bluuebunny/crossref_metadata_2025_split huggingface dataset:
Use of a Vertical Vorticity Equation in Variational Dual-Doppler Wind Analysis
Authors: Shapiro Alan , Potvin Corey K. , Gao Jidong 
Published: May 2009

Abstract
The utility of the anelastic vertical vorticity equation in a weak-constraint (least squares error) variational dual-Doppler wind analysis procedure is explored. The analysis winds are obtained by minimizing a cost function accounting for the discrepancies between observed and analyzed radial winds, errors in the mass conservation equation, errors in the anelastic vertical vorticity equation, and spatial smoothness constraints. By using Taylor’s frozen-turbulence hypothesis to shift analysis winds to observation points, discrepancies between radially projected analysis winds and radial wind observations can be calculated at the actual times and locations the data are acquired. The frozen-turbulence hypothesis is also used to evaluate the local derivative term in the vorticity equation. Tests of the analysis procedure are performed with analytical pseudo-observations of an array of translating and temporally decaying counterrotating updrafts and downdrafts generated from a Beltrami flow solution of the Navier–Stokes equations. The experiments explore the value added to the analysis by the vorticity equation constraint in the common scenario of substantial missing low-level data (radial wind observations at heights beneath 1.5 km are withheld from the analysis). Experiments focus on the sensitivity of the most sensitive analysis variable—the vertical velocity component—to values of the weighting coefficients, volume scan period, number of volume scans, and errors in the estimated frozen-turbulence pattern-translation components. Although the vorticity equation constraint is found to add value to many of these analyses, the analysis can become significantly degraded if estimates of the pattern-translation components are largely in error or if the frozen-turbulence hypothesis itself breaks down. However, tests also suggest that these negative impacts can be mitigated if data are available in a rapid-scan mode.
An Extratropical Air–Sea Interaction over the North Pacific in Association with a Preceding El Niño Episode in Early Summer
Authors: Wang Yafei , Lupo Anthony R. 
Published: May 2009

Abstract
Using data for the month of June from 1951 through 2000, this study examined the air–sea interactions over the North Pacific after El Niño matured during the preceding fall season. The principal findings of this work are the following: 1) a coherent region near the international date line (IDL) in the extratropical North Pacific revealed an area of significant negative correlations (SNCs) between the preceding November sea surface temperature (SST) in the Niño-3 region and the June SST in the North Pacific. Also, two indexes of the June Okhotsk high show a significant positive correlation with the November SST in the Niño-3 region during the 1963–2000 period. 2) The strong southeastward wave flux from the upstream area of the Okhotsk Sea over much of the North Pacific in the midlatitudes is associated with a strong preceding El Niño event, the development of the Okhotsk high, and a negative 500-hPa geopotential height/SST anomaly around the coherent region. The stationary wave propagation plays a major part in maintaining the low SSTs in the coherent region and suppressing the northward progress of the subtropical high. This process partially bridges the connection between the central equatorial Pacific warming (CEPW) and the East Asian summer monsoon. 3) A wave train–like anomaly in the SST (tilted northwest–southeast) was established and maintained in the North Pacific during the summer of 1998. This coincided with the direction of the atmospheric Rossby wave propagation as the strong southeastward wave flux was scattered over the midlatitude North Pacific. This event provides solid evidence that Rossby wave propagation plays an important role in forming an oceanic temperature wave train in the extratropical Pacific through the barotropic process.
The Method for Object-Based Diagnostic Evaluation (MODE) Applied to Numerical Forecasts from the 2005 NSSL/SPC Spring Program
Authors: Davis Christopher A. , Brown Barbara G. , Bullock Randy , Halley-Gotway John 
Published: May 2009

Abstract
The authors use a procedure called the method for object-based diagnostic evaluation, commonly referred to as MODE, to compare forecasts made from two models representing separate cores of the Weather Research and Forecasting (WRF) model during the 2005 National Severe Storms Laboratory and Storm Prediction Center Spring Program. Both models, the Advanced Research WRF (ARW) and the Nonhydrostatic Mesoscale Model (NMM), were run without a traditional cumulus parameterization scheme on horizontal grid lengths of 4 km (ARW) and 4.5 km (NMM). MODE was used to evaluate 1-h rainfall accumulation from 24-h forecasts valid at 0000 UTC on 32 days between 24 April and 4 June 2005. The primary variable used for evaluation was a “total interest” derived from a fuzzy-logic algorithm that compared several attributes of forecast and observed rain features such as separation distance and spatial orientation. The maximum value of the total interest obtained by comparing an object in one field with all objects in the comparison field was retained as the quality of matching for that object. The median of the distribution of all such maximum-interest values was selected as a metric of the overall forecast quality.
Results from the 32 cases suggest that, overall, the configuration of the ARW model used during the 2005 Spring Program performed slightly better than the configuration of the NMM model. The primary manifestation of the differing levels of performance was fewer false alarms, forecast rain areas with no observed counterpart, in the ARW. However, it was noted that the performance varied considerably from day to day, with most days featuring indistinguishable performance. Thus, a small number of poor NMM forecasts produced the overall difference between the two models.
A novel human gamma-globin gene vector for genetic correction of sickle cell anemia in a humanized sickle mouse model: critical determinants for successful correction
Authors: Perumbeti Ajay , Higashimoto Tomoyasu , Urbinati Fabrizia , Franco Robert , Meiselman Herbert J. , Witte David , Malik Punam 
Published: May 2009

Abstract
We show that lentiviral delivery of human γ-globin gene under β-globin regulatory control elements in hematopoietic stem cells (HSCs) results in sufficient postnatal fetal hemoglobin (HbF) expression to correct sickle cell anemia (SCA) in the Berkeley “humanized” sickle mouse. Upon de-escalating the amount of transduced HSCs in transplant recipients, using reduced-intensity conditioning and varying gene transfer efficiency and vector copy number, we assessed critical parameters needed for correction. A systematic quantification of functional and hematologic red blood cell (RBC) indices, organ pathology, and life span was used to determine the minimal amount of HbF, F cells, HbF/F-cell, and gene-modified HSCs required for correcting the sickle phenotype. We show that long-term amelioration of disease occurred (1) when HbF exceeded 10%, F cells constituted two-thirds of the circulating RBCs, and HbF/F cell was one-third of the total hemoglobin in sickle RBCs; and (2) when approximately 20% gene-modified HSCs repopulated the marrow. Moreover, we show a novel model using reduced-intensity conditioning to determine genetically corrected HSC threshold that corrects a hematopoietic disease. These studies provide a strong preclinical model for what it would take to genetically correct SCA and are a foundation for the use of this vector in a human clinical trial.
RhoGDIβ-induced hypertrophic growth in H9c2 cells is negatively regulated by ZAK
Authors: Huang Chih-Yang , Yang Li-Chiu , Liu Kuan-Yu , Liao Pao-Hsin , Chou Janet Ing-Yuh , Chou Ming-Yung , Lin Wei-Wen , Yang Jaw-Ji 
Published: May 2009

Abstract
We found that overexpression of RhoGDIβ, a Rho GDP dissociation inhibitor, induced hypertrophic growth and suppressed cell cycle progression in a cultured cardiomyoblast cell line. Knockdown of RhoGDIβ expression by RNA interference blocked hypertrophic growth. We further demonstrated that RhoGDIβ physically interacts with ZAK and is phosphorylated by ZAK in vitro, and this phosphorylation negatively regulates RhoGDIβ functions. Moreover, the ZAK-RhoGDIβ interaction may maintain ZAK in an inactive hypophosphorylated form. These two proteins could negatively regulate one another such that ZAK suppresses RhoGDIβ functions through phosphorylation and RhoGDIβ counteracts the effects of ZAK by physical interaction. Knockdown of ZAK expression in ZAK- and RhoGDIβ-expressing cells by ZAK-specific RNA interference restored the full functions of RhoGDIβ.
Effects of human parvovirus B19 VP1 unique region protein on macrophage responses
Authors: Tzang Bor-Show , Chiu Chun-Ching , Tsai Chun-Chou , Lee Yi-Ju , Lu I-Jung , Shi Jing-Yu , Hsu Tsai-Ching 
Published: May 2009

AbstractBackgroundActivity of secreted phospholipase A (sPLA2) has been implicated in a wide range of cellular responses. However, little is known about the function of human parvovirus B19-VP1 unique region (VP1u) with sPLA2 activity on macrophage.MethodsTo investigate the roles of B19-VP1u in response to macrophage, phospholipase A2 activity, cell migration assay, phagocytosis activity, metalloproteinase assay, RT-PCR and immunoblotting were performed.ResultsIn the present study, we report that migration, phagocytosis, IL-6, IL-1β mRNA, and MMP9 activity are significantly increased in RAW264.7 cells by B19-VP1u protein with sPLA2 activity, but not by B19-VP1uD175A protein that is mutated and lacks sPLA2 activity. Additionally, significant increases of phosphorylated ERK1/2 and JNK proteins were detected in macrophages that were treated with B19-VP1u protein, but not when they were treated with B19-VP1uD175A protein.ConclusionTaken together, our experimental results suggest that B19-VP1u with sPLA2 activity affects production of IL-6, IL-1β mRNA, and MMP9 activity, possibly through the involvement of ERK1/2 and JNK signaling pathways. These findings could provide clues in understanding the role of B19-VP1u and its sPLA2 enzymatic activity in B19 infection and B19-related diseases.
Dihydroartemisinin (DHA) induces caspase-3-dependent apoptosis in human lung adenocarcinoma ASTC-a-1 cells
Authors: Lu Ying-Ying , Chen Tong-Sheng , Qu Jun-Le , Pan Wen-Liang , Sun Lei , Wei Xun-Bin 
Published: May 2009

Abstract

Background
Dihydroartemisinin (DHA), a semi-synthetic derivative of artemisinin, isolated from the traditional Chinese herb Artemisia annua, is recommended as the first-line anti-malarial drug with low toxicity. DHA has been shown to possess promising anticancer activities and induce cancer cell death through apoptotic pathways, although the molecular mechanisms are not well understood.

Methods
In this study, cell counting kit (CCK-8) assay was employed to evaluate the survival of DHA-treated ASTC-a-1 cells. The induction of apoptosis was detected by Hoechst 33258 and PI staining as well as flow cytometry analysis. Collapse of mitochondrial transmembrane potential (ΔΨm) was measured by dynamic detection under a laser scanning confocal microscope and flow cytometry analysis using Rhodamine123. Caspase-3 activities measured with or without Z-VAD-fmk (a broad spectrum caspase inhibitor) pretreatment by FRET techniques, caspase-3 activity measurement, and western blotting analysis.

Results
Our results indicated that DHA induced apoptotic cell death in a dose- and time-dependent manner, which was accompanied by mitochondrial morphology changes, the loss of ΔΨm and the activation of caspase-3.

Conclusion
These results show for the first time that DHA can inhibit proliferation and induce apoptosis via caspase-3-dependent mitochondrial death pathway in ASTC-a-1 cells. Our work may provide evidence for further studies of DHA as a possible anticancer drug in the clinical treatment of lung adenocarcinoma.
Ischemic conditioning by short periods of reperfusion attenuates renal ischemia/reperfusion induced apoptosis and autophagy in the rat
Authors: Wu Hsing-Hui , Hsiao Tzu-Yu , Chien Chiang-Ting , Lai Ming-Kuen 
Published: May 2009

Abstract
Prolonged ischemia amplified iscehemia/reperfusion (IR) induced renal apoptosis and autophagy. We hypothesize that ischemic conditioning (IC) by a briefly intermittent reperfusion during a prolonged ischemic phase may ameliorate IR induced renal dysfunction. We evaluated the antioxidant/oxidant mechanism, autophagy and apoptosis in the uninephrectomized Wistar rats subjected to sham control, 4 stages of 15-min IC (I15 × 4), 2 stages of 30-min IC (I30 × 2), and total 60-min ischema (I60) in the kidney followed by 4 or 24 hours of reperfusion. By use of ATP assay, monitoring O2
-. amounts, autophagy and apoptosis analysis of rat kidneys, I60 followed by 4 hours of reperfusion decreased renal ATP and enhanced reactive oxygen species (ROS) level and proapoptotic and autophagic mechanisms, including enhanced Bax/Bcl-2 ratio, cytochrome C release, active caspase 3, poly-(ADP-ribose)-polymerase (PARP) degradation fragments, microtubule-associated protein light chain 3 (LC3) and Beclin-1 expression and subsequently tubular apoptosis and autophagy associated with elevated blood urea nitrogen and creatinine level. I30 × 2, not I15 × 4 decreased ROS production and cytochrome C release, increased Manganese superoxide dismutase (MnSOD), Copper-Zn superoxide dismutase (CuZnSOD) and catalase expression and provided a more efficient protection than I60 against IR induced tubular apoptosis and autophagy and blood urea nitrogen and creatinine level. We conclude that 60-min renal ischemia enhanced renal tubular oxidative stress, proapoptosis and autophagy in the rat kidneys. Two stages of 30-min ischemia with 3-min reperfusion significantly preserved renal ATP content, increased antioxidant defense mechanisms and decreased ischemia/reperfusion enhanced renal tubular oxidative stress, cytosolic cytochrome C release, proapoptosis and autophagy in rat kidneys.
STAT2 hypomorphic mutant mice display impaired dendritic cell development and antiviral response
Authors: Chen Lan-Sun , Wei Pei-Chi , Liu Taming , Kao Chung-Hsuan , Pai Li-Mei , Lee Chien-Kuo 
Published: May 2009

AbstractInterferons (IFNs) are key regulators for both innate and adaptive immune responses. By screening ENU-mutagenized mice, we identified a pedigree- P117 which displayed impaired response to type I, but not type II, IFNs. Through inheritance test, genetic mapping and sequencing, we found a T to A point mutation in the 5' splice site of STAT2 intron 4–5, leading to cryptic splicing and frame shifting. As a result, the expression of STAT2 protein was greatly diminished in the mutant mice. Nonetheless, a trace amount of functional STAT2 protein was still detectable and was capable of inducing, though to a lesser extent, IFNα-downstream gene expressions, suggesting that P117 is a STAT2 hypomorphic mutant. The restoration of mouse or human STAT2 gene in P117 MEFs rescued the response to IFNα, suggesting that the mutation in STAT2 is most likely the cause of the phenotypes seen in the pedigree. Development of different subsets of lymphocytes appeared to be normal in the mutant mice except that the percentage and basal expression of CD86 in splenic pDC and cDC were reduced. In addition,in vitroFlt3L-dependent DC development and TLR ligand-mediated DC differentiationwerealso defective in mutant cells. These results suggest that STAT2 positively regulates DC development and differentiation. Interestingly, a severe impairment of antiviral state and increased susceptibility to EMCV infection were observed in the mutant MEFs and mice, respectively, suggesting that the remaining STAT2 is not sufficient to confer antiviral response. In sum, the new allele of STAT2 mutant reported here reveals a role of STAT2 for DC development and a threshold requirement for full functions of type I IFNs.
Spatiotemporal expression of histone acetyltransferases, p300 and CBP, in developing embryonic hearts
Authors: Chen Guozhen , Zhu Jing , Lv Tiewei , Wu Gang , Sun Huichao , Huang Xupei , Tian Jie 
Published: May 2009

AbstractHistone acetyltransferases (HATs), p300 and cAMP response element binding protein (CREB)-binding protein (CBP) are two structurally related transcriptional co-activators that activate expression of many eukaryotic genes involved in cellular growth and signaling, muscle differentiation and embryogenesis. However, whether these proteins play important and different roles in mouse cardiogenesis is not clear. Here, we investigate the protein distributions and mRNA expression of the two HATs in embryonic and adult mouse heart during normal heart development by using immunohistochemical and RT-PCR techniques. The data from immunohistochemical experiments revealed that p300 was extensively present in nearly every region of the hearts from embryonic stages to the adulthood. However, no CBP expression was detected in embryonic hearts at day E7.5. CBP expression appeared at the later stages, and the distribution of CBP was less than that of p300. In the developmental hearts after E10.5, both for p300 and CBP, the mRNA expression levels reached a peak on day E10.5, and then were gradually decreased afterwards. These results reveal that both p300 and CBP are related to embryonic heart development. The dynamic expression patterns of these two enzymes during mouse heart development indicate that they may play an important role on heart development. However, there is a difference in spatiotemporal expression patterns between these two enzymes during heart development. The expression of p300 is earlier and more predominate, suggesting that p300 may play a more important role in embryonic heart development especially during cardiac precursor cell induction and interventricular septum formation.
Genistein-mediated inhibition of glycosaminoglycan synthesis, which corrects storage in cells of patients suffering from mucopolysaccharidoses, acts by influencing an epidermal growth factor-dependent pathway
Authors: Jakóbkiewicz-Banecka Joanna , Piotrowska Ewa , Narajczyk Magdalena , Barańska Sylwia , Węgrzyn Grzegorz 
Published: May 2009

Abstract

Background
Mucopolysaccharidoses (MPS) are inherited metabolic disorders caused by mutations leading to dysfunction of one of enzymes involved in degradation of glycosaminoglycans (GAGs). Due to their impaired degradation, GAGs accumulate in cells of patients, which results in dysfunction of tissues and organs. Substrate reduction therapy is one of potential treatment of these diseases. It was demonstrated previously that genistein (4', 5, 7-trihydroxyisoflavone) inhibits synthesis and reduces levels of GAGs in cultures of fibroblasts of MPS patients. Recent pilot clinical study indicated that such a therapy may be effective in MPS III (Sanfilippo syndrome).

Methods
To learn on details of the molecular mechanism of genistein-mediated inhibition of GAG synthesis, efficiency of this process was studied by measuring of incorporation of labeled sulfate, storage of GAGs in lysosomes was estimated by using electron microscopic techniques, and efficiency of phosphorylation of epidermal growth factor (EGF) receptor was determined by using an ELISA-based assay with fluorogenic substrates.

Results
Effects of genistein on inhibition of GAG synthesis and accumulation in fibroblasts from patients suffering from various MPS types were abolished in the presence of an excess of EGF, and were partially reversed by an increased concentration of genistein. No such effects were observed when an excess of 17β-estradiol was used instead of EGF. Moreover, EGF-mediated stimulation of phsophorylation of the EGF receptor was impaired in the presence of genistein in both wild-type and MPS fibroblasts.

Conclusion
The results presented in this report indicate that the mechanism of genistein-mediated inhibition of GAG synthesis operates through epidermal growth factor (EGF)-dependent pathway.
In vitro study of the tocolytic effect of oroxylin A from Scutellaria baicalensis root
Authors: Shih Huey-Chuan , Hsu Chun-Sen , Yang Ling-Ling 
Published: May 2009

Abstract
Scutellariae Radix is one of the well-known tocolytic Chinese herbs. Oroxylin A is isolated from the root of Scutellaria baicalensis. The main syndrome of preterm birth is caused by uterus contractions from excitatory factors. Administration of tocolytic agents is a strategy to prevent the occurrence of preterm births. The aim of this study was to investigate the effects of oroxylin A on contractions of uterine strips isolated from non-pregnant female Wistar rats (250~350 g). Contractions of the uterus were induced with acetylcholine (Ach) (1 μM), PGF2α (0.1 μM), oxytocin (10-3 U/ml), KCl (56.3 mM), tetraethylammonium (TEA; 1 and 10 mM), 4-aminopyridine (4-AP; 5 mM), glipizide (30 μM), a nitric oxide synthase (NOS) inhibitor (LNNA; 10-3M), a β-receptor blocker (propranolol; 10 μM), and a cyclooxygenase inhibitor (indomethacin; 60 μM). The inhibitory effects of the amplitude and frequency of spontaneous contractions by oroxylin A were antagonized with Ach (IC50 22.85 μM), PGF2α (IC5027.28 μM), oxytocin (IC50 12.34 μM), TEA; 1 and 10 mM (IC50 52.73 and 76.43 μM), 4-AP (IC50 67.16 μM), and glipizide (IC5027.53 μM), but oroxylin A was not influenced by Ca2+-free medium, LNNA, propranolol, or indomethacin. Otherwise, oroxylin A-mediated relaxation of the rat uterus might occur through opening of uterine calcium-dependent potassium channels or adenosine triphosphate potassium channel activation. This suggests that oroxylin A is the tocolytic principle constituent of Scutellariae Radix, and oroxylin A may provide a lead compound for new tocolytic drug development in the future.
Antigen-driven bystander effect accelerates epicutaneous sensitization with a new protein allergen
Authors: Wang Li-Fang , Chen Jau-Shiuh , Hsu Chih-Jung , Liu Ching-Yi , Yu Jhang-Sian , Miaw Shi-Chuen 
Published: May 2009

AbstractExposure to protein allergen epicutaneously, inducing a Th2-dominant immune response, sensitizes the host to the development of atopic disease. Antigen-driven bystander effect demonstrates that polarized T cells could instruct naïve T cells to differentiate into T cells with similar phenotype. In this study, we aimed to determine the contribution of antigen-driven bystander effect on epicutaneous sensitization with a newly introduced protein allergen. BALB/c mice were immunized intraperitoneally with BSA emulsified in alum, known to induce a Th2 response, three weeks before given BSA and OVA epicutaneously. Lymph node cells from these mice restimulated with OVA secreted higher levels IL-4, IL-5 and IL-13 as compared with cells from mice without BSA immunization. In addition, BALB/c mice immunized subcutaneously with BSA emulsified in complete Freund's adjuvant, known to induce a Th1-predominant response, also induced higher Th1 as well as Th2 cytokine response when restimulated with OVA as compared with mice without immunization. We demonstrated that subcutaneous immunization with BSA in CFA induced Th2 as well as Th1 response. The threshold of epicutaneous sensitization to OVA was also reduced, possibly due to increased expressions of IL-4 and IL-10 in the draining lymph nodes during the early phase of sensitization. In conclusion, antigen-driven bystander effect, whether it is of Th1- or Th2-predominant nature, can accelerate epicutaneous sensitization by a newly introduced protein allergen. These results provide a possible explanation for mono- to poly-sensitization spread commonly observed in atopic children.