bluuebunny/crossref_metadata_2025_split huggingface dataset:
Morphological diversity and development of glia in Drosophila
Authors: Hartenstein Volker 
Published: March 2011

AbstractInsect glia represents a conspicuous and diverse population of cells and plays a role in controlling neuronal progenitor proliferation, axonal growth, neuronal differentiation and maintenance, and neuronal function. Genetic studies in Drosophila have elucidated many aspects of glial structure, function, and development. Just as in vertebrates, it appears as if different classes of glial cells are specialized for different functions. On the basis of topology and cell shape, glial cells of the central nervous system fall into three classes (Fig. 1A–C): (i) surface glia that extend sheath‐like processes to wrap around the entire brain; (ii) cortex glia (also called cell body‐associated glia) that encapsulate neuronal somata and neuroblasts which form the outer layer (cortex) of the central nervous system; (iii) neuropile glia that are located at the interface between the cortex and the neuropile, the central domain of the nervous system formed by the highly branched neuronal processes and their synaptic contacts. Surface glia is further subdivided into an outer, perineurial layer, and an inner, subperineurial layer. Likewise, neuropile glia comprises a class of cells that remain at the surface of the neuropile (ensheathing glia), and a second class that forms profuse lamellar processes around nerve fibers within the neuropile (astrocyte‐like or reticular glia). Glia also surrounds the peripheral nerves and sensory organs; here, one also recognizes perineurial and subperineurial glia, and a third type called “wrapping glia” that most likely corresponds to the ensheathing glia of the central nervous system. Much more experimental work is needed to determine how fundamental these differences between classes of glial cells are, or how and when during development they are specified. To aid in this work the following review will briefly summarize our knowledge of the classes of glial cells encountered in the Drosophila nervous system, and then survey their development from the embryo to adult. © 2011 Wiley‐Liss, Inc.
Hippocampal but not amygdalar volume affects contextual fear conditioning in humans
Authors: Pohlack Sebastian T. , Nees Frauke , Liebscher Claudia , Cacciaglia Raffaele , Diener Slawomira J. , Ridder Stephanie , Woermann Friedrich G. , Flor Herta 
Published: March 2011

AbstractBoth animal and human studies have identified a critical role of the hippocampus in contextual fear conditioning. In humans mainly functional magnetic resonance imaging has been used. To extend these findings to volumetric properties, 58 healthy participants underwent structural magnetic resonance imaging and participated in a differential fear conditioning paradigm with contextual stimuli. Ratings of emotional valence, arousal, and contingency as well as skin conductance responses (SCRs) were used as indicators of conditioning. Twenty‐nine participants with the smallest hippocampal volumes were compared with 29 persons with the largest hippocampal volumes. Persons with larger hippocampal volume (especially on the right side) learned to discriminate between two conditioned contexts, whereas those with small hippocampal volumes did not, as indicated by SCRs. Further analyses showed that these results could not be explained by amygdalar volumes. In contrast, the participant answers on the self‐report measures were not significantly influenced by hippocampal or amygdalar, but by total brain volume, suggesting a role of cortical structures in these more cognitive evaluation processes. Reanalysis of the self‐report data using partial hippocampal volumes revealed a significant influence of the posterior but not anterior subvolumes, which is in accordance with theories and empirical findings on hippocampal functioning. This study shows the relevance of hippocampal volume for contextual fear conditioning in healthy volunteers and may have important implications for anxiety disorders. Hum Brain Mapp, 2012. © 2011 Wiley Periodicals, Inc.
Budget allocation and the revealed social rate of time preference for health
Authors: Paulden Mike , Claxton Karl 
Published: March 2011

SUMMARYAppropriate decisions based on cost‐effectiveness evaluations of health‐care technologies depend upon the cost‐effectiveness threshold and its rate of growth as well as some social rate of time preference for health. A more traditional approach to this problem is outlined before a social decision‐making approach is developed, which demonstrates that social time preference for health is revealed through the budget allocations made by a socially legitimate higher authority. The relationship between the social time preference rate for health, the growth rate of the cost‐effectiveness threshold and the rate at which the higher authority can borrow or invest is then examined. We establish that the social time preference rate for health is implied by the budget allocation and the health production functions in each period. As such, the social time preference rate for health depends not on the social time preference rate for consumption or growth in the consumption value of health but on growth in the cost‐effectiveness threshold and the rate at which the higher authority can save or borrow between periods. The implications for discounting and the policies of bodies such as NICE are then discussed. Copyright © 2011 John Wiley & Sons, Ltd.
Valproic acid: Growth inhibition of head and neck cancer by induction of terminal differentiation and senescence
Authors: Gan Chai Phei , Hamid Sharifah , Hor Seen Yii , Zain Rosnah Binti , Ismail Siti Mazlipah , Wan Mustafa Wan Mahadzir , Teo Soo Hwang , Saunders Nicholas , Cheong Sok Ching 
Published: March 2011

AbstractBackgroundThere are limited studies on the effects of drugs that modulate epigenetic regulation for head and neck squamous cell carcinoma (HNSCC). This study determined the effect of valproic acid (VPA) on HNSCC.MethodsGrowth inhibition effects of VPA alone or in combination with 5‐aza‐2′deoxycytidine (5‐aza‐dC) or all‐trans retinoic acid (ATRA) was evaluated with MTT and clonogenic assays on 5 HNSCC cell lines. The mechanism of growth inhibition was investigated by looking at markers of terminal differentiation and senescence.ResultsGrowth inhibition profiles of HNSCC cell lines varied in response to VPA. Inhibition of clonogenic survival in response to VPA was associated with an upregulation of p21, expression of terminal differentiation markers, and cellular senescence. Notably, a combination treatment of 5‐Aza‐dC‐VPA‐ATRA enhanced growth inhibition in cells resistant to VPA.ConclusionVPA is a potent inhibitor of proliferation in some HNSCC cell lines, and may be used to treat HNSCC. © 2011 Wiley Periodicals, Inc. Head Neck, 2012
Development and evaluation of sediment quality guidelines based on benthic macrofauna responses
Authors: Ritter Kerry J. , Bay Steven M. , Smith Robert W. , Vidal-Dorsch Doris E. , Field L. Jay 
Published: March 2011

Abstract
Toxicity-based sediment quality guidelines (SQGs) are often used to assess the potential of sediment contamination to adversely affect benthic macrofauna, yet the correspondence of these guidelines to benthic community condition is poorly documented. This study compares the performance of 5 toxicity-based SQG approaches to a new benthos-based SQG approach relative to changes in benthic community condition. Four of the toxicity-based SQG approaches—effects range median, logistic regression modeling (LRM), sediment quality guideline quotient 1 (SQGQ1), and consensus—were derived in previous national studies in the United States, and one was developed as a regional variation of LRM calibrated to California data. The new benthos-based SQG approach, chemical score index, was derived from Southern California benthic community data. The chemical-specific guidelines for each approach were applied to matched chemical concentration, amphipod mortality, and benthic macrofauna abundance data for Southern California. Respective results for each SQG approach were then combined into a summary metric describing the overall contamination magnitude (e.g., mean quotient) and assessed in accordance with a set of thresholds in order to classify stations into 4 categories of expected biological effect. Results for each SQG approach were significantly correlated with changes in sediment toxicity and benthic community condition. Cumulative frequency plots and effect category thresholds for toxicity and benthic community condition were similar, indicating that both types of effect measures had similar sensitivity and specificity of response to contamination level. In terms of discriminating among multiple levels of benthic community condition, the toxicity-based SQG indices illustrated moderate capabilities, similar to those for multiple levels of toxicity. The National LRM, California LRM, and the chemical score index had the highest overall agreement with benthic categories. However, only the benthos-based chemical score index was consistently among the highest performing SQG indices for all measures of association (correlation, percent agreement, and weighted kappa) for both toxicity and benthos. Integr Environ Assess Manag 2012; 8: 610–624. © 2011 SETAC
Determining the insolvent estate – A comparative analysis
Authors: Rajak Harry 
Published: March 2011

AbstractThis article is part of a comparative research project in which the provisions of several different jurisdictions concerning the determination of the insolvent estate are examined. In particular, this part of the project examines those provisions which enable the administrator of the insolvent estate to seek to increase the size of the estate by (a) setting aside pre‐insolvency transactions and (b) seeking compensation from those who allegedly were negligent or fraudulent in the management of the debtor prior to the onset of the latter's insolvency. The overall purpose of the research study is to establish a basis for the possible substantive harmonization of the different provisions in those countries, which constitute the European Union. Copyright © 2011 John Wiley & Sons, Ltd.
AIF‐mediated caspase‐independent necroptosis: A new chance for targeted therapeutics
Authors: Delavallée Laure , Cabon Lauriane , Galán‐Malo Patricia , Lorenzo Hans K. , Susin Santos A. 
Published: March 2011

AbstractCell death has been initially divided into apoptosis, in which the cell plays an active role, and necrosis, which is considered a passive cell death program. Intense research performed in the last decades has concluded that “programmed” cell death (PCD) is a more complex physiological process than initially thought. Indeed, although in most cases the PCD process is achieved via a family of Cys proteases known as caspases, an important number of regulated PCD pathways do not involve this family of proteases. As a consequence, active forms of PCD are initially referred to as caspase‐dependent and caspase‐independent. More recent data has revealed that there are also active caspase‐independent necrotic pathways defined as necroptosis (programmed necrosis). The existence of necroptotic forms of death was corroborated by the discovery of key executioners such as the kinase RIP1 or the mitochondrial protein apoptosis‐inducing factor (AIF). AIF is a Janus protein with a redox activity in the mitochondria and a pro‐apoptotic function in the nucleus. We have recently described a particular form of AIF‐mediated caspase‐independent necroptosis that also implicates other molecules such as PARP‐1, calpains, Bax, Bcl‐2, histone H2AX, and cyclophilin A. From a therapeutic point of view, the unraveling of this new form of PCD poses a question: is it possible to modulate this necroptotic pathway independently of the classical apoptotic paths? Because the answer is yes, a wider understanding of AIF‐mediated necroptosis could theoretically pave the way for the development of new drugs that modulate PCD. To this end, we present here an overview of the current knowledge of AIF and AIF‐mediated necroptosis. We also summarize the state of the art in some of the most interesting therapeutic strategies that could target AIF or the AIF‐mediated necroptotic pathway. © 2011 IUBMB IUBMB Life, 63(4): 221–232, 2011
Physiological unfolded protein response regulated by OASIS family members, transmembrane bZIP transcription factors
Authors: Kondo Shinichi , Saito Atsushi , Asada Rie , Kanemoto Soshi , Imaizumi Kazunori 
Published: March 2011

AbstractThe endoplasmic reticulum (ER) plays role in the maintenance of numerous aspects of cellular and organismal homeostasis by folding, modifying, and exporting nascent secretory and transmembrane proteins. Failure of the ER's adaptive capacity results in accumulation of unfolded or malfolded proteins in the ER lumen (ER stress). To avoid cellular damage, mammalian cells activate the specific signals from the ER to the cytosol or nucleus to enhance the capacity for protein folding, attenuate the synthesis of proteins, and degrade unfolded proteins. These signaling pathways are collectively known as the unfolded protein response (UPR). The canonical branches of the UPR are mediated by three ER membrane‐bound proteins, PERK, IRE1, and ATF6. These ER stress transducers basically play important roles in cell survival after ER stress. Recently, novel types of ER stress transducers, OASIS family members that share a region of high sequence similarity with ATF6 have been identified. They have a transmembrane domain, which allows them to associate with the ER, and possess a transcription‐activation domain and a bZIP domain. OASIS family proteins include OASIS, BBF2H7, CREBH, AIbZIP, and Luman. Despite the structural similarities among OASIS family proteins and ATF6, differences in activating stimuli, tissue distribution, and response element binding indicate specialized functions of each member on regulating the UPR in the specific organs and tissues. Here, we summarize our current understanding of biochemical characteristics and in vivo functions of OASIS family proteins, particularly focusing on OASIS and BBF2H7. A growing body of new works suggests that the UPR branches regulated by OASIS family members play essential roles in cell differentiation and maturation or maintenance of basal cellular homeostasis in mammals. © 2011 IUBMB IUBMB Life, 63(4): 233–239, 2011
Toxicity of methyl tertiary‐butyl ether (MTBE) following exposure of Wistar Rats for 13 weeks or one year via drinking water
Authors: Bermudez Edilberto , Willson Gabrielle , Parkinson Horace , Dodd Darol 
Published: March 2011

ABSTRACTThirteen‐week and one‐year toxicity studies of methyl tertiary‐butyl ether (MTBE) administered in drinking water to Wistar rats were conducted. Male and female rats were exposed to MTBE in drinking water at 0.5, 3, 7.5 and 15 mg ml−1 for 13 weeks and at 0.5, 3 and 7.5 (males) or 0.5, 3 and 15 mg ml−1 (females) for 1 year. Body weights were reduced only in males following 13 weeks of exposure. Reduced water consumption and urine output were observed in males and females exposed to MTBE. Kidney cell replication and α2u‐globulin levels in males were increased at 1 and 4 weeks of MTBE exposure and tubular cell regeneration was increased in male kidneys exposed to MTBE concentrations of 7.5 mg ml−1 or greater for 13 weeks. Wet weights of male kidneys were increased following 13 weeks, 6 months and 1 year of exposure to MTBE concentrations of 7.5 mg ml−1 or greater. Kidney wet weights were increased in females at MTBE concentrations of 15 mg ml−1 for 13 weeks. Tertiary‐butyl alcohol blood levels increased linearly with dose in males and females following 1 year of exposure. Chronic progressive nephropathy (CPN), of minimal to mild severity, increased in males, but not females, with 1 year of MTBE exposure. In summary, exposure of Wistar rats to MTBE in the drinking water resulted in minimal exposure‐related effects including limited renal changes in male rats suggestive of α2u‐globulin nephropathy following 13 weeks of exposure and an exacerbation of CPN in males at the end of 1 year of exposure. Copyright © 2011 John Wiley & Sons, Ltd.
Elastin‐like recombinamers as substrates for retinal pigment epithelial cell growth
Authors: Srivastava Girish K. , Martín Laura , Singh Amar K. , Fernandez‐Bueno Ivan , Gayoso Manuel J. , Garcia‐Gutierrez Maria T. , Girotti Alessandra , Alonso Matilde , Rodríguez‐Cabello José C. , Pastor José C. 
Published: March 2011

AbstractThe aim of this study is to investigate the use of elastin‐like recombinamers (ELRs) as a substrate that can maintain the growth, phenotype, and functional characteristics of retinal pigment epithelial (RPE) cells efficiently and as a suitable carrier for the transplantation of autologous RPE cells for treatment of age‐related macular degeneration (AMD). ELR films containing a bioactive sequence, RGD (ELR‐RGD), and one with no specific sequence (ELR‐IK) as control, were obtained by solvent‐casting onto glass and subsequent cross‐linking. ARPE19 cells were seeded on sterilized ELR films as well as on the control surfaces. Cells were analysed after 4, 24, 72, and 120 h to study cell adhesion, proliferation, cell viability, morphology, and specificity by staining with Trypan blue, DAPI, Rhodamin‐Phalloidin and RPE65, ZO‐1 antibodies and observing under fluorescence as well as electron microscope. ARPE19 cells seeded on both ELR films and controls were 100% viable and maintained their morphology and set of characteristics at the different time points studied. Cell proliferation on ELR‐RGD was significantly higher than that found on ELR‐IK at all time points, although it was less than the growth rate on polystyrene. ARPE19 cells grow well on ELR‐RGD maintaining their phenotype. These results should be extended to further studies with fresh human RPE cells and in vivo studies to determine whether this ELR‐RGD matrix could be used as a Bruch's membrane prosthesis and carrier for transplantation of RPE cells in patients suffering with AMD. © 2011 Wiley Periodicals, Inc. J Biomed Mater Res Part A:, 2011.
Transforming growth factor‐β1 suppression of endotoxin‐induced heme oxygenase‐1 in macrophages involves activation of Smad2 and downregulation of Ets‐2
Authors: Chung Su Wol , Kwon Min‐Young , Kang Young‐Ho , Chung Hun‐Taeg , Lee Seon‐Jin , Kim Hong Pyo , Perrella Mark A. 
Published: March 2011

AbstractHeme oxygenase (HO)‐1 is a cytoprotective molecule that is induced during the response to injury. An increase in HO‐1 is an acute indicator of inflammation, and early induction of HO‐1 has been suggested to correlate with severity of injury. While a great deal is known about the induction of HO‐1 by inflammatory mediators and bacterial lipopolysaccharide (LPS), much less is known about the effects of anti‐inflammatory mediators on HO‐1 expression. Transforming growth factor (TGF)‐β is known to play a critical role in suppressing the immune response, and the TGF‐β1 isoform is expressed in inflammatory cells. Thus, we wanted to investigate whether TGF‐β1 could inhibit the expression of HO‐1 during exposure to an inflammatory stimulus in macrophages. Here we demonstrate that TGF‐β1 is able to downregulate LPS‐induced HO‐1 in mouse macrophages, and this reduction in HO‐1 occurred through signaling of TGF‐β1 via its type I receptor, and activation of Smad2. This TGF‐β1 response is dependent on an intact Ets‐binding site (EBS) located 93 base pairs upstream from the mouse HO‐1 transcription start site. This EBS is known to be important for Ets‐2 transactivation of HO‐1 by LPS stimulation, and we show that TGF‐β1 is able to suppress LPS‐induced Ets‐2 mRNA and protein levels in macrophages. Moreover, silencing of Smad2 is able to prevent the suppression of both HO‐1 and Ets‐2 by TGF‐β1 during exposure to LPS. These data suggest that the return of HO‐1 to basal levels during the resolution of an inflammatory response may involve its downregulation by anti‐inflammatory mediators. J. Cell. Physiol. 227: 351–360, 2012. © 2011 Wiley Periodicals, Inc.
Bone marrow and peripheral white blood cells number is affected by sleep deprivation in a murine experimental model
Authors: Guariniello Luciana Doria , Vicari Perla , Lee Kil Sun , de Oliveira Allan Chiaratti , Tufik Sergio 
Published: March 2011

AbstractSleep deficit and related disorders are becoming increasingly prevalent in modern life and an extensive literature has documented that acute or chronic sleep deprivation can lead to several physiological consequences. Here, we evaluated the effects of sleep deprivation on hematopoietic composition of either bone marrow or peripheral blood. Mice were subjected to paradoxical sleep deprivation (PSD) for 72 h by modified multiple platform method, with or without an additional sleep recovery (SR) period of 10 days. PSD decreased total cellularity of the bone marrow and peripheral blood concomitantly. Subsequent analysis of cell composition showed that absolute number of hematopoietic stem/progenitor cells and colony‐forming units was decreased. Moreover, the absolute number of granulocytes and monocytes in bone marrow was reduced in PSD group. These alterations were paralleled by an accumulation of neutrophils and monocytes in peripheral blood. PSD also induced lymphopenia in the circulation. To the best of our knowledge, this is the first study that demonstrates the importance of sleep on the hematopoietic microenvironment and provides new insights into the relationship between sleep and the immune system. J. Cell. Physiol. 227: 361–366, 2012. © 2011 Wiley Periodicals, Inc.
Ceramide metabolism is affected by obesity and diabetes in human adipose tissue
Authors: Błachnio‐Zabielska A.U. , Pułka M. , Baranowski M. , Nikołajuk A. , Zabielski P. , Górska M. , Górski J. 
Published: March 2011

AbstractCeramide is involved in development of insulin resistance. However, there are no data on ceramide metabolism in human adipose tissue. The aim of our study was to examine sphingolipid metabolism in fat tissue from obese nondiabetic (n = 11), obese diabetic (n = 11), and lean nondiabetic (n = 8) subjects. The content of ceramide (Cer), dihydroceramide (dhCer), sphingosine (SPH), sphinganine (SPA), sphingosine‐1‐phosphate (S1P; pmol/mg of protein), the expression (mRNA) and activity of key enzymes responsible for Cer metabolism: serine palmitoyltransferase (SPT), neutral and acidic sphingomyelinase (nSMase and aSMase, respectively), and neutral and acidic ceramidase (nCDase and aCDase, respectively) were examined in human adipose tissue. The contents of SPA and Cer were significantly lower whereas the content of dhCer was higher in both obese groups than the respective values in the lean subjects. The expression of examined enzymes was elevated in both obese groups. The SPT and CDases activity increased whereas aSMase activity deceased in both obese groups. We have found correlation between adipose tissue Cer content and plasma adiponectin concentration (r = 0.69, P < 0.001) and negative correlation between total Cer content and HOMA‐IR index (homeostasis model of insulin resistance) (r = −0.67, P < 0.001). We have found that both obesity and diabetes affected pathways of sphingolipid metabolism in the adipose tissue. J. Cell. Physiol. 227: 550–557, 2012. © 2011 Wiley Periodicals, Inc.