bluuebunny/crossref_metadata_2025_split huggingface dataset:
Targeting NOX, INOS and COX‐2 in inflammatory cells: Chemoprevention using food phytochemicals
Authors: Murakami Akira , Ohigashi Hajime 
Published: September 2007

AbstractBiological, biochemical and physical stimuli activate inflammatory leukocytes, such as macrophages, resulting in induction and synthesis of proinflammatory proteins and enzymes, together with free radicals, as innate immune responses. On the other hand, chronic and dysregulated activation of some inducible enzymes, including NADPH oxidase (NOX), inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)‐2, have been shown to play pivotal roles in the development of certain inflammatory diseases such as oncogenesis. While the use of synthetic agents, especially those targeting molecules, is an attractive and reasonable approach to prevent carcinogenesis, it should be noted that traditional herbs and spices also exist along with their active constituents, which have been demonstrated to disrupt inflammatory signal transduction pathways. In this mini‐review, the molecular mechanisms of activation or induction of NOX, iNOS and COX‐2, as well as some food phytochemicals with marked potential to regulate those key inflammatory molecules, are highlighted. For example, 1′‐acetoxychavicol acetate, which occurs in the rhizomes of the subtropical Zingiberaceae plant, has been shown to attenuate NOX‐derived superoxide generation in macrophages, as well as lipopolysaccharide‐induced nitric oxide and prostaglandin E2 production through the suppression of iNOS and COX‐2 synthesis, respectively. Notably, this phytochemical has exhibited a wide range of cancer prevention activities in several rodent models of inflammation‐associated carcinogenesis. Herein, the cancer preventive potentials of several food phytochemicals targeting the induction of NOX, iNOS and COX‐2 are described. © 2007 Wiley‐Liss, Inc.
Chronic inflammation and oxidative stress in human carcinogenesis
Authors: Federico Alessandro , Morgillo Floriana , Tuccillo Concetta , Ciardiello Fortunato , Loguercio Carmela 
Published: September 2007

AbstractA wide array of chronic inflammatory conditions predispose susceptible cells to neoplastic transformation. In general, the longer the inflammation persists, the higher the risk of cancer. A mutated cell is a sine qua non for carcinogenesis. Inflammatory processes may induce DNA mutations in cells via oxidative/nitrosative stress. This condition occurs when the generation of free radicals and active intermediates in a system exceeds the system's ability to neutralize and eliminate them. Inflammatory cells and cancer cells themselves produce free radicals and soluble mediators such as metabolites of arachidonic acid, cytokines and chemokines, which act by further producing reactive species. These, in turn, strongly recruit inflammatory cells in a vicious circle. Reactive intermediates of oxygen and nitrogen may directly oxidize DNA, or may interfere with mechanisms of DNA repair. These reactive substances may also rapidly react with proteins, carbohydrates and lipids, and the derivative products may induce a high perturbation in the intracellular and intercellular homeostasis, until DNA mutation. The main substances that link inflammation to cancer via oxidative/nitrosative stress are prostaglandins and cytokines. The effectors are represented by an imbalance between pro‐oxidant and antioxidant enzyme activities (lipoxygenase, cyclooxygenase and phospholipid hydroperoxide glutathione‐peroxidase), hydroperoxides and lipoperoxides, aldehydes and peroxinitrite. This review focalizes some of these intricate events by discussing the relationships occurring among oxidative/nitrosative/metabolic stress, inflammation and cancer. © 2007 Wiley‐Liss, Inc.
Preliminary explorations of the role of mitochondrial proteins in refractory epilepsy: Some Findings From Comparative Proteomics
Authors: Jiang WenJing , Du BinFeng , Chi ZhaoFu , Ma Lin , Wang ShengJun , Zhang XuHua , Wu Wei , Wang XiaoHua , Xu GuangRun , Guo ChunNi 
Published: September 2007

AbstractApproximately 20–30% of patients with epilepsy continue to have seizures despite carefully monitored treatment with antiepileptic drugs. The mechanisms that underlie why some patients are responsive and others prove resistant to antiepileptic drugs are poorly understood. Increasing evidence supports a role for altered mitochondrial function in the pathogenesis of epilepsy. To gain greater molecular insight in the pathogenesis of intractable epilepsy, we undertook a global analysis of protein expressions in a pharmacoresistant epileptic model selected by phenytoin in electrical amygdala‐kindled rats by using two‐dimensional gel electrophoresis coupled with matrix‐assisted laser desorption/ionization time of flight (MALDI‐TOF‐TOF). We identified five increased proteins and 14 decreased proteins including voltage‐dependent anion channel 1 (VDAC1) with a 2.82‐fold increased level (P < 0.05) and voltage‐dependent anion channel 2 (VDAC2) with a 3.97‐fold decreased level (P < 0.05) in hippocampus of pharmacoresistant rats. The increased VDAC1 and decreased VDAC2 were confirmed by Western blot analysis and immunohistochemistry. Vascular mitochondria and apoptosis neurons were observed through electron microscopy. Energy contents, the adenine nucleotides, were measured by high‐performance liquid chromatography (HPLC). The correlation analyses were carried out between VDAC and the energy charge. These findings indicate that the increase of VDAC1 and the decrease of VDAC2 play an important role during the process and provide new molecular evidence in understanding mechanism of refractory epilepsy. © 2007 Wiley‐Liss, Inc.
Endogenous neurogenesis and neovascularization in the neocortex of the rat after focal cerebral ischemia
Authors: Shin Hye Young , Kim Jin Hyun , Phi Ji Hoon , Park Chul‐Kee , Kim Jung Eun , Kim Jong‐Hoon , Paek Sun Ha , Wang Kyu‐Chang , Kim Dong Gyu 
Published: September 2007

AbstractThe present study was designed to examine whether endogenous neurogenesis and neovascularization occur in the neocortex of the ischemic rat brain after unilateral middle cerebral artery occlusion (MCAO). Sprague‐Dawley rats were divided into six groups (n = 29): one control group (n = 4) and five groups composed of animals sacrificed at increasing times post‐MCAO (2 days and 1, 2, 4, and 8 weeks; n = 5 per group). To determine the presence of neurogenesis and neovascularization in the ischemic brain, nestin, Tuj1, NeuN, GFAP, Tie2, RECA, and 5‐bromo‐2′‐deoxyuridine (BrdU) were analyzed immunohistochemically. In addition, nestin, GFAP, and Tie2 expression was determined by Western blotting. Triple‐labeling of nestin, BrdU, and laminin was performed to visualize the interaction between endogenous neurogenesis and neovascularization. The number of BrdU‐ and nestin‐colabeled cells increased markedly in the neocortex and border zone of the ischemic area up to 1 week after MCAO and decreased thereafter. Western blot analysis revealed that the expression of nestin, Tie‐2, and GFAP was amplified in the ipsilateral hemisphere 2days after MCAO and peaked 1 week after MCAO, compared with that in the normal brain. After ischemic injury, nestin‐ and BrdU‐colabeled cells were observed in the vicinity of the endothelial cells lining cerebral vessels in the ipsilateral neocortex of the ischemic brain. Endogenous neurogenesis and neovascularization were substantially activated and occurred in close proximity to one other in the ipsilateral neocortex of the ischemic rat brain. © 2007 Wiley‐Liss, Inc.
Up‐regulation of platelet‐derived growth factor by peripheral‐blood leukocytes during experimental allergic encephalomyelitis
Authors: Koehler Niklas K. U. , Roebbert Markus , Dehghani Kourosh , Ballmaier Matthias , Claus Peter , von Hoersten Stephan , Shing Mona , Odin Per , Strehlau Jürgen , Heidenreich Fedor 
Published: September 2007

AbstractIn multiple sclerosis (MS) and its animal model, experimental allergic encephalomyelitis (EAE), clinical disease is associated with infiltration of the central nervous system (CNS) by immune cells. Subsequent remission with remyelination has been linked to an increased occurrence of oligodendrocyte progenitor (O2A) cells. Platelet‐derived growth factor (PDGF) and fibroblast growth factor–2 (FGF‐2) are key growth factors for O2A cells, yet little is known about their relevance in EAE and MS. We analyzed the expression of PDGF, FGF‐2, and their receptors by peripheral‐blood leukocytes (PBLs) and lymphocyte subsets during MBP‐induced EAE. Strong up‐regulation of PDGF, but not FGF‐2, was observed in PBLs, with the highest expression after the disease maximum. T, NK, and NKT cells expressed PDGF, which is a novel observation because thus far only monocytes/macrophages have been reported to express PDGF. These results extend the idea that growth factors may contribute to improved CNS tissue repair, including PDGF, which is secreted by lesion‐homing immune cells. The production of PDGF by lymphocytes may have potential therapeutic value when activating or modulating T‐cell responses in demyelinating diseases. © 2007 Wiley‐Liss, Inc.
L‐DOPA‐induced activation of striatal p38MAPK and CREB in neonatal dopaminergic denervated rat: Relevance to self‐injurious behavior
Authors: Sivam Subbiah P. , Pugazhenthi Subbiah , Pugazhenthi Vidya , Brown Heath 
Published: September 2007

AbstractThe destruction of nigrostriatal dopaminergic neurons with 6‐hydroxydopamine (6OHDA) during the neonatal period results in dopamine (DA) loss and susceptibility for self‐injurious behavior (SIB) when challenged with L‐dihydroxyphenylalanine (L‐DOPA), via a supersensitive D1 receptor‐mediated mechanism. However, there are no changes in D1 receptor binding or mRNA levels, suggesting a potential postreceptor signaling mechanism(s). Here, we examined whether L‐DOPA‐induced SIB is associated with altered MAPK signaling (p38MAPK, ERK1/2, and JNK) and their nuclear target, CREB. Neonatal dopaminergic lesioned animals were challenged, as adults, with L‐DOPA, observed for SIB for 6 hr, and then sacrificed. The data were grouped as follows: control, lesioned rats without SIB (SIB–), and lesioned rats that were positive for SIB (SIB+). HPLC analysis of striatal extracts revealed a more significant loss of DA and an increase of serotonin in the SIB+than in the SIB–group. The striatal levels of TH protein were severely decreased, but D1 receptor levels were unaltered in the lesioned groups. These results confirm and extend previous studies indicating that SIB is associated with a near‐total loss of DA and TH, an increase in serotonin, and no change in D1 receptor levels. The present studies further revealed that the levels of active phosphorylated forms of p38MAPK and CREB were significantly higher in the SIB+group than in the SIB–group in the striatum, but not in cortex or olfactory tubercle. The results indicate an induction of striatal p38MAPK and an activation of its nuclear target, CREB, as additional mechanisms in the genesis of L‐DOPA‐induced SIB. © 2007 Wiley‐Liss, Inc.
Purkinje cell survival in organotypic cultures: Implication of Rho and its downstream effector ROCK
Authors: Julien Sylvie , Schnichels Sven , Teng Henry , Tassew Nardos , Henke‐Fahle Sigrid , Mueller Bernhard K. , Monnier Philippe P. 
Published: September 2007

AbstractOrganotypic cultures of postnatal day 1 (P1) to P7 mouse cerebella are well‐established models for studying cell survival. In the present work, we investigate the involvement of the Rho/ROCK intracellular pathway in Purkinje cell survival by using organotypic cultures of P3 Swiss mice. Specific inhibitors of Rho or ROCK were applied at different concentrations to the slice cultures, which were maintained for 5 days in vitro. We show that the bacterial exoenzyme C3 transferase, a specific inhibitor of the small GTPase Rho, increases Purkinje cell survival. There is a 4.5‐ and 2.5‐fold increase in Purkinje cell survival when C3 intracellular uptake is promoted either by the PEP‐1 peptide or by the C2IN carrier protein, respectively, and not with the commonly used TAT peptide. Moreover, treatment with Y27632 and H‐1152, two specific inhibitors of the Rho kinase ROCK, also strongly reduces apoptotic cell death and results in 6.5‐ and 8.5‐fold increases in cell survival, respectively. In immunohistochemical analysis, we also show that H‐1152 did not change either glial fibrillary acidic protein or isolectin‐B4 staining, indicating that this compound did not alter the cellular composition in our cultures. Thus, our data demonstrate that inhibition of Rho and its downstream effector ROCK may be used to enhance cell survival in neurodegenerative diseases. © 2007 Wiley‐Liss, Inc.
Role of endothelins as mediators of injury‐induced alterations of glial glutamate turnover
Authors: Lehmann Claudia , Eisner Friederike , Engele Jürgen 
Published: September 2007

AbstractAstroglia terminate glutamatergic neurotransmission and prevent excitotoxic extracellular glutamate concentration by clearing synaptically released glutamate through the high‐affinity, sodium‐dependent glutamate transporters GLT‐1 and GLAST. Many brain injures are associated with the disturbed expression of glial glutamate transporters and a subsequent increase of extracellular glutamate to neurotoxic levels. We have now followed up initial hints pointing to endothelins, a family of injury‐regulated peptides, as mediators of this injury‐induced loss of glial glutamate transporter expression. We observed that, in line with such a role, endothelins not only act as potent inhibitors of basal and exogenously (dbcAMP)‐induced expression of GLT‐1 in cortical astrocytes as shown before, but likewise inhibit expression of GLT‐1 or GLAST in astrocytes cultured from the diencephalon, mesencephalon, cerebellum, and spinal cord. We further demonstrate that endothelins equally inhibit GLT‐1 expression in cortical slice cultures, a culture system closely resembling the in vivo situation. Although brain injuries are usually associated with an increase in the expression of the glutamate‐converting enzyme glutamine synthetase, cultured cortical astrocytes maintained with endothelins showed an almost complete loss of glutamine synthetase. Interestingly, the inhibitory effects of endothelins on the expression of glutamine synthetase, but not of glutamate transporters, was overridden by high extracellular glutamate, indicating that the primarily inhibitory action of endothelins on the various components of glial glutamate turnover dissociates in the injured brain. © 2007 Wiley‐Liss, Inc.
Cardiovascular responses to noradrenaline microinjection in the ventrolateral periaqueductal gray of unanesthetized rats
Authors: Pelosi Gislaine Garcia , Tavares Rodrigo Fiacadori , Antunes‐Rodrigues José , Corrêa Fernando Morgan Aguiar 
Published: September 2007

AbstractThe periaqueductal gray area (PAG) is a mesencephalic area involved in cardiovascular modulation. Noradrenaline (NA), a neurotransmitter involved in central blood pressure control, is present in the rat PAG. We report here on the cardiovascular effects caused by NA microinjection into the ventrolateral PAG (vlPAG) of unanesthetized rats and the peripheral mechanism involved in their mediation. NA microinjection in the vlPAG of unanesthetized rats evoked dose‐related pressor and bradycardiac responses. No significant cardiovascular responses were observed in urethane‐anesthetized rats. The pressor response was potentiated by pretreatment with the ganglion blocker pentolinium (5 or 10 mg/kg, intravenously). Pretreatment with the vasopressin antagonist dTyr(CH2)5 (Me)AVP (50 μg/kg, intravenously) blocked the pressor response evoked by the NA microinjection into the vlPAG. Additionally, circulating vasopressin content was found to be significantly increased after NA microinjection in the vlPAG. The results suggest that activation of noradrenergic synapses within the vlPAG modulates vasopressin release in unanesthetized rats. © 2007 Wiley‐Liss, Inc.
Developmental expression of histone deacetylase 11 in the murine brain
Authors: Liu Hedi , Hu Qichen , Kaufman Amanda , D'Ercole A. Joseph , Ye Ping 
Published: September 2007

AbstractRecent studies indicate that neural cell development in the central nervous system (CNS) correlates with a reduction in acetylation of histone core proteins. Moreover, histone hypoacetylation is thought to be important to oligodendrocyte lineage development. The mechanisms mediating the reduction in acetylation during postnatal neural development remain to be defined. To begin to understand these mechanisms, we investigated the expression of histone deacetylase 11 (HDAC11), a newly identified HDAC, in mouse brain during postnatal development. We show that HDAC11 was widely expressed in the brain and that this expression gradually increased in a region‐specific pattern between birth and 4 weeks of age. At the cellular level HDAC11 protein was predominately localized in the nuclei of mature oligodendrocytes but only minimally in astrocytes. Although dentate gyrus granule neurons abundantly expressed HDAC11, granule neuron precursors in the subgranule layer exhibited little HDAC11 immunoreactivity. Double‐immunostaining of the corpus callosum and dentate gyrus demonstrated that HDAC11 and Ki67, a cell‐proliferating marker, are rarely colocalized in same cells. Our data show that HDAC11 was expressed in the developing brain in a temporal and spatial pattern that correlates with the maturation of neural cells, including cells of the oligodendrocyte lineage. These findings support a role for HDAC11 in CNS histone deacetylation and the development of oligodendrocytes and neurons during postnatal development. © 2007 Wiley‐Liss, Inc.
A contextual examination of new venture performance: entrepreneur leadership behavior, top management team heterogeneity, and environmental dynamism
Authors: Hmieleski Keith M. , Ensley Michael D. 
Published: September 2007

AbstractThis study examined the relationship of entrepreneur leadership behavior (empowering and directive), top management team heterogeneity (functional, educational specialty, educational level, and skill) and industry environmental dynamism (rate of unpredicted change in number of industry establishments, number of industry employees, industry revenue, and industry research and development intensity) on new venture performance (revenue growth and employment growth) using two different samples—theInc. 500 list of America's fastest growing startups and a national (United States) random sample of new ventures. In dynamic industry environments, startups with heterogeneous top management teams were found to perform best when led by directive leaders and those with homogenous top management teams performed best when led by empowering leaders. Conversely in stable industry environments, startups with heterogeneous top management teams were found to perform best when led by empowering leaders and those with homogenous top management teams performed best when led by directive leaders. These findings were consistent across both samples and demonstrate the value in a contextual approach to leadership, which considers adjusting leadership behavior in accordance to factors that are both internal and external to the firm. Copyright © 2007 John Wiley & Sons, Ltd.
Lattice dynamics of tetragonal Nd2BaZnO5
Authors: Gupta H. C. , Sharma V. 
Published: September 2007

AbstractA short‐range force constant model (SRFCM) has been applied to investigate the Raman and the infrared wavenumbers in Nd2BaZnO5 in its tetragonal phase of space group I4/mcm. Calculations of zone‐center phonons are made with five stretching and five bending force constants. All the Raman and infrared values are then assigned to their corresponding modes. Two Raman modes are reassigned on the basis of group theoretical calculations. The calculated Raman wavenumbers exhibit good agreement with the observed values. Copyright © 2007 John Wiley & Sons, Ltd.
Characterization of deep‐fat frying in a wheat flour–water mixture model using a state diagram
Authors: Thanatuksorn Pariya , Kajiwara Kazuhito , Suzuki Toru 
Published: September 2007

AbstractBACKGROUND: Crispness is an important characteristic to be controlled in deep‐fat fried products. The physical state of food polymers influences the development of cellular structure and textural qualities of fried food. Glassy state is believed to play an important role in the mechanical properties of low‐moisture food. Therefore, an understanding of the physicochemical phenomena in the development of fried food structure using a state diagram of the frying process is discussed.RESULTS: Wheat flour models containing 400 and 600 g kg−1 initial moisture content were fried in frying oil at 150 °C for 1–7 min. Thermal properties of wheat flour, structure alteration and textural properties of fried samples were evaluated. The porous structure continuously enlarged when the sample was in the rubbery state. As the frying time was prolonged, the state of the product became glassy due to a decrease in water content, resulting in the ceasing of porous enlargement.Conclusion: The results revealed that physicochemical changes during frying influence the alteration of microstructure and quality of fried food, and the state diagram could be applied to explain the formation of microstructure during the frying process and used as a decision‐making tool to choose the proper conditions to provide desirable qualities in fried food. Copyright © 2007 Society of Chemical Industry
Optimization of the porous structure and polarity of polymethacrylate‐based monolithic capillary columns for the LC‐MS separation of enzymatic digests
Authors: Eeltink Sebastiaan , Geiser Laurent , Svec Frantisek , Fréchet Jean M. J. 
Published: September 2007

AbstractThe porous structure as well as the polarity of methacrylate ester‐based monolithic stationary phases has been optimized to achieve the separation of various peptides originating from enzymatic digestion. The porous structure, determined by the size of both pores and microglobules, was varied through changes in the composition of porogenic solvents in the polymerization mixture, while the polarity was controlled through the incorporation of butyl, lauryl, or octadecyl methacrylate in the polymer backbone. Both the morphology and the chemistry of the monoliths had a significant effect on the retention and efficiency of the capillary columns. The best resolution of peptidic fragments obtained by digestion of Cytochrome c with trypsin in solution was obtained in a gradient LC‐MS mode using a monolithic capillary column of poly(lauryl methacrylate‐co‐ethylene dimethacrylate) featuring small pores and small microglobules. Raising the temperature from 25 to 60°C enabled separations to be carried out at 40% higher flow rates. Separations carried out at 60°C with a steeper gradient proceeded without loss of performance in half the time required for a comparable separation at room temperature. Our preparation technique affords monolithic columns with excellent column‐to‐column and run‐to‐run repeatability of retention times and pressure drops.