bluuebunny/crossref_metadata_2025_split huggingface dataset:
Thermal tolerance of juvenile freshwater mussels (Unionidae) under the added stress of copper
Authors: Pandolfo Tamara J. , Cope W. Gregory , Arellano Consuelo 
Published: March 2010

Abstract
Freshwater mussels fulfill an essential role in aquatic communities, but are also one of the most sensitive and rapidly declining faunal groups in North America. Rising water temperatures, caused by global climate change or industrial discharges, can further challenge impaired unionid communities, but thermal stress is almost certainly not the only stressor affecting freshwater mussels. Metals, such as copper (Cu), are a common source of toxicant exposure in aquatic environments. The toxic effects of Cu on the early life stages of freshwater mussels have been well studied, and freshwater mussels are more sensitive to Cu than most aquatic organisms. The purpose of the present study was to determine the effect of a sublethal copper concentration on the upper thermal tolerance of three species, Lampsilis siliquoidea, Potamilus alatus, and Ligumia recta, of juvenile freshwater mussels in 48- and 96-h tests. Thermal tolerance was determined over a range of experimental temperatures (20–42°C) at three acclimation temperatures (17, 22, and 27°C). Median lethal temperatures (LT50s) were calculated in the absence and presence of Cu, and at 48 h ranged from 34.6 to 44.4°C (mean 37.7°C) without Cu, and from 33.8 to 38.9°C (mean 35.8°C) with Cu. The LT50s at 96 h ranged from 32.5 to 35.6°C (mean 34.5°C) without Cu and from 33.0 to 35.4°C (mean 34.2°C) with Cu. Potamilus alatus had a significantly lower 48 h LT50 with Cu than without Cu at the 22°C acclimation temperature; there were no other significant differences in LT50s attributed to Cu. Survival trends showed limited evidence of interactive effects between copper and temperature for all three species, suggesting the combined stress of elevated temperatures and copper exposure to freshwater mussels should be further explored. Environ. Toxicol. Chem. 2010;29:691–699. © 2009 SETAC
Genetic costs of tolerance to metals in Daphnia longispina populations historically exposed to a copper mine drainage
Authors: Agra Ana Raquel , Guilhermino Lúcia , Soares Amadeu M.V.M. , Barata Carlos 
Published: March 2010

Abstract
The present study was conducted to assess three microevolutionary aspects of adaptation to pollution in Daphnia longispina populations historically exposed to an acid mine drainage from an abandoned pyrite mine: pollution mediated effects in acute tolerance to copper (Cu) and zinc (Zn); pollution-mediated effects on genetic variability of tolerant and physiological traits related to fitness (feeding rates); and fitness costs of tolerance measured as genetic trade-offs between tolerance and feeding rates under none and low levels of contamination. These objectives were addressed by comparing broad sense heritabilities and genetic correlations using up to 20 distinct clonal lineages randomly obtained from two populations: one located in a water reservoir contaminated by the acid mine drainage, and the other located in a nearby clean water reservoir. Results showed that only sensitive and resistant lineages to Cu were present in the reference and contaminated site, respectively. For Zn, however, both populations had a similar distribution pattern of sensitivities. Heritability values for tolerant and feeding traits across metal exposure levels was similar in both populations being in most cases greater than 50%. Fitness costs of tolerance were illustrated by lower feeding rates of the tolerant population compared to the reference one and negative genetic correlations between mean clonal feeding rates and median clonal survival time in control conditions (no added Cu or Zn). The results obtained thus support the view that tolerance to pollution is ecologically costly. Environ. Toxicol. Chem. 2010;29:939–946. © 2009 SETAC
Effects of pesticides and antibiotics on penaeid shrimp with special emphases on behavioral and biomarker responses
Authors: Tu Huynh Thi , Silvestre Frederic , Phuong Nguyen Thanh , Kestemont Patrick 
Published: March 2010

Abstract
The purpose of the present study is to provide information on the current state of knowledge regarding the effects of pesticides and antibiotics used in aquaculture on penaeid shrimp, one of the most common aquatic products for human consumption, with a special emphasis on the use of behavioral, physiological, and biochemical response. These include behavior; feeding rate changes; respiration rate, oxygen consumption, and osmoregulation alterations; nucleic acids, protein, and glycogen synthesis; cholinesterase activity inhibition; ATPase activity; and oxidative stress responses. This paper also deals with residues of antibiotics and pesticides in penaeid shrimp. Antibiotics and pesticides used in aquaculture may have adverse effects on treated animals and human consumers health if they are not correctly used. As a complement to the measurement of antibiotic and pesticide residues in tissues, the use of behavioral and biomarker responses can provide more relevant biological information on the potential adverse effects of antibiotics and pesticides on penaeid shrimp health. Environ. Toxicol. Chem. 2010;29:929–938. © 2009 SETAC
Efficacy of plant essential oils on postharvest control of rot caused by fungi on four cultivars of apples in vivo
Authors: Lopez‐Reyes Jorge Giovanny , Spadaro Davide , Gullino Maria Lodovica , Garibaldi Angelo 
Published: March 2010

AbstractThe efficacy of plant essential oils was evaluated on apples, cv. Golden Delicious, cv. Granny Smith, cv. Red Chief and cv. Royal Gala, at postharvest to control Botrytis cinerea and Penicillium expansum. The essential oils from basil (Ocimum basilicum), fennel (Foeniculum sativum), lavender (Lavandula officinalis), marjoram (Origanum majorana), oregano (Origanum vulgare), peppermint (Mentha piperita), rosemary (Rosmarinus officinalis), sage (Salvia officinalis), savory (Satureja montana), thyme (Thymus vulgaris) and wild mint (Mentha arvensis) were tested at different concentrations. All the essential oils were from mediterranean plants. The fruits were artificially wounded and inoculated with a suspension at 1 × 105 conidia/ml of each pathogen. After 12 h, emulsions at 1% and 10% of each essential oil were dropped into each inoculated wound. A tebuconazole chemical control and an inoculated control were also included. All the treated fruit were stored at 4 ± 1°C. After 15 and 30 days, the diameter of the rot around each wound was measured. The results revealed that the efficacies of the essential oils tested were cultivar‐ and storage time‐dependent. In any case, treatments with essential oils from oregano, savory and thyme showed significant efficacy in all apple cultivars tested. Treatments with essential oil emulsions at 10% were phytotoxic for all the apple cultivars evaluated. Copyright © 2010 John Wiley & Sons, Ltd.
Heparin treatment of vascular smooth muscle cells results in the synthesis of the dual‐specificity phosphatase MKP‐1
Authors: Blaukovitch Cheryl Isleib , Pugh Raymond , Gilotti Albert C. , Kanyi Daniela , Lowe‐Krentz Linda J. 
Published: March 2010

AbstractThe ability of heparin to block proliferation of vascular smooth muscle cells has been well documented. It is clear that heparin treatment can decrease the level of ERK activity in vascular smooth muscle cells that are sensitive to heparin. In this study, the mechanism by which heparin induces decreases in ERK activity was investigated by evaluating the dual specificity phosphatase, MKP‐1, in heparin treated cells. Heparin induced MKP‐1 synthesis in a time and concentration dependent manner. The time‐course of MKP‐1 expression correlated with the decrease in ERK activity. Over the same time frame, heparin treatment did not result in decreases in MEK‐1 activity which could have, along with constitutive phosphatase activity, accounted for the decrease in ERK activity. Antibodies against a heparin receptor also induced the synthesis of MKP‐1 along with decreasing ERK activity. Blocking either phosphatase activity or synthesis also blocked heparin‐induced decreases in ERK activity. Consistent with a role for MKP‐1, a nuclear phosphatase, heparin treated cells exhibited decreases in nuclear ERK activity more rapidly than cells not treated with heparin. The data support MKP‐1 as a heparin‐induced phosphatase that dephosphorylates ERK, decreasing ERK activity, in vascular smooth muscle cells. J. Cell. Biochem. 110: 382–391, 2010. © 2010 Wiley‐Liss, Inc.
A novel zinc finger protein Zfp637 behaves as a repressive regulator in myogenic cellular differentiation
Authors: Li Kai , Zhang Jie , Ren Jing‐jing , Wang Qi , Yang Kai‐yong , Xiong Zhu‐juan , Mao Yong‐qiu , Qi Yan‐yu , Chen Xiao‐wei , Lan Feng , Wang Xiu‐jie , Xiao Heng‐yi , Lin Ping , Wei Yu‐quan 
Published: March 2010

AbstractZinc finger proteins have been implicated as transcription factors in the differentiation and development of cells and tissues in higher organisms. The classical C2H2 zinc finger motif is one main type of motif of zinc finger proteins. Our previous studies have shown that Zfp637, which comprises six consecutively typical and one atypical C2H2 zinc finger motifs, is highly expressed in undifferentiated or poorly differentiated cell lines, but is moderately or slightly expressed in normal tissues. We have also demonstrated that Zfp637 can promote cell proliferation. However, its role in the regulation of cell differentiation remains unknown. We report here that endogenous Zfp637 as well as mTERT is expressed in proliferating C2C12 myoblasts and that their expression is downregulated during myogenic differentiation. Constitutive expression of Zfp637 in C2C12 myoblasts increased mTERT expression and telomerase activity, and promoted the progression of the cell cycle and cell proliferation. By contrast, endogenous repression of Zfp637 expression by RNA interference downregulated the mTERT gene and the activity of telomerase, and markedly reduced cell proliferation. Overexpression of Zfp637 also inhibited the expression of myogenic differentiation‐specific genes such as MyoD and myogenin, and prevented C2C12 myoblast differentiation. Our results suggest that Zfp637 inhibits muscle differentiation through a defect in the cell cycle exit by potentially regulating mTERT expression in C2C12 myoblasts. This may provide a new research line for studying muscle differentiation. J. Cell. Biochem. 110: 352–362, 2010. © 2010 Wiley‐Liss, Inc.
A redox‐linked novel pathway for arsenic‐mediated RET tyrosine kinase activation
Authors: Kato Masashi , Takeda Kozue , Hossain Khaled , Thang Nguyen D. , Kaneko Yu , Kumasaka Mayuko , Yamanoshita Osamu , Uemura Noriyuki , Takahashi Masahide , Ohgami Nobutaka , Kawamoto Yoshiyuki 
Published: March 2010

AbstractWe examined the biochemical effects of arsenic on the activities of RET proto‐oncogene (c‐RET protein tyrosine kinases) and RET oncogene (RET‐MEN2A and RET‐PTC1 protein tyrosine kinases) products. Arsenic activated c‐RET kinase with promotion of disulfide bond‐mediated dimerization of c‐RET protein. Arsenic further activated RET‐MEN2A kinase, which was already 3‐ to 10‐fold augmented by genetic mutation compared with c‐RET kinase activity, with promotion of disulfide bond‐mediated dimerization of RET‐MEN2A protein (superactivation). Arsenic also increased extracellular domain‐deleted RET‐PTC1 kinase activity with promotion of disulfide bond‐mediated dimerization of RET‐PTC1 protein. Arsenic increased RET‐PTC1 kinase activity with cysteine 365 (C365) replaced by alanine with promotion of dimer formation but not with cysteine 376 (C376) replaced by alanine. Our results suggest that arsenic‐mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET‐PTC1 protein). Moreover, arsenic enhanced the activity of immunoprecipitated RET protein with increase in thiol‐dependent dimer formation. As arsenic (14.2 µM) was detected in the cells cultured with arsenic (100 µM), direct association between arsenic and RET in the cells might modulate dimer formation. Thus, we demonstrated a novel redox‐linked mechanism of activation of arsenic‐mediated RET proto‐oncogene and oncogene products. J. Cell. Biochem. 110: 399–407, 2010. © 2010 Wiley‐Liss, Inc.
Curcumin suppresses constitutive activation of STAT‐3 by up‐regulating protein inhibitor of activated STAT‐3 (PIAS‐3) in ovarian and endometrial cancer cells
Authors: Saydmohammed Manush , Joseph Doina , Syed Viqar 
Published: March 2010

AbstractSignal transducer and activator of transcription‐3 (STAT‐3) is constitutively activated in ovarian and endometrial cancers and is implicated in uncontrolled cell growth. Thus, its disruption could be an effective approach to control tumorigenesis. Curcumin is a dihydroxyphenolic compound, with proven anti‐cancer efficacy in various cancer models. We examined the anti‐tumor mechanism of curcumin on STAT‐3 and on the negative regulators of STAT‐3, including suppressors of cytokine signaling proteins (SOCS‐1 and SOCS‐3), protein inhibitors of activated STAT (PIAS‐1 and PIAS‐3), and SH2 domain‐containing phosphatases (SHP‐1 and SHP‐2) in ovarian and endometrial cancer cell lines. Treatment of cancer cells with curcumin induced a dose‐ and time‐dependent decrease of constitutive IL‐6 expression and of constitutive and IL‐6‐induced STAT‐3 phosphorylation, which is associated with decreased cell viability and increased cleavage of caspase‐3. The inhibition of STAT‐3 activation by curcumin was reversible, and phosphorylated STAT‐3 levels returned to control levels 24 h after curcumin removal. Compared to normal cells baseline expression of SOCS‐3 was high in cancer cells and a marked decrease in SOCS‐3 expression was seen following curcumin treatment. Overexpression of SOCS‐3 in curcumin‐treated cells increased expression of phosphorylated STAT‐3 and resulted in increased cell viability. Normal ovarian and endometrial cells exhibited high expression of PIAS‐3 protein, whereas in cancer cells the expression was greatly reduced. Curcumin increased PIAS‐3 expression in cancer cells. Of significance, siRNA‐mediated knockdown of PIAS‐3 overcomes the inhibitory effect of curcumin on STAT‐3 phosphorylation and cell viability. In conclusion, curcumin suppresses JAK‐STAT signaling via activation of PIAS‐3, thus attenuating STAT‐3 phosphorylation and tumor cell growth. J. Cell. Biochem. 110: 447–456, 2010. © 2010 Wiley‐Liss, Inc.
Connective tissue growth factor (CTGF) transactivates nuclear factor of activated T‐cells (NFAT) in cells of the osteoblastic lineage
Authors: Smerdel‐Ramoya Anna , Zanotti Stefano , Canalis Ernesto 
Published: March 2010

AbstractConnective tissue growth factor (CTGF), a member of the Cyr 61, CTGF, Nov (CCN) family of proteins, regulates multiple cellular functions. Overexpression of CTGF in vivo causes osteopenia, but in vitro CTGF can induce osteoblastogenesis. To investigate mechanisms involved in the effects of CTGF on osteoblastic cell differentiation, we examined whether CTGF modifies the activity of nuclear factor of activated T‐cells (NFATc) 1, a transcription factor that cooperates with osterix in the formation of new bone. CTGF increased the transactivation of a transiently transfected reporter construct, where 9 NFAT binding sites direct the expression of luciferase (9xNFAT‐Luc) and the activity of the Regulators of calcineurin 1 exon 4 (Rcan1.4) promoter, an NFAT target gene. We postulated that CTGF could modify the phosphorylation of NFAT by regulating glycogen synthase kinase 3β (GSK3β). CTGF increased the mRNA levels of Protein kinase cyclic guanosine monophosphate (cGMP) dependent type II (Prkg2), the gene encoding for cGMP dependent protein kinase II (cGKII) which phosphorylates GSK3β. Accordingly, CTGF induced GSK3β phosphorylation and decreased the active pool of GSK3β, a kinase that phosphorylates NFAT and leads to its nuclear export. As a consequence, CTGF favored the nuclear localization of NFATc1. Downregulation of PRKG2 by RNA interference reversed the effect of CTGF on the transactivation of the 9xNFAT reporter construct and the Rcan 1.4 promoter, confirming the role of cGKII in the activation of NFAT by CTGF. In conclusion, CTGF enhances NFAT signaling through the induction of cGKII and the phosphorylation of GSK3β. J. Cell. Biochem. 110: 477–483, 2010. © 2010 Wiley‐Liss, Inc.
In vitro evaluation of novel antisense oligonucleotides is predictive of in vivo exon skipping activity for Duchenne muscular dystrophy
Authors: Wang Qingsong , Yin HaiFang , Camelliti Patrizia , Betts Corinne , Moulton Hong , Lee Hyunil , Saleh Amer F. , Gait Michael J. , Wood Matthew J. A. 
Published: March 2010

AbstractBackgroundTargeted splice modulation of pre‐mRNA transcripts by antisense oligonucleotides (AOs) can correct the function of aberrant disease‐related genes. Duchenne muscular dystrophy (DMD) arises as a result of mutations that interrupt the open‐reading frame in the DMD gene encoding dystrophin such that dystrophin protein is absent, leading to fatal muscle degeneration. AOs have been shown to correct this dystrophin defect via exon skipping to yield functional dystrophin protein in animal models of DMD and also in DMD patients via intramuscular administration. To advance this therapeutic method requires increased exon skipping efficiency via an optimized AO sequence, backbone chemistry and additional modifications, and the improvement of methods for evaluating AO efficacy.MethodsIn the present study, we establish the conditions for rapid in vitro AO screening in H2K muscle cells, in which we evaluate the exon skipping properties of a number of known and novel AO chemistries [2′‐O‐methyl, peptide nucleic acid, phosphorodiamidate morpholino (PMO)] and their peptide‐conjugated derivatives and correlate their in vitro and in vivo exon skipping activities.ResultsThe present study demonstrates that using AO concentrations of 300 nM with analysis at a single time‐point of 24 h post‐transfection allowed the effective in vitro screening of AO compounds to yield data predictive of in vivo exon skipping efficacy. Peptide‐conjugated PMO AOs provided the highest in vitro activity. We also show for the first time that the feasibility of rapid AO screening extends to primary cardiomyocytes.ConclusionsIn vitro screening of different AOs within the same chemical class is a reliable method for predicting the in vivo exon skipping efficiency of AOs for DMD. Copyright © 2010 John Wiley & Sons, Ltd.
Antibiotic prescription patterns in hospitalized patients with nursing home–acquired pneumonia
Authors: El‐Solh Ali A. , Peter Misha , Alfarah Ziad , Akinnusi Morohunfolu E. , Alabbas Abbas , Pineda Lilibeth A. 
Published: March 2010

AbstractBACKGROUND:Considerable research has increased our understanding of antibiotic prescribing practices in hospital settings when it comes to nosocomial pneumonia. Much less is known about the antibiotic prescribing patterns for hospitalized non‐critically ill patients with nursing home‐acquired pneumonia (NHAP).OBJECTIVE:As part of a multisite quality improvement project, we sought to examine patterns of antibiotic prescription among healthcare providers as a function of underlying comorbid, functional, and clinical factors.SETTING:Three tertiary care centers.INTERVENTION:Chart reviews of 397 individual admissions were performed on patients admitted from nursing homes with the diagnosis of pneumonia between January 2005 and September 2007.RESULTS:Compliance with national guidelines for the treatment of NHAP was poor. Overall, the 3 most commonly used compounds for inpatient treatment were fluoroquinolones (51.4%), ceftriaxone (45.0%), and azithromycin (42.1%). Monotherapy was prescribed in 57.1%. Fluoroquinolones represented 79.5% of these cases. Patients with higher acuity of illness were more likely to receive a combination of vancomycin plus piperacillin/tazobactam (P < 0.001). Median duration of treatment was 8.0 (range, 3‐21) days. Stratified analyses showed that combination therapy was used more often on University‐affiliated services than on private service (54% vs. 35%; P < 0.001).CONCLUSIONS:There was poor adherence with antibiotic guidelines for the treatment of NHAP. In the absence of outcome data on guidelines compliance, antibiotic use was influenced by patients' age, severity of illness, and providers' academic affiliation. Future research should focus on outcome measures and physicians factors that influence nonadherence. Journal of Hospital Medicine 2010;5:E5–E10. © 2010 Society of Hospital Medicine.
Hospitalist use of hand‐carried ultrasound: Preparing for battle
Authors: Kimura Bruce J. , Amundson Stan A. , Shaw David J. 
Published: March 2010

AbstractHand‐carried ultrasound (HCU) is a burgeoning technology at a critical point in its development as a general diagnostic technique. Despite the known safety and accuracy of ultrasound in radiology and echocardiography, the use of HCU to augment physical diagnosis by all physicians has yet unrealized potential. In order to incorporate ultrasound into a diagnostic model of routine bedside application, simple imaging and training protocols must first be derived and validated. Simplified cardiac ultrasound exams have already been validated to detect evidence‐based targets such as subclinical atherosclerosis, heart failure, and elevated central venous pressures. However, for general examination of the acutely ill patient, it is the internist‐hospitalist who should derive a full‐body ultrasound examination, balancing training requirements with the numerous clinical applications potentially available. As the hospital's leading diagnostician with ultrasound expertise available in‐house, the hospitalist could develop HCU so as to triage and refer more appropriately and limit unnecessary testing and hospital stays. Active involvement by hospitalists now in the planning of outcome, validation, and training studies, will be invaluable in the formation of an “ultrasound‐assisted” physical examination in the future and will promote competent, cost‐effective applications of HCU within general medical practice. Journal of Hospital Medicine 2010;5:163–167. © 2010 Society of Hospital Medicine.