse and microenvironment, we experimentally subdivided the myeloid cell population and revealed that uptake of fluorescent dextran defined a low-motility subpopulation expressing markers of tumor-promoting, alternatively activated macrophages. In contrast, fluorescent anti-Gr1 antibodies marked myeloid cells patrolling inside tumor vessels and in the stroma. Our techniques allow real-time combinatorial analysis of cell populations based on spatial location, gene expression, behavior and cell surface molecules within intact tumors. The techniques are not limited to investigations in cancer, but could give new insights into cell behavior more broadly in development and disease.
Cellular mechanisms of Cnidarian bleaching: stress causes the collapse of symbiosis
Authors: Weis Virginia M. 
Published: September 2008

SUMMARYCnidarian bleaching is a breakdown in the mutualistic symbiosis between host Cnidarians, such as reef building corals, and their unicellular photosynthetic dinoflagellate symbionts. Bleaching is caused by a variety of environmental stressors, most notably elevated temperatures associated with global climate change in conjunction with high solar radiation, and it is a major contributor to coral death and reef degradation. This review examines the underlying cellular events that lead to symbiosis dysfunction and cause bleaching, emphasizing that, to date, we have only some pieces of a complex cellular jigsaw puzzle. Reactive oxygen species (ROS), generated by damage to both photosynthetic and mitochondrial membranes, is shown to play a central role in both injury to the partners and to inter-partner communication of a stress response. Evidence is presented that suggests that bleaching is a host innate immune response to a compromised symbiont, much like innate immune responses in other host–microbe interactions. Finally, the elimination or exit of the symbiont from host tissues is described through a variety of mechanisms including exocytosis, host cell detachment and host cell apoptosis.
A glucagon-like endocrine pathway inDrosophilamodulates both lipid and carbohydrate homeostasis
Authors: Bharucha K. N. , Tarr P. , Zipursky S. L. 
Published: September 2008

SUMMARYThe regulation of energy homeostasis is fundamental to all organisms. The Drosophila fat body serves as a repository for both triglycerides and glycogen, combining the energy storage functions of mammalian adipose and hepatic tissues, respectively. Here we show that mutation of the Drosophila adipokinetic hormone receptor (AKHR), a functional analog of the mammalian glucagon receptor, leads to abnormal accumulation of both lipid and carbohydrate. As a consequence of their obese phenotypes, AKHR mutants are markedly starvation resistant. We show that AKHR is expressed in the fat body, and, intriguingly, in a subset of gustatory neurons that mediate sweet taste. Genetic rescue experiments establish that the metabolic phenotypes arise exclusively from the fat body AKHR expression. Behavioral experiments demonstrate that AKHR mutants are neither sedentary nor hyperphagic, suggesting the metabolic abnormalities derive from a genetic propensity to retain energy stores. Taken together, our results indicate that a single endocrine pathway contributes to both lipid and carbohydrate catabolism in the Drosophila fat body.
Suction generation in white-spotted bamboo sharksChiloscyllium plagiosum
Authors: Wilga Cheryl D. , Sanford Christopher P. 
Published: September 2008

SUMMARYAfter the divergence of chondrichthyans and teleostomes, the structure of the feeding apparatus also diverged leading to alterations in the suction mechanism. In this study we investigated the mechanism for suction generation during feeding in white-spotted bamboo sharks, Chiloscyllium plagiosum and compared it with that in teleosts. The internal movement of cranial elements and pressure in the buccal, hyoid and pharyngeal cavities that are directly responsible for suction generation was quantified using sonomicrometry and pressure transducers. Backward stepwise multiple linear regressions were used to explore the relationship between expansion and pressure, accounting for 60–96% of the variation in pressure among capture events. The progression of anterior to posterior expansion in the buccal, hyoid and pharyngeal cavities is accompanied by the sequential onset of subambient pressure in these cavities as prey is drawn into the mouth. Gape opening triggers the onset of subambient pressure in the oropharyngeal cavities. Peak gape area coincides with peak subambient buccal pressure. Increased velocity of hyoid area expansion is primarily responsible for generating peak subambient pressure in the buccal and hyoid regions. Pharyngeal expansion appears to function as a sink to receive water influx from the mouth, much like that of compensatory suction in bidirectional aquatic feeders. Interestingly, C. plagiosum generates large suction pressures while paradoxically compressing the buccal cavity laterally,delaying the time to peak pressure. This represents a fundamental difference from the mechanism used to generate suction in teleost fishes. Interestingly,pressure in the three cavities peaks in the posterior to anterior direction. The complex shape changes that the buccal cavity undergoes indicate that, as in teleosts, unsteady flow predominates during suction feeding. Several kinematic variables function together, with great variation over long gape cycles to generate the low subambient pressures used by C. plagiosumto capture prey.
Effects of hypothermia on gene expression in zebrafish gills:upregulation in differentiation and function of ionocytes as compensatory responses
Authors: Chou Ming-Yi , Hsiao Chung-Der , Chen Shyh-Chi , Chen I-Wen , Liu Sian-Tai , Hwang Pung-Pung 
Published: September 2008

SUMMARY
Ectothermic vertebrates are different from mammals that are sensitive to hypothermia and have to maintain core temperature for survival. Why and how ectothermic animals survive, grow and reproduce in low temperature have been for a long time a scientifically challenging and important inquiry to biologists. We used a microarray to profile the gill transcriptome in zebrafish (Danio rerio) after exposure to low temperature. Adult zebrafish were acclimated to a low temperature of 12°C for 1 day and up to 30 days, and the gill transcriptome was compared with that of control fish in 28°C by oligonucleotide microarray hybridization. Results showed 11 and 22 transcripts were found to be upregulated, whereas 56 and 70 transcripts were downregulated by low-temperature treatment for 1 day and 30 days,respectively. The gill transcriptome profiles revealed that ionoregulation-related genes were highly upregulated in cold-acclimated zebrafish. This paved the way to investigate the role of ionoregulatory genes in zebrafish gills during cold acclimation. Cold acclimation caused upregulation of genes that are essential for ionocyte specification,differentiation, ionoregulation, acid–base balance and the number of cells expressing these genes increased. For instance, epithelial Ca2+ channel (EcaC; an ionoregulatory protein) mRNA increased in parallel with the level of Ca2+ influx, revealing a functional compensation after long-term acclimation to cold. Phosphohistone H3 and TUNEL staining showed that the cell turnover rate was retarded in cold-acclimated gills. Altogether, these results suggest that gills may sustain their functions by producing mature ionocytes from pre-existing undifferentiated progenitors in low-temperature environments.
Systematic differences in membrane acyl composition associated with varying body mass in mammals occur in all phospholipid classes: an analysis of kidney and brain
Authors: Nealon Jessica R. , Blanksby Stephen J. , Mitchell Todd W. , Else Paul L. 
Published: September 2008

SUMMARYThe acyl composition of membrane phospholipids in kidney and brain of mammals of different body mass was examined. It was hypothesized that reduction in unsaturation index (number of double bonds per 100 acyl chains)of membrane phospholipids with increasing body mass in mammals would be made-up of similar changes in acyl composition across all phospholipid classes and that phospholipid class distribution would be regulated and similar in the same tissues of the different-sized mammals. The results of this study supported both hypotheses. Differences in membrane phospholipid acyl composition (i.e. decreased omega-3 fats, increased monounsaturated fats and decreased unsaturation index with increasing body size) were not restricted to any specific phospholipid molecule or to any specific phospholipid class but were observed in all phospholipid classes. With increase in body mass of mammals both monounsaturates and use of less unsaturated polyunsaturates increases at the expense of the long-chain highly unsaturated omega-3 and omega-6 polyunsaturates, producing decreases in membrane unsaturation. The distribution of membrane phospholipid classes was essentially the same in the different-sized mammals with phosphatidylcholine (PC) and phosphatidylethanolamine (PE) together constituting ∼91% and ∼88% of all phospholipids in kidney and brain, respectively. The lack of sphingomyelin in the mouse tissues and higher levels in larger mammals suggests an increased presence of membrane lipid rafts in larger mammals. The results of this study support the proposal that the physical properties of membranes are likely to be involved in changing metabolic rate.
Investigating onychophoran gas exchange and water balance as a means to inform current controversies in arthropod physiology
Authors: Clusella-Trullas Susana , Chown Steven L. 
Published: September 2008

SUMMARY
Several controversies currently dominate the fields of arthropod metabolic rate, gas exchange and water balance, including the extent to which modulation of gas exchange reduces water loss, the origins of discontinuous gas exchange,the relationship between metabolic rate and life-history strategies, and the causes of Palaeozoic gigantism. In all of these areas, repeated calls have been made for the investigation of groups that might most inform the debates,especially of taxa in key phylogenetic positions. Here we respond to this call by investigating metabolic rate, respiratory water loss and critical oxygen partial pressure (Pc) in the onychophoran Peripatopsis capensis, a member of a group basal to the arthropods, and by synthesizing the available data on the Onychophora. The rate of carbon dioxide release (V̇CO2) at 20°C in P. capensis is 0.043 ml CO2 h–1, in keeping with other onychophoran species; suggesting that low metabolic rates in some arthropod groups are derived. Continuous gas exchange suggests that more complex gas exchange patterns are also derived. Total water loss in P. capensis is 57 mg H2O h–1 at 20°C,similar to modern estimates for another onychophoran species. High relative respiratory water loss rates (∼34%; estimated using a regression technique) suggest that the basal condition in arthropods may be a high respiratory water loss rate. Relatively high Pc values(5–10% O2) suggest that substantial safety margins in insects are also a derived condition. Curling behaviour in P. capensisappears to be a strategy to lower energetic costs when resting, and the concomitant depression of water loss is a proximate consequence of this behaviour.
The use of autologous femoral vein for the repair of the common iliac vein after resection of a pheochromocytoma
Authors: Simms M , Mehat M S , Buckels J A C 
Published: September 2008

Aim To illustrate the use of autologous femoral vein for grafting ilio-caval vein defects following abdomino-pelvic tumour resections. Methods Case report and literature review. Results Durable restoration of ilio-caval patency was achieved, with minimal morbidity from graft harvesting. Conclusions Autologous femoral vein presents a viable graft option for the immediate reconstruction of large intra-abdominal vein deficits.
Using a Speech-Generating Device to Enhance Communicative Abilities for an Adult With Moderate Intellectual Disability
Authors: Cheslock Melissa A. , Barton-Hulsey Andrea , Romski MaryAnn , Sevcik Rose A. 
Published: September 2008

Abstract
For adults with disabilities who are unable to speak, the literature recommends that intervention include augmentative and alternative communication (AAC) to improve communication and interactions with others. Some adults with moderate intellectual disabilities who exhibit limited functional speech are often overlooked as candidates for AAC interventions because they have some speech abilities. The perception is that they are too old to improve their language and communication skills. This article presents a case report of a 30-year-old woman with a moderate intellectual disability and a severe expressive language disorder who uses a speech-generating device as a compensatory strategy to facilitate her communicative abilities, independence, and self-determination.
Increased Plasma Concentrations of Cytoskeletal and Ca2+-Binding Proteins and Their Peptides in Psoriasis Patients
Authors: Plavina Tatiana , Hincapie Marina , Wakshull Eric , Subramanyam Meena , Hancock William S 
Published: September 2008

AbstractBackground: The mechanisms underlying psoriatic pathogenesis are not fully understood and might be elucidated by identifying novel disease-related molecular markers, including autoantigens.Methods: We used 2 proteomic methods to analyze plasma samples from 20 psoriasis patients and 20 matched healthy donors. The first method focused on evaluating changes in glycoprotein concentrations and the plasma proteome, and the second method assessed endogenous proteolytic activity by analyzing the low molecular weight component of plasma.Results: The integrated proteomic and peptidomic analysis identified a number of proteins and their fragments present at different concentrations in the plasma of psoriasis patients and healthy donors. We used ELISA to independently verify the changes in the concentrations of several of these proteins. One intriguing finding, increased concentrations of cytoskeletal and actin-binding proteins and their peptides in psoriatic plasma, suggested disease-related cell leakage of these proteins and their increased proteolysis. Among the increased proteins and peptides were thymosin β 4, talin 1, actin γ, filamin, and profilin. Increased concentrations of Ca2+-binding proteins calgranulins A and B in psoriatic plasma were also observed, confirming previous reports, and appeared to be relevant to the increase of cytoskeletal components. Another notable change in psoriatic plasma was a striking decrease in fibrinogen fragments.Conclusions: The identified increased concentrations of cytoskeletal proteins, their peptides, and calgranulins in psoriatic plasma, as well as the underlying altered protease activity, are proposed to be related to psoriasis pathogenesis.