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Selected AbstractsThe Potential for Species Conservation in Tropical Secondary ForestsCONSERVATION BIOLOGY, Issue 6 2009ROBIN L. CHAZDON especialización de hábitat; biodiversidad forestal; bosque secundario; bosque tropical; sucesión Abstract:,In the wake of widespread loss of old-growth forests throughout the tropics, secondary forests will likely play a growing role in the conservation of forest biodiversity. We considered a complex hierarchy of factors that interact in space and time to determine the conservation potential of tropical secondary forests. Beyond the characteristics of local forest patches, spatial and temporal landscape dynamics influence the establishment, species composition, and persistence of secondary forests. Prospects for conservation of old-growth species in secondary forests are maximized in regions where the ratio of secondary to old-growth forest area is relatively low, older secondary forests have persisted, anthropogenic disturbance after abandonment is relatively low, seed-dispersing fauna are present, and old-growth forests are close to abandoned sites. The conservation value of a secondary forest is expected to increase over time, as species arriving from remaining old-growth forest patches accumulate. Many studies are poorly replicated, which limits robust assessments of the number and abundance of old-growth species present in secondary forests. Older secondary forests are not often studied and few long-term studies are conducted in secondary forests. Available data indicate that both old-growth and second-growth forests are important to the persistence of forest species in tropical, human-modified landscapes. Resumen:,A raíz de la pérdida generalizada de los bosques maduros en el trópico, los bosques secundarios probablemente jugarán un mayor papel en la conservación de la biodiversidad forestal. Consideramos una jerarquía compleja de factores que interactúan en el espacio y tiempo para determinar el potencial de conservación de los bosques tropicales secundarios. Más allá de las características de los fragmentos de bosque locales, la dinámica espacial y temporal del paisaje influye en el establecimiento, la composición de especies y la persistencia de bosques secundarios. Los prospectos para la conservación de especies primarias en los bosques secundarios se maximizan en regiones donde la proporción de superficie de bosque maduro-bosque secundario es relativamente baja, los bosques secundarios más viejos han persistido, la perturbación antropogénica después del abandono es relativamente baja, hay presencia de fauna dispersora de semillas y donde hay bosques primarios cerca de sitios abandonados. Se espera que el valor de conservación de un bosque secundario incremente en el tiempo, a medida que se acumulan especies provenientes de los fragmentos de bosque primario remanentes. Muchos estudios están pobremente replicados, lo que impide evaluaciones robustas del número y abundancia de especies primarias presentes en bosques secundarios. Los bosques secundarios más viejos generalmente no son estudiados y son pocos los estudios a largo plazo en bosques secundarios. Los datos disponibles indican que tanto los bosques primarios como los secundarios son importantes para la persistencia de especies forestales en paisajes tropicales modificados por humanos. [source] Transesophageal Echocardiography Risk Factors for Stroke in Nonvalvular Atrial FibrillationECHOCARDIOGRAPHY, Issue 4 2000F.R.C.P.C., SUSAN M. FAGAN M.D. Atrial fibrillation is a common arrhythmia, particularly in the older age groups. It confers an increased risk of thromboembolism to these patients, and multiple clinical risk factors have been identified to be useful in predicting the risks of thromboembolic events. Recent studies have evaluated the role of transesophageal echocardiography (TEE) in the evaluation of patients with atrial fibrillation. The purpose of this review is to evaluate the significance of transesophageal echocardiography findings in the prediction of thromboembolic events, particularly stroke, in patients with nonvalvular atrial fibrillation, with an emphasis on recently reported prospective studies. Aortic plaque and left atrial appendage abnormalities are identified as independent predictors of thromboembolic events. Although they are associated with clinical events, they also have independent incremental prognostic values. Other transesophageal echocardiographic findings, such as patent foramen ovale and atrial septal aneurysm, have not been found to be predictors of thromboembolic events in this patient group. Thus, TEE is a useful tool in stratifying patients with nonvalvular atrial fibrillation into different risk groups in terms of thromboembolic events, and it will likely play an important role in future studies to assess new treatment strategies in high-risk patients with atrial fibrillation. [source] Emergence of larval yellow perch, Perca flavescens, in South Dakota lakes: potential implications for recruitmentFISHERIES MANAGEMENT & ECOLOGY, Issue 4 2008D. A. ISERMANN Abstract, Temporal patterns in length frequency distributions and hatch dates were described for larval yellow perch, Perca flavescens (Mitchill), captured in surface ichthyoplankton trawls from late April to mid-June 2000 to 2002 in six South Dakota, USA lakes. Fewer than 15 larval yellow perch were collected in four of six lakes during 2002, suggesting that in some cases factors prior to, during or immediately after hatching likely play a critical role in the perch recruitment process. When larval yellow perch were encountered in larger numbers, temporal trends in total length (TL) frequencies indicated that only a single cohort was produced annually in each lake. Most yellow perch in these lakes hatched between 29 April and 17 May, and most hatching occurred during 5,11 days each year. Larval TL was not related to hatch date. The apparent prevalence of relatively short hatch periods in these yellow perch populations probably increases the risk of catastrophic losses resulting from periods of poor environmental conditions. [source] Spatial patterns of simulated transpiration response to climate variability in a snow dominated mountain ecosystemHYDROLOGICAL PROCESSES, Issue 18 2008Lindsey Christensen Abstract Transpiration is an important component of soil water storage and stream-flow and is linked with ecosystem productivity, species distribution, and ecosystem health. In mountain environments, complex topography creates heterogeneity in key controls on transpiration as well as logistical challenges for collecting representative measurements. In these settings, ecosystem models can be used to account for variation in space and time of the dominant controls on transpiration and provide estimates of transpiration patterns and their sensitivity to climate variability and change. The Regional Hydro-Ecological Simulation System (RHESSys) model was used to assess elevational differences in sensitivity of transpiration rates to the spatiotemporal variability of climate variables across the Upper Merced River watershed, Yosemite Valley, California, USA. At the basin scale, predicted annual transpiration was lowest in driest and wettest years, and greatest in moderate precipitation years (R2 = 0·32 and 0·29, based on polynomial regression of maximum snow depth and annual precipitation, respectively). At finer spatial scales, responsiveness of transpiration rates to climate differed along an elevational gradient. Low elevations (1200,1800 m) showed little interannual variation in transpiration due to topographically controlled high soil moistures along the river corridor. Annual conifer stand transpiration at intermediate elevations (1800,2150 m) responded more strongly to precipitation, resulting in a unimodal relationship between transpiration and precipitation where highest transpiration occurred during moderate precipitation levels, regardless of annual air temperatures. Higher elevations (2150,2600 m) maintained this trend, but air temperature sensitivities were greater. At these elevations, snowfall provides enough moisture for growth, and increased temperatures influenced transpiration. Transpiration at the highest elevations (2600,4000 m) showed strong sensitivity to air temperature, little sensitivity to precipitation. Model results suggest elevational differences in vegetation water use and sensitivity to climate were significant and will likely play a key role in controlling responses and vulnerability of Sierra Nevada ecosystems to climate change. Copyright © 2008 John Wiley & Sons, Ltd. [source] Participation of the Fas and Fas ligand systems in apoptosis during atrophy of the rat submandibular glandsINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 1 2007Shigeru Takahashi Summary Most acinar cells and some duct cells undergo apoptosis during atrophy of the submandibular gland. The present study was designed to elucidate whether Fas and its receptor ligand (FasL) are involved during apoptotic atrophy of the gland. The excretory duct of the right submandibular gland of rats was doubly ligated with metal clips from 1 to 14 days for induction of gland atrophy. Control rats were untreated. Fas and FasL expression in the atrophied submandibular gland was detected using immunohistochemistry (IHC) and Western immunoblot. Expression of activated caspase 8 and activated caspase 3 was also detected with IHC. Fas-positive acinar and duct cells and FasL-positive duct cells increased in the atrophic glands at 3 and 5 days after duct ligation when apoptotic cells were commonly observed. Thereafter, Fas- and FasL-positive cells declined in number. Patterns of expression of Fas and FasL using Western immunoblots concurred with the IHC results. Activated caspase 8-positive cells were present at every time interval but peaked at 3 and 5 days following duct ligation. The cells showing immunoreaction for activated caspase 3 first appeared on day 3, with the peak in apoptosis, after which they decreased. The results indicate that the Fas/FasL systems likely play an important role in apoptotic pathways during atrophy of the submandibular gland. [source] Adapter protein CRKII signaling is involved in the rat pancreatic acini response to reactive oxygen speciesJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2006Alberto G. Andreolotti Abstract Recent studies demonstrate that reactive oxygen species (ROS) are important mediators of acute pancreatitis, whether induced experimentally or in necrotizing pancreatitis in humans; however, the cellular processes involved remain unclear. Adapter protein CrkII, plays a central role for convergence of cellular signals from different stimuli. Cholecystokinin (CCK), which induces pancreatitis, stimulates CrkII tyrosine phosphorylation and CrkII protein complexes, raising the possibility it can be important in the acinar cell responses to ROS. Therefore, our aim was to investigate whether CrkII signaling is involved in the biological response of rat pancreatic acini to H2O2 and the intracellular mediators implicated. Treatment of isolated rat pancreatic acini with H2O2 rapidly stimulates CrkII phosphorylation, measured as electrophoretic mobility shift and by using a phosphospecific antibody (pTyr221). Tyrosine kinase blocker B44 inhibits the higher phosphorylation state, demonstrating that it occurs mainly in tyrosine residues. H2O2 -induced CrkII phosphorylation is time- and concentration-dependent, showing maximal effect with 3 mM H2O2 at 5 min. The intracellular pathways induced by H2O2 leading to CrkII tyrosine phosphorylation do not involve PKC, intracellular calcium, PI3-K or the actin cytoskeleton integrity. ROS generation clearly promotes the formation of protein complex CrkII,PYK2. In conclusion, ROS clearly affect the key adapter protein CrkII signaling by two ways: stimulation of CkII phosphorylation and a functional consequence: formation of CrkII,protein complexes. Because of its central role in activating more distal pathways, CrkII might likely play an important role in the ability of ROS to induce pancreatic cellular injury and pancreatitis. J. Cell. Biochem. © 2005 Wiley-Liss, Inc. [source] Contribution of the striatum to the effects of 5-HT1A receptor stimulation in L-DOPA-treated hemiparkinsonian ratsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 7 2009Christopher Bishop Abstract Clinical and experimental studies implicate the use of serotonin (5-HT)1A receptor agonists for the reduction of L -3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID). Although raphe nuclei likely play a role in these antidyskinetic effects, an unexplored population of striatal 5-HT1A receptors (5-HT1AR) may also contribute. To better characterize this mechanism, L-DOPA-primed hemiparkinsonian rats received the 5-HT1AR agonist ±8-OH-DPAT (0, 0.1, 1.0 mg/kg, i.p.) with or without cotreatment with the 5-HT1AR antagonist WAY100635 (0.5 mg/kg, i.p.) 5 min after L-DOPA, after which abnormal involuntary movements (AIMs), rotations, and forelimb akinesia were quantified. To establish the effects of 5-HT1AR stimulation on L-DOPA-induced c-fos and preprodynorphin (PPD) mRNA within the dopamine-depleted striatum, immunohistochemistry and real-time reverse transcription polymerase chain reaction, respectively, were used. Finally, to determine the contribution of striatal 5-HT1AR to these effects, L-DOPA-primed hemiparkinsonian rats received bilateral intrastriatal microinfusions of ±8-OH-DPAT (0, 5, or 10 ,g/side), WAY100635 (5 ,g/side), or both (10 ,g + 5 ,g/side) 5 min after L-DOPA, after which AIMs and rotations were examined. Systemic ±8-OH-DPAT dose- and receptor-dependently attenuated L-DOPA-mediated AIMs and improved forelimb akinesia. Striatal c-fos immunoreactivity and PPD mRNA ipsilateral to the lesion were strongly induced by L-DOPA, while ±8-OH-DPAT suppressed these effects. Finally, intrastriatal infusions of ±8-OH-DPAT reduced AIMs while coinfusion of WAY100635 reversed its antidyskinetic effect. Collectively, these results support the hypothesis that the cellular and behavioral properties of 5-HT1AR agonists are conveyed in part via a population of functional 5-HT1AR within the striatum. © 2008 Wiley-Liss, Inc. [source] Gene expression in peripheral arterial chemoreceptorsMICROSCOPY RESEARCH AND TECHNIQUE, Issue 3 2002Estelle B. Gauda Abstract The peripheral arterial chemoreceptors of the carotid body participate in the ventilatory responses to hypoxia and hypercapnia, the arousal responses to asphyxial apnea, and the acclimatization to high altitude. In response to an excitatory stimuli, glomus cells in the carotid body depolarize, their intracellular calcium levels rise, and neurotransmitters are released from them. Neurotransmitters then bind to autoreceptors on glomus cells and postsynaptic receptors on chemoafferents of the carotid sinus nerve. Binding to inhibitory or excitatory receptors on chemoafferents control the electrical activity of the carotid sinus nerve, which provides the input to respiratory-related brainstem nuclei. We and others have used gene expression in the carotid body as a tool to determine what neurotransmitters mediate the response of peripheral arterial chemoreceptors to excitatory stimuli, specifically hypoxia. Data from physiological studies support the involvement of numerous putative neurotransmitters in hypoxic chemosensitivity. This article reviews how in situ hybridization histochemistry and other cellular localization techniques confirm, refute, or expand what is known about the role of dopamine, norepinephrine, substance P, acetylcholine, adenosine, and ATP in chemotransmission. In spite of some species differences, review of the available data support that 1) dopamine and norepinephrine are synthesized and released from glomus cells in all species and play an inhibitory role in hypoxic chemosensitivity; 2) substance P and acetylcholine are not synthesized in glomus cells of most species but may be made and released from nerve fibers innervating the carotid body in essentially all species; 3) adenosine and ATP are ubiquitous molecules that most likely play an excitatory role in hypoxic chemosensitivity. Microsc. Res. Tech. 59:153,167, 2002. © 2002 Wiley-Liss, Inc. [source] New insights into the effect of amorolfine nail lacquerMYCOSES, Issue 2 2005C. Flagothier Summary Despite improvements in antifungal strategies, the outcome of treating onychomycoses often remains uncertain. Several factors account for treatment failure, of which the pharmacokinetics and pharmacodynamics of the antifungal are of importance. The taxonomic nature and ungual location of the fungus cannot be neglected, besides the type of nail and its growth rate. In addition, the biological cycle of the fungus and the metabolic activity of the pathogen likely play a marked influence in drug response. The presence of natural antimicrobial peptides in the nail is also probably a key feature controlling the cure rates. There are many outstanding publications that cover the full spectrum of the field. The purpose of this review is to put in perspective some facets of activity of the topical treatment using amorolfine nail laquer. The antifungal activity of the drug is likely less pronounced in onychomycosis than that expected from conventional in vitro studies. However, the nail laquer formulation should reduce the propensity to form antifungal-resistant spores and limit the risk of reinfection. [source] Chlororespiration and cyclic electron flow around PSI during photosynthesis and plant stress responsePLANT CELL & ENVIRONMENT, Issue 9 2007DOMINIQUE RUMEAU ABSTRACT Besides major photosynthetic complexes of oxygenic photosynthesis, new electron carriers have been identified in thylakoid membranes of higher plant chloroplasts. These minor components, located in the stroma lamellae, include a plastidial NAD(P)H dehydrogenase (NDH) complex and a plastid terminal plastoquinone oxidase (PTOX). The NDH complex, by reducing plastoquinones (PQs), participates in one of the two electron transfer pathways operating around photosystem I (PSI), the other likely involving a still uncharacterized ferredoxin-plastoquinone reductase (FQR) and the newly discovered PGR5. The existence of a complex network of mechanisms regulating expression and activity of the NDH complex, and the presence of higher amounts of NDH complex and PTOX in response to environmental stress conditions the phenotype of mutants, indicate that these components likely play a role in the acclimation of photosynthesis to changing environmental conditions. Based on recently published data, we propose that the NDH-dependent cyclic pathway around PSI participates to the ATP supply in conditions of high ATP demand (such as high temperature or water limitation) and together with PTOX regulates cyclic electron transfer activity by tuning the redox state of intersystem electron carriers. In response to severe stress conditions, PTOX associated to the NDH and/or the PGR5 pathway may also limit electron pressure on PSI acceptor and prevent PSI photoinhibition. [source] Novel role of plasmacytoid dendritic cells in humans: Induction of interleukin-10,producing treg cells by plasmacytoid dendritic cells in patients with rheumatoid arthritis responding to therapyARTHRITIS & RHEUMATISM, Issue 1 2010Melina Kavousanaki Objective Reestablishing immune tolerance and long-term suppression of disease represent major therapeutic goals in rheumatoid arthritis (RA). Dendritic cells (DCs) likely play a central role in such regulation via the expansion and/or induction of Treg cells. The present study was undertaken to explore the contribution of DCs to the development of Treg cells in a human autoimmune disease setting. Methods DC subsets were characterized by flow cytometry in the peripheral blood and synovial fluid of patients with RA. Proliferation of and cytokine release by naive CD4+CD25, T cells were measured in cocultures of these cells with DCs from patients with RA and healthy controls. The suppressive capacity of DC-polarized T cells was explored in vitro by a standard suppression assay. Results Only very low numbers of both plasmacytoid DCs (CD303+) and myeloid DCs (CD1c+) were present in the peripheral blood of patients with active RA. In contrast, patients with therapy-induced remission of RA exhibited higher numbers of circulating plasmacytoid DCs. Mature plasmacytoid DCs from RA patients with low disease activity, but not those from healthy controls, expressed high levels of indoleamine 2,3-dioxygenase and promoted the differentiation of allogeneic naive CD4+CD25, T cells into interleukin-10,secreting Treg cells, or Tr1 cells, that showed poor proliferation in vitro. Importantly, these plasmacytoid DC,primed Treg cells potently suppressed the proliferation of autologous naive CD4+ T cells, in a dose-dependent manner. Conclusion These results demonstrate, for the first time, that human plasmacytoid DCs may be educated within the rheumatoid microenvironment to acquire a tolerogenic phenotype. Modulation of the immune response by plasmacytoid DCs might provide novel immune-based therapies in autoimmunity and transplantation. [source] Comparisons and connections between mean field dynamo theory and accretion disc theoryASTRONOMISCHE NACHRICHTEN, Issue 1 2010E.G. Blackman Abstract The origin of large scale magnetic fields in astrophysical rotators, and the conversion of gravitational energy into radiation near stars and compact objects via accretion have been subjects of active research for a half century. Magnetohydrodynamic turbulence makes both problems highly nonlinear, so both subjects have benefitted from numerical simulations.However, understanding the key principles and practical modeling of observations warrants testable semi-analytic mean field theories that distill the essential physics. Mean field dynamo (MFD) theory and alpha-viscosity accretion disc theory exemplify this pursuit. That the latter is a mean field theory is not always made explicit but the combination of turbulence and global symmetry imply such. The more commonly explicit presentation of assumptions in 20th century textbook MFDT has exposed it to arguably more widespread criticism than incurred by 20th century alpha-accretion theory despite complementary weaknesses. In the 21st century however, MFDT has experienced a breakthrough with a dynamical saturation theory that consistently agrees with simulations. Such has not yet occurred in accretion disc theory, though progress is emerging. Ironically however, for accretion engines, MFDT and accretion theory are presently two artificially uncoupled pieces of what should be a single coupled theory. Large scale fields and accretion flows are dynamically intertwined because large scale fields likely play a key role in angular momentum transport. I discuss and synthesize aspects of recent progress in MFDT and accretion disc theory to suggest why the two likely conspire in a unified theory (© 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source] Arabidopsis thaliana protein, ATK1, is a minus-end directed kinesin that exhibits non-processive movementCYTOSKELETON, Issue 3 2002Adam I. Marcus Abstract The microtubule cytoskeleton forms the scaffolding of the meiotic spindle. Kinesins, which bind to microtubules and generate force via ATP hydrolysis, are also thought to play a critical role in spindle assembly, maintenance, and function. The A. thaliana protein, ATK1 (formerly known as KATA), is a member of the kinesin family based on sequence similarity and is implicated in spindle assembly and/or maintenance. Thus, we want to determine if ATK1 behaves as a kinesin in vitro, and if so, determine the directionality of the motor activity and processivity character (the relationship between molecular "steps" and microtubule association). The results show that ATK1 supports microtubule movement in an ATP-dependent manner and has a minus-end directed polarity. Furthermore, ATK1 exhibits non-processive movement along the microtubule and likely requires at least four ATK1 motors bound to the microtubule to support movement. Based on these results and previous data, we conclude that ATK1 is a non-processive, minus-end directed kinesin that likely plays a role in generating forces in the spindle during meiosis. Cell Motil. Cytoskeleton 52:144,150, 2002. © 2002 Wiley-Liss, Inc. [source] Role of Sun Exposure in MelanomaDERMATOLOGIC SURGERY, Issue 4 2006GIL B. IVRY BS BACKGROUND Malignant melanoma is the third most common skin cancer in the United States. It is commonly thought that sun exposure is causative in these tumors. Recently, however, the significance of the role of sun exposure in melanoma has come into question. Some have suggested that other factors, such as genetics, play a larger role, and that sun protection may even be harmful. OBJECTIVE AND METHODS To investigate the role of sun exposure in melanoma etiology. An extensive review of basic science and clinical literature on this subject was conducted. RESULTS Although exceptions exist, sun exposure likely plays a large role in most melanomas. The pattern of this exposure, however, is not fully known, and controversy exists, especially in the use of sunscreens. Sun exposure may interact with genetic factors to cause melanomas, and sun protective measures appear to be prudent. CONCLUSIONS The cause of melanoma is probably variable and multifactorial. Sun exposure may play a primary or supporting role in most melanoma tumors. [source] Sieving mechanisms in polymeric matricesELECTROPHORESIS, Issue 3 2003Anna Sartori Abstract A critical review of the existing theoretical models and experimental evidences for sieving mechanisms during separation of macromolecules, paying particular attention to capillary electrophoresis applications is presented. Gel models (Ogston and reptation) have been successfully applied to highly entangled polymer solutions, where fast and efficient separations can occur. In order to account for the DNA/polymers collision-interaction mechanisms during separation in dilute solutions , characterized by a poorer resolution ,, approximated analytical models have been developed. An insight in the mechanism regulating the intermediate case of moderately entangled polymer solutions, for low fields and concentrations of small multiples of the overlap concentration c*, is given by the constraint release approach. This model proposes an upper limit of size separation, increasing with matrix concentration and molecular mass. Finally, the coupling between the reptative motion of the analytes and the effect of matrix constraint release very likely plays a fundamental role in the separation mechanism and requires therefore further and deeper investigation, both theoretically and experimentally. [source] Metabolic syndrome and three of its components as risk factors for recurrent ischaemic stroke presenting as large-vessel infarctionEUROPEAN JOURNAL OF NEUROLOGY, Issue 8 2008C.-W. Liou Background and purpose:, Although a clear protocol for reduction of recurrent ischaemic stroke (RIS) has been established, few studies have compared the stroke subtype distribution and risk factors between RIS and first-ever stroke (FES). Methods:, This one-year hospital-based study enrolled 587 FES and 475 RIS patients. Patients were categorized into four stroke subtypes according to a modified TOAST stroke subtype classification system. Risk factor profiles were compared between the two major stroke groups and between the corresponding four subtypes to discriminate the significant risk factors for RIS. Results:, A multivariate regression analysis identified hypertension (OR, 1.87; 95% CI, 1.34,2.62), diabetes mellitus (DM) (OR, 1.57; 95% CI, 1.22,2.02), low high-density lipoprotein (LHDL) (OR, 1.43; 95% CI, 1.08,1.88) and older age as significant RIS risk factors. The significance of the former three RIS factors was further recognized in its large-vessel subtype. Moreover, metabolic syndrome was significantly more common in the recurrent stroke group (P = 0.01), including its large-vessel subtype (P = 0.04). Progressively increasing odds ratios from 1.49 to 2.02, in accordance with increased number of diagnostic components of metabolic syndrome for recurrent large-vessel ischaemic stroke, were noted. Conclusions:, Metabolic syndrome likely plays a crucial role in the development of RIS, including large-vessel infarction in modern-day Taiwan. [source] Gonadal hormone modulation of hippocampal neurogenesis in the adultHIPPOCAMPUS, Issue 3 2006Liisa A.M. Galea Abstract Gonadal hormones modulate neurogenesis in the dentate gyrus (DG) of adult rodents in complex ways. Estradiol, the most potent estrogen, initially enhances and subsequently suppresses cell proliferation in the dentate gryus of adult female rodents. Much less is known about how estradiol modulates neurogenesis in the adult male rodent; however, recent evidence suggests that estradiol may have a moderate effect on cell proliferation but enhances cell survival in the DG of newly synthesized cells but only when estradiol is administered during a specific stage in the cell maturation cycle in the adult male rodent. Testosterone likely plays a role in adult neurogenesis, although there have been no direct studies to address this. However, pilot studies from our laboratory suggest that testosterone up-regulates cell survival but not cell proliferation in the DG of adult male rats. Progesterone appears to attenuate the estradiol-induced enhancement of cell proliferation. Neurosteroids such as allopregnalone decrease neurogenesis in adult rodents, while pregnancy and motherhood differentially regulate adult neurogenesis in the adult female rodent. Very few studies have investigated the effects of gonadal hormones on male rodents; however, studies have indicated that there is a gender difference in the response to hormone-regulated hippocampal neurogenesis in the adult. Clearly, more work needs to be done to elucidate the effects of gonadal hormones on neurogenesis in the DG of both male and female rodents. © 2006 Wiley-Liss Inc. [source] Involvement of IQGAP3, a regulator of Ras/ERK-related cascade, in hepatocyte proliferation in mouse liver regeneration and development,JOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2009Koshi Kunimoto The spatio-temporal regulation of hepatocyte proliferation is a critical issue in liver regeneration. Here, in normal and regenerating liver as well as in developing liver, we examined its expression/localization of IQGAP3, which was most recently reported as a Ras/Rac/Cdc42-binding proliferation factor associated with cell,cell contacts in epithelial-type cells. In parallel, the expression/localization of Rac/Cdc42-binding IQGAP1/2 was examined. IQGAP3 showed a specific expression in proliferating hepatocytes positive for the proliferating marker Ki-67, the levels of expressions of mRNAs and proteins were significantly increased in hepatocytes in liver regeneration and development. In immunofluorescence, IQGAP3 was highly enriched at cell,cell contacts of hepatocytes. IQGAP1 and IQGAP2 were exclusively expressed in Kupffer and sinusoidal endothelial cells, respectively, in normal, regenerating, and developing liver. The expression of IQGAP1, but not of IQGAP2, was increased in CCl4 -induced (but not in partial hepatectomy-induced) liver regeneration. Exclusive expression/localization of IQGAP3 to hepatocytes in the liver likely reflects the specific involvement of the IQGAP3/Ras/ERK signaling cascade in hepatocyte proliferation in addition to the previously identified signaling pathways, possibly by integrating cell,cell contact-related proliferating signaling events. On the other hand, the Rac/Cdc42-binding properties of IQGAP1/2/3 may be related to the distinct modes of remodeling due to the different strategies which induced proliferation of liver cells; partial hepatectomy, CCl4 injury, or embryonic development. Thus, the functional orchestration of Ras and the Ras homologous (Rho) family proteins Rac/Cdc42 likely plays a critical role in liver regeneration and development. J. Cell. Physiol. 220: 621,631, 2009. © 2009 Wiley-Liss, Inc. [source] The zinc-finger protein ZFR is critical for Staufen 2 isoform specific nucleocytoplasmic shuttling in neuronsJOURNAL OF NEUROCHEMISTRY, Issue 1 2006George Elvira Abstract In mammalian neurons, transport and translation of mRNA to individual potentiated synapses is believed to occur via a heterogeneous population of RNA granules. To identify components of Staufen2-containing granules, we used the yeast two-hybrid system. A mouse fetal cDNA library was screened with the N-terminal fragment of Staufen2 as bait. ZFR, a three zinc finger protein, was identified as an interacting protein. Confocal microscopy showed that ZFR, although mainly nuclear, was also found in the somatodendritic compartment of primary hippocampal neurons where it localized as granule-like structures. Co-localization with Staufen2 was observed in several granules. Biochemical analyses (immunoprecipitation, cell fractionation) further confirmed the ZFR/Staufen2 association. ZFR was shown to interact with at least the Staufen262 isoform, but not with Staufen1. ZFR also co-fractionated with ribosomes and Staufen259 and Staufen252 in a sucrose gradient. Interestingly, knockdown expression of ZFR through RNA interference in neurons relocated specifically the Staufen262, but not the Staufen259, isoform to the nucleus. Our results demonstrate that ZFR is a native component of Staufen2-containing granules and likely plays its role during early steps of RNA transport and localization. They also suggest that one of these roles may be linked to Staufen262 -containing RNA granule formation in the nucleus and/or to their nucleo-cytoplasmic shuttling. [source] Dynamic expression of de novo DNA methyltransferases Dnmt3a and Dnmt3b in the central nervous systemJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2005Jian Feng Abstract To explore the role of DNA methylation in the brain, we examined the expression pattern of de novo DNA methyltransferases Dnmt3a and Dnmt3b in the mouse central nervous system (CNS). By comparing the levels of Dnmt3a and Dnmt3b mRNAs and proteins in the CNS, we showed that Dnmt3b is detected within a narrow window during early neurogenesis, whereas Dnmt3a is present in both embryonic and postnatal CNS tissues. To determine the precise pattern of Dnmt3a and Dnmt3b gene expression, we carried out X-gal histochemistry in transgenic mice in which the lacZ marker gene is knocked into the endogenous Dnmt3a or Dnmt3b gene locus (Okano et al. [1999] Cell 99:247,257). In Dnmt3b - lacZ transgenic mice, X-gal-positive cells are dispersed across the ventricular zone of the CNS between embryonic days (E) 10.5 and 13.5 but become virtually undetectable in the CNS after E15.5. In Dnmt3a - lacZ mice, X-gal signal is initially observed primarily in neural precursor cells within the ventricular and subventricular zones between E10.5 and E17.5. However, from the newborn stage to adulthood, Dnmt3a X-gal signal was detected predominantly in postmitotic CNS neurons across all the regions examined, including olfactory bulb, cortex, hippocampus, striatum, and cerebellum. Furthermore, Dnmt3a signals in CNS neurons increase during the first 3 weeks of postnatal development and then decline to a relatively low level in adulthood, suggesting that Dnmt3a may be of critical importance for CNS maturation. Immunocytochemistry experiments confirmed that Dnmt3a protein is strongly expressed in neural precursor cells, postmitotic CNS neurons, and oligodendrocytes. In contrast, glial fibrillary acidic protein-positive astrocytes exhibit relatively weak or no Dnmt3a immunoreactivity in vitro and in vivo. Our data suggest that whereas Dnmt3b may be important for the early phase of neurogenesis, Dnmt3a likely plays a dual role in regulating neurogenesis prenatally and CNS maturation and function postnatally. © 2005 Wiley-Liss, Inc. [source] Identification and characterization of TSAP, a novel gene specifically expressed in testis during spermatogenesisMOLECULAR REPRODUCTION & DEVELOPMENT, Issue 9 2007Li Bin Abstract Through in silico screens, we have identified many previously uncharacterized genes that display similar expression patterns as the mouse Dazl gene, a germ line-specific marker. Here, we report the identification and characterization of one of these novel genes. TSAP gene encodes a protein with 350 amino acids and contains five ankyrin repeats and a PEST sequence motif. Furthermore, we have generated an anti-TSAP antibody and have used three different approaches (RT-PCR, in situ hybridization, and immunohistochemistry) to investigate the expression profiles of TSAP mRNAs and proteins. TSAP is specifically expressed in testis, but not in other tissues such as ovary. Within the testis, TSAP is detected 10 days after birth and is mainly expressed in spermatocytes (ST) and later stage of germ cells, but not in spermatogonia (SG) or sertoli cells. Therefore, TSAP protein likely plays a role in spermatogenesis. Mol. Reprod. Dev. 74: 1141,1148, 2007. © 2007 Wiley-Liss, Inc. [source] Parkinson's disease, stroke, and related epidemiologyMOVEMENT DISORDERS, Issue 11 2005Andrew Nataraj MD Abstract We investigated the prevalence of cerebrovascular disease and other comorbidities in Parkinson's disease (PD) patients compared to the general population. Five hundred PD patients were chosen randomly from one author's (A.H.R.) database. Age- and sex-matched controls were derived from 270 patients with essential tremor from the same database and from 490 patients in a general practitioner's database. Age, hypertensive status, smoking status, coronary artery disease, orthostatic hypotension, diabetes mellitus, and symptomatic cerebrovascular disease (stroke or transient ischemic attack) were assessed. Statistical analysis was performed using Pearson ,2 testing and binary logistic regression analysis. The prevalence of coronary artery disease, hypertension, diabetes mellitus, and orthostatic hypotension was similar among groups. The PD group had more patients who never smoked and less current smokers than the other groups. While there were similar frequencies of symptomatic cerebrovascular disease among groups, the prevalence of stroke was lower in PD patients. This difference disappeared upon stratification into groups based on smoking status and in the addition of smoking as a covariate in the multivariate analysis. Diminished smoking in PD patients likely plays a role in our finding of decreased stroke in patients with PD. Increased access to appropriate neurological care and subsequent prevention of stroke after a warning transient ischemic attack may also play a role, as may diminished levels of excitotoxic neurotransmitters in PD patients. © 2005 Movement Disorder Society [source] The differential regulation of Smad7 in kidney tubule cells by connective tissue growth factor and transforming growth factor-beta1NEPHROLOGY, Issue 3 2007WEIER QI Summary: Aims: Smad7 is an inhibitory Smad that regulates transforming growth factor-, (TGF-,) signaling. Connective tissue growth factor (CTGF) is recognized as a potent downstream mediator of the fibrogenic effects of TGF-,1. SMAD binding sites have been identified in both TGF-, and CTGF promoters. The effect of CTGF on Smad7 expression and its role in the regulation of Smad7 induced by TGF-,1 in renal tubular cells is unknown. Methods: Human model of proximal tubular cells (HK-2 cells) was used and confirmed using a diabetic rat model. RT-PCR was performed to measure Smad7, TGF-,1 and Smad2 and ELISA was performed to measure active TGF-,1. CTGF or TGF-,1 was silenced in HK-2 cells using siRNA methodology. Results: TGF-,1 induced Smad7 in a time-dependent manner, peaking at 30 min (P < 0.0005) but sustained up to 24 hrs (p < 0.005). Conversely, CTGF reduced Smad7, which was maximal at 24 hrs (p < 0.05). This was supported by our in vivo data demonstrating that CTGF protein significantly increased while Smad7 mRNA level was reduced in a diabetic rat model. The basal expression level of Smad7 decreased in TGF-,1 silenced cells compared to cells transfected with non-specific siRNA (p < 0.0005). The basal expression level of Smad7 increased in CTGF silenced cells (p < 0.05), which was increased by TGF-,1 (p < 0.005). Both mRNA and protein levels of TGF-,1 decreased in CTGF silenced cells (p < 0.05 and p < 0.005 respectively) accompanied by reduction in Smad2 mRNA level in CTGF silenced cells. Conclusions: Smad7 is induced rapidly by TGF-,1 limiting the response to TGF-,1. CTGF likely plays a key role in promoting TGF-,1 activity by decreasing the availability of Smad7 and increasing Smad2. [source] Wallerian Degeneration: A Major Component of Early Axonal Pathology in Multiple SclerosisBRAIN PATHOLOGY, Issue 5 2010Tomasz Dziedzic Abstract Axonal loss is a major component of the pathology of multiple sclerosis (MS) and the morphological basis of permanent clinical disability. It occurs in demyelinating plaques but also in the so-called normal-appearing white matter (NAWM). However, the contribution of Wallerian degeneration to axonal pathology is not known. Here, we analyzed the extent of Wallerian degeneration and axonal pathology in periplaque white matter (PPWM) and lesions in early multiple sclerosis biopsy tissue from 63 MS patients. Wallerian degeneration was visualized using an antibody against the neuropeptide Y receptor Y1 (NPY-Y1R). The number of SMI-32-positive axons with non-phosphorylated neurofilaments was significantly higher in both PPWM and plaques compared to control white matter. APP-positive, acutely damaged axons were found in significantly higher numbers in plaques compared to PPWM. Strikingly, the number of NPY-Y1R-positive axons undergoing Wallerian degeneration was significantly higher in PPWM and plaques than in control WM. NPY-Y1R-positive axons in PPWM were strongly correlated to those in the lesions. Our results show that Wallerian degeneration is a major component of axonal pathology in the periplaque white matter in early MS. It may contribute to radiological changes observed in early MS and most likely plays a major role in the development of disability. [source] Genetic link between p53 and genes required for formation of the zonula adherens junctionCANCER SCIENCE, Issue 5 2004Masamitsu Yamaguchi Ectopic expression of human p53 in Drosophila eye imaginal disc cells induces apoptosis and results in a rough eye phenotype in the adult flies. We have screened Drosophila stocks to identify mutations that enhance or suppress the p53-induced rough eye phenotype. One of the dominant enhancers of the p53-induced rough eye phenotype corresponds to a loss-of-function mutation of the crumbs gene, which is essential for the biogenesis of the zonula adherens junction and the establishment of apical polarity in epithelial cells. Enhancement of p53-induced apoptosis in the eye imaginal discs by a half-reduction of the crumbs gene dose was confirmed by a TUNEL method. Furthermore, mutations of genes for Shotgun (Drosophila E-cadherin) and Armadillo (Drosophila,-catenin), the two main components of the adherens junction, also strongly enhanced the p53-induced rough eye phenotype. These results suggest that human p53 senses subtle abnormality at the adherens junction or in signals derived from the junction, and consequently induces apoptosis to remove abnormal cells from tissue. Thus p53 likely plays a role as a guardian of the tissue not only by sensing the damaged DNA, but also by sensing signals from the adherens junction. [source] | |||||||||||||||||||||||||