bluuebunny/crossref_metadata_2025_split huggingface dataset:
Muscle‐specific expression of the smyd1 gene is controlled by its 5.3‐kb promoter and 5′‐flanking sequence in zebrafish embryos
Authors: Du Shao Jun , Rotllant Josep , Tan Xungang 
Published: October 2006

AbstractZebrafish SmyD1 is a SET and MYND domain‐containing protein that plays an important role in myofiber maturation and muscle contraction. SmyD1 is required for myofibril organization and sarcomere assembly during myofiber maturation. Whole‐mount in situ hybridization revealed that smyd1 mRNAs are specifically expressed in skeletal and cardiac muscles in zebrafish embryos. However, it is unknown if smyd1 is expressed in other striated muscles, such as cranial and fin muscles, and moreover, the regulatory elements required for its muscle‐specific expression. We report here the analyses of smyd1 expression using smyd1‐gfp transgenic zebrafish. smyd1‐gfp transgenic zebrafish were generated using the 5.3‐kb smyd1 promoter and its 5′‐flanking sequence. GFP expression was found in the skeletal and cardiac muscles of smyd1‐gfp transgenic embryos. GFP expression appeared stronger in slow muscles than fast muscles in transgenic zebrafish larvae. In addition, GFP expression was also detected in cranial and fin muscles of smyd1‐gfp transgenic zebrafish larvae. In situ hybridization confirmed smyd1 mRNA expression in these tissues, suggesting that the expression of the smyd1‐gfp transgene recapitulated that of the endogenous smyd1 gene. Deletion analysis revealed that the 0.5‐kb sequence in the proximal promoter of smyd1 was essential for its muscle specificity. Together, these data indicate that smyd1 is specifically expressed in most, if not all, striated muscles, and the muscle specificity is controlled by the 5.3‐kb promoter and flanking sequences. Developmental Dynamics 235:3306–3315, 2006. © 2006 Wiley‐Liss, Inc.
Development of an anti‐IL‐17A auto‐vaccine that prevents experimental auto‐immune encephalomyelitis
Authors: Uyttenhove Catherine , Van Snick Jacques 
Published: October 2006

AbstractIL‐17 has been associated with multiple inflammatory disorders such as rheumatoid arthritis, asthma and multiple sclerosis. As these diseases require long‐term treatment we turned to an auto‐vaccine strategy for IL‐17 neutralization in vivo. Mouse IL‐17A was covalently linked to ovalbumin and used to immunize C57BL/6 mice. This vaccine induced the production of antibodies that blocked IL‐17A bioactivity in vitro but did not react with the other IL‐17 isoforms, including IL‐17F. As the half‐life of the Ab titers after the last immunogen administration was approximately 4 months, the vaccine provides for long lasting and selective inhibition of IL‐17A activity in vivo. A monoclonal Ab (mAb) derived from these mice showed the same specificity for IL‐17A. To test the ability of the vaccine to confer protection against an IL‐17‐dependent disorder, SJL mice were vaccinated with IL‐17‐OVA and encephalomyelitis (EAE) was induced by proteolipid protein (PLP) peptide 139–151. Vaccinated mice were completely protected against the disease. The above‐mentioned anti‐IL‐17A mAb also prevented EAE development. The absence of clinical symptoms contrasted with unaltered PLP‐induced cytokine production in vitro and unmodified anti‐PLP IgG titers and isotypes. These results suggest that an anti‐IL‐17A auto‐vaccine offers new perspectives for therapy of autoimmune diseases.See accompanying commentary: http://dx.doi.org/10.1002/eji.200636760
Hopeanol: A Potent Cytotoxin with A Novel Skeleton from Hopea exalata
Authors: Ge Hui Ming , Xu Chen , Wang Xiao Ting , Huang Bo , Tan Ren Xiang 
Published: October 2006

AbstractHopeanol, a rearranged resveratrol dimer ester with an unprecedent carbon skeleton, was isolated from the bark ofHopea exalata. Its structure was determined by comprehensive spectroscopic analysis. Hopeanol exhibited potent cytotoxicity against six human cancer cell lines with its IC50 = 0.52–19.36 μM. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Hydrological processes and streamflow in a lake dominated watercourse
Authors: Spence Christopher 
Published: October 2006

AbstractThis paper discusses results of a nested basin study investigating run‐off responses along the watercourse in a 137 km2 subarctic Canadian Shield watershed. Catchment areas contributing surface run‐off to the basin outlet shrink after a maximum during spring snowmelt because of storage demands in headwater wetlands and lakes. This decrease is significant as summer contributing areas to the basin outlet are only 4% the size of spring melt contributing areas. This reduction in contributing area and decrease in antecedent lake levels lead to a two order of magnitude decrease in run‐off ratios from spring snowmelt to midsummer. Furthermore, the attenuating influence of lakes on the run‐off hydrograph increases the opportunity for evaporative losses, which prevents small run‐off events from maintaining a measurable flood wave through the basin. The location at which a run‐off event is interrupted in the watercourse is a function of lake size relative to upstream run‐off inputs. Run‐off is more susceptible to evaporative losses in large receiving lakes where inflow per unit area is less. These processes cause intermittent streamflow through the basin. These results have repercussions for coupled atmospheric/hydrological models whose resolution is approaching the basin scale. The incorporation of lateral transfer schemes that encompass these processes and physiographic influences on streamflow response is encouraged. Copyright © 2006 Crown in the right of Canada. Published by John Wiley & Sons, Ltd.
Energy and water vapour exchanges over a mixedwood boreal forest in Ontario, Canada
Authors: Pejam M. R. , Arain M. A. , McCaughey J. H. 
Published: October 2006

AbstractMeasurements of energy, carbon dioxide and water vapour fluxes and supporting meteorological variables were made from 1 September 2003 to 31 August 2004 in a 74‐year‐old mixedwood forest in northern Ontario, Canada, using the eddy covariance technique. Land surface cover data analysis showed that although this forest is comprised of deciduous and coniferous species, their proportion throughout the forest was almost equal, resulting in a homogeneously mixedwood stand. The seasonal pattern of albedo showed a distinct pattern as a result of mixed deciduous and coniferous species with the first low radiation reflection period in early spring (between snowmelt and deciduous leaf‐out), and the second low reflection period in late autumn (between senescence and snowfall). Root zone soil water content remained above 0·32 throughout the growing season, which is characteristic of wet soil conditions. The evaporative flux exceeded the sensible heat flux during most of the growing season. Daily mean evapotranspiration values during the peak growing season were about 2–2·5 mm day−1 with maximum values reaching up to 4–5 mm day−1 on sunny days. The total water loss over the 12‐month measurement period was 480 ± 30 mm, while the total precipitation was 835 mm. Despite high soil water content, bulk surface conductance calculated using the inverted Penman–Monteith formulation, showed a strong correlation with vapour pressure deficit (VPD), indicating stomatal control on water loss during the afternoons with high atmospheric demand and during occasional dry periods. Bulk surface conductance values in this mixedwood forest were relatively higher than those in other boreal coniferous forests and were more similar to values observed in the southern boreal deciduous forests. The Priestley–Taylor α values showed a wide range but during most of the growing season its values were close to unity, indicating that water stress does not play a major role in the overall water loss from this boreal forest ecosystem, while energy supply has a strong control on evapotranspiration. These results will help parameterize accurately energy and water exchanges for the moist mixedwood forests in land surface‐atmosphere interaction and hydrologic models. Copyright © 2006 John Wiley & Sons, Ltd.
Lead‐induced experimental lesions of the testis and their treatment
Authors: Ghelberg Naum W. , Bordas Emeric 
Published: October 2006

AbstractThirty‐six healthy albino rats were divided into three groups and the histologic structure of the testes was examined after treatment: group ‘C’–10 healthy control rats were untreated; group ‘Pb’ – eight rats received intraperitoneal injections of 8.5 mg per kg body weight lead acetate for 154 days (15 doses in all); group ‘PbA’ – eight rats intoxicated with lead, like group ‘Pb’ but which, during the last 21 days before killing, were treated with 5 ml per kg body weight per day of a 2% injectable solution of sodium aspartate. As compared with the controls, group ‘Pb’ showed alteration of the histopathologic pattern and reduction in the size of seminiferous tubules, basal membrane separation and a decrease in the cell content of the germinal layer, lesions of the spermatocytes and spermatids, and slight oedematous dissociation in the interstice. In 75% of the group ‘PbA’ animals, normal aspects similar to those of group ‘C’ were found.
Mutagenicity study on mice given mercuric chloride
Authors: Poma Kathleen , Kirsch‐Volders Micheline , Susanne Charles 
Published: October 2006

AbstractThe mutagenic activity of different roncentrations of mercuric chloride (0, 2, 4 and 6 mg HgCl2 per kg body wt) has been analysed in Swiss Albino mice at several periods (12, 24, 36 and 48 h) after intraperitoneal injection. No increased frequency of chromosomal aberrations was observed in bone marrow cells or in spermatogonia.
The metabolism and distribution of 4,4′‐Methylene‐bis(2‐chloroaniline) (MBOCA) in rats
Authors: Farmer P. B. , Rickard J. , Robertson S. 
Published: October 2006

Abstract4,4′‐Methylene‐bis(2‐chloroaniline) (MBOCA), a known carcinogen in several animal species, is frequently found in the urine of humans exposed to the compound in the plastics industry. A knowledge of the metabolism and tissue distribution of MBOCA would be of value in monitoring exposure to this potential human carcinogen. Following intraperitoneal (i.p.) or oral administration of [14C]MBOCA to rats, approximately one third of the radioactivity was excreted in the urine. Only 1–2% of the radioactivity was identified as MBOCA by high performance liquid chromatography (HPLC) and gas chromatography–mass spectrometry. At least nine other metabolites were separated by reversed‐phase HPLC. Treatment of the urine with sulphatase–glucuronidase liberated two major deconjugated metabolites. No evidence was obtained for any major long‐term retention of MBOCA in the rat, although 48h after dosing approximately 2% of the administered radioactivity was associated with the liver. Despite the extensive metabolism of MBOCA in the rat, analysis of the urine of exposed workers showed only MBOCA at concentrations up to 1500 nmol 1−1. No evidence was found for the major metabolites identified in the rat.
Porous polylactide/chitosan scaffolds for tissue engineering
Authors: Wan Ying , Fang Ya , Wu Hua , Cao Xiaoying 
Published: October 2006

AbstractNovel porous scaffolds were fabricated using biodegradable polylactide/chitosan blends. A combinational technique involving solvent‐extracting, liquid‐solid separation, and freeze‐drying paths were employed. The processing parameters were optimized in order to produce desired porous scaffolds and thus obtained scaffolds showed well distributed and interconnected porous structures with controllable porosities varying from around 50–85% and regulative pore sizes being distributed within a region between 2 and 190 μm. These scaffolds exhibited remarkably improved hydrophilicity based on the measurements for their swelling index. The results obtained from in vitro incubation of scaffolds in phosphate buffered saline solutions at 37°C during various periods up to 10 weeks indicated that chitosan component inside the scaffolds, on the one hand, effectively buffered the acidic degradation products of polylactide/chitosan scaffolds and on the other hand, the degradation of the scaffolds was also conspicuously delayed. These porous scaffolds maintained well‐defined compressive mechanical properties and by well‐blending polylactide with chitosan component, improved toughness on the resultant porous scaffolds was also observed. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Changes in collagen cross‐linking in bleomycin‐induced pulmonary fibrosis
Authors: Reiser Karen M. , Tryka A. Francine , Lindenschmidt Robert C. , Last Jerold A. , Witschi Hanspeter R. 
Published: October 2006

AbstractCollagen cross‐linking was analyzed in lungs of rats two, four, and ten weeks after intratracheal instillation of 1.5 units of bleomycin. Similar analyses were performed on lungs of mice 18 months after intratracheal instillation of bleomycin with or without subsequent exposure to 70% oxygen (O2) for 72 hours. Lungs were analyzed to determine the content of the reduced difunctional cross‐links dihydroxylysinonorleucine (DHLNL) and hydroxylysinonorleucine (HLNL) and of the nonreducible trifunctional cross‐link hydroxypyridinium (OHP). Ratios of DHLNL:HLNL were elevated in the rat lungs at two and four weeks, due to increased levels of DHLNL. There were no changes in the difunctional cross‐links in any of the mouse lungs. Hydroxypyridinium content was elevated in the rat lungs at ten weeks and in the mouse lungs exposed to bleomycin and oxygen. We conclude that increases in DHLNL may serve as an early indicator that potentially “fibrotic collagen” is being synthesized in lungs acutely exposed to fibrogenic stimuli, while increases in OHP may serve as a permanent marker of a fibrogenic event that could have occurred months to years earlier.
The binding of reactive metabolites of the carcinogen N‐hydroxy‐2‐acetylaminofluorene to DNA and protein in isolated rat liver nuclei: Effects of glutathione and methionine
Authors: Meerman John H. N. , Tijdens Roeline B. , Mulder Gerard J. 
Published: October 2006

AbstractThe covalent binding of reactive metabolites of the carcinogen N‐hydroxy‐2‐acetylaminofluorene to DNA and protein in isolated, intact rat liver nuclei was studied. The chemically synthesized 2‐acetylaminofluorene‐N‐sulfate became covalently bound to DNA and protein to form adducts, 50% to 60% of which retained the N‐acetyl group. Glutathione decreased the covalent binding of acetylated adducts to DNA by 18% and to protein by 50%. Methionine was more effective; it decreased DNA binding by 52% and protein binding by 79%.N‐Hydroxy‐2‐acetylaminofluorene was deacetylated by the nuclear preparation. Almost exclusively, deacetylated 2‐aminofluorene adducts to DNA and protein were formed. Glutathione decreased the covalent binding of deacetylated adducts to DNA by only 14%. Protein binding, however, was decreased by 57%. Methionine had no effect on the formation of these adducts to DNA and protein. Formation of 2‐aminofluorene‐glutathione conjugates was reduced by ascorbic acid by 65%. Covalent binding of deacetylated adducts to DNA and protein, however, was not decreased by ascorbic acid.These data suggest that “harder” nucleophiles like methionine can be used to protect macromolecules in vivo from damage by “hard” electrophiles such as those generated from the reactive 2‐acetylaminofluorene‐N‐sulfate. However, such nucleophiles seem not to be effective with N‐hydroxylamines, such as N‐hydroxy‐2‐aminofluorene, formed by deacetylation of N‐hydroxy‐2‐acetylaminofluorene.
Stereoselective formation of a cholesterol ester conjugate from fenvalerate by mouse microsomal carboxyesterase(s)
Authors: Miyamoto Junshi , Kaneko Hideo , Takamatsu Yasuko 
Published: October 2006

AbstractIn accordance with in vivo findings, of the four chiral isomers of fenvalerate (S‐5602 SumicidinR, PydrinR, [RS]‐α‐cyano‐3‐phenoxybenzyl [RS]‐2‐(4‐chlorophenyl)isovalerate), only the [2R,αS]‐isomer (B‐isomer) yielded cholesteryl [2R]‐2‐(4‐chlorophenyl)isovalerate (CPIA‐cholesterol ester) in the in vitro study using several tissue homogenates of mice, rats, dogs, and monkeys. There were species differences in the extent of CPIA‐cholesterol‐ester formation, with mouse tissues showing relatively higher activity than those of other animals. The kidney, brain, and spleen of mice showed relatively higher capacities to form this ester compared to other tissues, and the enzyme activity was mainly localized in microsomal fractions. The CPIA‐cholesterol ester did not seem to be produced by three known biosynthetic pathways of endogenous cholesterol esters–acyl‐CoA:cholesterol O‐acyltransferase (ACAT),2 lecithin:cholesterol O‐acyltransferase (LCAT)3 and cholesterol esterase.4 Carboxyesterase(s) of mouse kidney microsomes solubilized by digitonin hydrolyzed only the Bα‐isomer of fenvalerate, yielding CPIA, whereas they yielded the corresponding cholesterol ester in the presence of artificial liposomes containing cholesterol. Thus, it appears that the stereoselective formation of the CPIA‐cholesterol ester results from the stereoselective formation of the CPIA‐carboxyesterase complex only from the Bα‐isomer, which subsequently undergoes cleavage by cholesterol to yield the CPIA‐cholesterol ester.
Effects of cadmium in vitro on microsomal steroid metabolism in the inner and outer zones of the guinea pig adrenal cortex
Authors: Colby H. D. , Pope M. R. , Johnson P. B. , Sherry J. H. 
Published: October 2006

AbstractStudies were carried out to evaluate the effects of cadmium in vitro on microsomal steroid metabolism in the inner (zona reticularis) and outer (zona fasciculata and zona glomerulosa) zones of the guinea pig adrenal cortex. Microsomes from the inner zone have greater 21‐hydroxylase than 17α‐hydroxylase activity, resulting in the conversion of progesterone primarily to 11‐deoxycorticosterone and of 17α‐hydroxy progesterone principally to its 21‐hydroxylated metabolite, 11‐deoxycortisol. Microsomes from the outer zones, by contrast, have far greater 17α‐hydroxylase and C17,20‐lyase activities than 21‐hydroxylase activity. As a result, progesterone is converted primarily to its 17‐hydroxylated metabolite, 17α‐hydroxyprogesterone; and 17α‐hydroxyprogesterone is converted principally to δ4‐androstenedione, with only small amounts of 21‐hydroxylated metabolites being produced. Addition of cadmium to incubations with inner zone microsomes causes concentration‐dependent decreases in 21‐hydroxylation and increases in 17α‐hydroxylase and C17,20‐lyase activities, resulting in a pattern of steroid metabolism similar to that in normal outer zone microsomes. Cadmium similarly decreases 21‐hydroxylation by outer zone microsomes but has no effect on the formation of 17‐hydroxylated metabolites or on androgen (Δ4‐androstenedione) production. In neither inner nor outer zone microsomes did cadmium affect cytochrome P‐450 concentrations, steroid interactions with cytochrome(s) P‐450, or NADPH–cytochrome P‐450 reductase activities. The results indicate that cadmium produces both quantitative and qualitative changes in adrenal microsomal steroid metabolism and that the nature of the changes differs in the inner and outer adrenocortical zones. In inner zone microsomes, there appears to be a reciprocal relationship between 21‐hydroxylase and 17α‐hydroxylase/C17,20‐lyase activities which may influence the physiological function(s) of that zone.
Inhibition of prostaglandin H synthase–catalyzed cooxidation of diethylstilbestrol by α‐naphthoflavone and β‐naphthoflavone
Authors: Degen Gisela H. 
Published: October 2006

AbstractProstaglandin H synthase (PHS) has gained interest as a drugmetabolizing enzyme and has been shown to cooxidize and metabolically activate diethylstilbestrol (DES) in vitro. Both 7,8‐benzoflavone (α‐naphthoflavone, ANF) and 5,6‐benzoflavone (β‐naphthoflavone, BNF) have now been studied for their effects on PHS from ram seminal vesicle microsomes by means of several in vitro assays.The PHS‐catalyzed cooxidation of DES, as measured by high‐performance liquid chromatography (HPLC) analysis, is inhibited by BNF and ANF at micromolar concentrations, with median inhibitory concentrations (IC‐50) of<20 and 40 μM, respectively. The oxidation of DES is inhibited whether it is initiated by arachidonic acid or by hydrogen peroxide, indicating that the benzoflavones inhibit PHS by a mechanism different from that of indomethacin. Monitoring of cyclooxygenase activity in an oxygraph also reveals an inhibition of PHS by BNF which depends only weakly on arachidonic acid concentration; inhibition by ANF is less pronounced under these conditions. Since PHS‐catalyzed conversion of the benzoflavone compounds was detected under conditions permitting cooxidation, the inhibition of PHS by benzoflavones in vitro could either be a direct effect or possibly mediated via metabolites.Our data imply that ANF and BNF, in addition to their well‐known role as modifiers of mixed‐function oxidases, can affect the PHS‐catalyzed metabolism of xenobiotics. This is discussed in the context of adverse effects caused by DES in vivo and in cell culture and must be taken into account when interpreting the modifying effect of benzoflavones on these endpoints.
Evaluation of the calcium mobilizing action of acetaminophen and bromobenzene in rat hepatocyte cultures
Authors: Long R. M. , Moore L. 
Published: October 2006

AbstractAcetaminophen (APAP) and bromobenzene (BrB) are reported to selectively inhibit plasma membrane (PM) but not endoplasmic reticulum (ER) Ca2+ transport in rat liver (1). The ability of these hepatotoxicants to increase cytoplasmic Ca2+ levels as a result of disrupted Ca2+ pumping was determined in cultured rat hepatocytes by monitoring the activity of glycogen phosphorylase a, a Ca2+ ‐sensitive (via phosphorylase kinase) enzyme. Following exposure to 2.5 to 10 mM APAP for five minutes, dose‐dependent increases in phosphorylase a activity were observed (58 to 190 U/g protein). Endoplasmic reticulum Ca2+ pump activity was not inhibited after any dose of APAP (56 nmol Ca2+ per milligram protein per 30 minutes). Phosphorylase a activity remained elevated for 60 minutes after exposure to APAP (124 μl/g protein). Following exposure to 0.5 to 2 mM BrB for five minutes, phosphorylase a activity also increased (58 to 229 U/g protein) in a dose‐related manner. Endoplasmic reticulum Ca2+ pump activity was inhibited after BrB exposure (from 58 to 16 nmol Ca2+ per milligram protein per 30 minutes). Phosphorylase a activity remained elevated for 60 minutes after exposure to BrB (147 U/g protein). Evidence of elevated cytoplasmic Ca2+ is consistent with the inhibition of Ca2+ ‐extruding/sequestering mechanisms at hepatocyte PM and/or ER. Prolonged elevation of cytosolic Ca2+ levels could overstimulate Ca2+ ‐sensitive processes within liver cells and thus initiate or contribute to hepatotoxic injury.
The inactivation of rhodanese by nitrite and inhibition by other anions in vitro
Authors: Alexander Keith , Procell Lawrence R. , Kirby Stephen D. , Baskin Steven I. 
Published: October 2006

AbstractCyanide detoxification in mammals occurs, in part, by sulfur transfer by rhodanese to form the less toxic thiocyanate. Thiosulfate and nitrite are often used in combination for the treatment of cyanide intoxication. This report shows that nitrite can inhibit the rate of sulfur transfer by rhodanese in vitro. Nitrate, chloride, sulfate, and acetate were also examined as inhibitors. Inhibition by nitrite appeared to be more complex than for the other anions tested. Closer examination showed that nitrite can inactivate the sulfur‐free rhodanese. Our observation leads to the suggestion that, in vivo, either rhodanese is maintained in its more stable sulfur‐substituted form or cellular compartmentalization prevents inactivation by nitrite.