bluuebunny/crossref_metadata_2025_split huggingface dataset:
Suppression of stretch reflex activity after spinal or systemic treatment with AMPA receptor antagonist NGX424 in rats with developed baclofen tolerance
Authors: Oshiro Masakatsu , Hefferan Michael P , Kakinohana Osamu , Lukacova Nadezda , Sugahara Kazuhiro , Yaksh Tony L , Marsala Martin 
Published: July 2010

BACKGROUND AND PURPOSEBaclofen (a GABABreceptor agonist) is the most commonly used anti‐spasticity agent in clinical practice. While effective when administered spinally or systemically, the development of progressive tolerance represents a serious limitation for its long‐term use. The goal of the present study was to characterize the treatment potency after intrathecal or systemic treatment with the selective AMPA receptor antagonist NGX424 on stretch reflex activity (SRA) and background muscle activity (BMA) in rats with developed baclofen tolerance.EXPERIMENTAL APPROACHAnimals were exposed to 10 min of spinal ischaemia to induce an increase in BMA and SRA. Selected animals were implanted with an intrathecal PE‐5 catheter and infused intrathecally with baclofen (1 µg·h−1) for 14 days. Before and after baclofen infusion, changes in BMA and SRA were measured at 2 day intervals. After development of baclofen tolerance, the animals were injected intrathecally (1 µg) or subcutaneously (3, 6 or 12 mg·kg−1) with NGX424, and changes in BMA and SRA were measured.KEY RESULTSIntrathecal or systemic delivery of NGX424 significantly suppressed the BMA and SRA in baclofen‐tolerant animals. This effect was dose dependent. The magnitude of BMA and SRA suppression seen after 1 µg (intrathecal) or 12 mg·kg−1(s.c.) of NGX424 injection was similar to that seen during the first 5 days of baclofen infusion.CONCLUSIONS AND IMPLICATIONSThese data demonstrate that the use of NGX424 can represent an effective therapy to modulate chronic spasticity in patients who are refractory or tolerant to baclofen treatment.LINKED ARTICLEThis article is commented on by Gómez‐Sorianoet al., pp. 972–975 of this issue. To view this commentary visithttp://dx.doi.org/10.1111/j.1476‐5381.2010.00964.x
Phosphatidylinositol 3‐kinase‐δ up‐regulates L‐type Ca2+ currents and increases vascular contractility in a mouse model of type 1 diabetes
Authors: Pinho JF , Medeiros MAA , Capettini LSA , Rezende BA , Campos PP , Andrade SP , Cortes SF , Cruz JS , Lemos VS 
Published: July 2010

BACKGROUND AND PURPOSE Vasculopathies represent the main cause of morbidity and mortality in diabetes. Vascular malfunctioning in diabetes is associated with abnormal vasoconstriction and Ca2+ handling by smooth muscle cells (SMC). Phosphatidylinositol 3‐kinases (PI3K) are key mediators of insulin action and have been shown to modulate the function of voltage‐dependent L‐type Ca2+ channels (CaV1.2). In the present work, we investigated the involvement of PI3K signalling in regulating Ca2+ current through CaV1.2 (ICa,L) and vascular dysfunction in a mouse model of type I diabetes.EXPERIMENTAL APPROACH Changes in isometric tension were recorded on myograph. Ca2+ currents in freshly dissociated mice aortic SMCs were measured using the whole‐cell patch‐clamp technique. Antisense techniques were used to knock‐down the PI3Kδ isoform.KEY RESULTS Contractile responses to phenylephrine and KCl were strongly enhanced in diabetic aorta independent of a functional endothelium. The magnitude of phenylephrine‐induced ICa,L was also greatly augmented. PI3Kδ expression, but not PI3Kα, PI3Kβ, PI3Kγ, was increased in diabetic aortas and treatment of vessels with a selective PI3Kδ inhibitor normalized ICa,L and contractile response of diabetic vessels. Moreover, knock‐down of PI3Kδin vivo decreased PI3Kδ expression and normalized ICa,L and contractile response of diabetic vessels ex vivo.CONCLUSIONS AND IMPLICATIONS Phosphatidylinositol 3‐kinase δ was essential to the increased vascular contractile response in our model of type I diabetes. PI3Kδ signalling was up‐regulated and most likely accounted for the increased ICa,L, leading to increased vascular contractility. Blockade of PI3Kδ may represent a novel therapeutic approach to treat vascular dysfunction in diabetic patients.LINKED ARTICLE This article is commented on by Sturek, pp. 1455–1457 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00997.x
The Interaction of Gestational and Postnatal Ethanol Experience on the Adolescent and Adult Odor‐Mediated Responses to Ethanol in Observer and Demonstrator Rats
Authors: Eade Amber M. , Youngentob Steven L. 
Published: July 2010

Background:  Gestational ethanol exposure enhances the adolescent reflexive sniffing response to ethanol odor. Postnatal exposures of naïve animals as either an observer (i.e., conspecific) or demonstrator (i.e., intoxicated peer) using a social transmission of food odor preference paradigm also yields enhanced odor‐mediated responses. Studies on the interaction of fetal and postnatal exposures using the social transmission paradigm have been limited to the responses of observers. When combined, the enhanced response is greater than either form of exposure alone and, in observer females, yields adult persistence. The absence of a male effect is noteworthy, given that chemosensory mechanisms are suggested to be an important antecedent factor in the progression of ethanol preference. Observers gain odor information on the breath of the demonstrator through social interaction. Demonstrators experience the pharmacologic properties of ethanol along with retronasal and hematogenic olfaction. Thus, we tested whether augmentation of the fetal ethanol‐induced behavioral response with postnatal exposure as a demonstrator differed from that as an observer. We also examined whether re‐exposure as a demonstrator yields persistence in both sexes.Methods:  Pregnant dams were fed an ethanol containing or control liquid diet throughout gestation. Progeny received four ethanol or water exposures: one every 48 hours through either intragastric infusion or social interaction with the infused peer beginning on P29. The reflexive behavioral sniffing response to ethanol odor was tested at postnatal (P) day 37 or P90, using whole‐body plethysmography.Results:  When tested in either adolescence or adulthood ‐ fetal ethanol exposed adolescent ethanol observers and demonstrators significantly differed in their odor‐mediated response to ethanol odor both between themselves and from their respective water controls. Nonetheless, adolescent ethanol re‐exposure as a demonstrator, like an observer, enhanced the reflexive sniffing response to ethanol odor at both testing ages by augmenting the known effects of prior fetal ethanol experience. At each age, the magnitude of the enhanced odor response in demonstrators was similar to that of observers. Interestingly, only re‐exposure as a demonstrator resulted in persistence of the behavioral response into adulthood in both sexes.Conclusions:  The method of ethanol re‐exposure plays an important role in prolonging the odor‐mediated effects of fetal exposure. While ethanol odor‐specific exposure through social interaction is important, additional factors such as the pairing of retronasal and hematogenic olfaction with ethanol’s intoxicating properties appear necessary to achieve persistence in both sexes.
Ethanol Alters the Osteogenic Differentiation of Amniotic Fluid‐Derived Stem Cells
Authors: Hipp Jennifer A. , Hipp Jason D. , Atala Anthony , Soker Shay 
Published: July 2010

Background:  Fetal alcohol spectrum disorder (FASD) is a set of developmental defects caused by prenatal alcohol exposure. Clinical manifestations of FASD are highly variable and include mental retardation and developmental defects of the heart, kidney, muscle, skeleton, and craniofacial structures. Specific effects of ethanol on fetal cells include induction of apoptosis as well as inhibition of proliferation, differentiation, and migration. This complex set of responses suggests that a bioinformatics approach could clarify some of the pathways involved in these responses.Methods:  In this study, the responses of fetal stem cells derived from the amniotic fluid (AFSCs) to treatment with ethanol have been examined. Large‐scale transcriptome analysis of ethanol‐treated AFSCs indicates that genes involved in skeletal development and ossification are up‐regulated in these cells. Therefore, the effect of ethanol on osteogenic differentiation of AFSCs was studied.Results:  Exposure to ethanol during the first 48 hours of an osteogenic differentiation protocol increased in vitro calcium deposition by AFSCs and increased alkaline phosphatase activity. In contrast, ethanol treatment later in the differentiation protocol (day 8) had no significant effect on the activity of alkaline phosphatase.Conclusions:  These results suggest that transient exposure of AFSCs to ethanol during early differentiation enhances osteogenic differentiation of the cells.
Assemblage patterns of fish functional groups relative to habitat connectivity and conditions in floodplain lakes
Authors: Miyazono S. , Aycock J. N. , Miranda L. E. , Tietjen T. E. 
Published: July 2010

Miyazono S, Aycock JN, Miranda LE, Tietjen TE. Assemblage patterns of fish functional groups relative to habitat connectivity and conditions in floodplain lakes. Ecology of Freshwater Fish 2010: 19: 578–585. © 2010 John Wiley & Sons A/SAbstract –  We evaluated the influences of habitat connectivity and local environmental factors on the distribution and abundance patterns of fish functional groups in 17 floodplain lakes in the Yazoo River Basin, USA. The results of univariate and multivariate analyses showed that species–environmental relationships varied with the functional groups. Species richness and assemblage structure of periodic strategists showed strong and positive correlations with habitat connectivity. Densities of most equilibrium and opportunistic strategists decreased with habitat connectivity. Densities of certain equilibrium and opportunistic strategists increased with turbidity. Forested wetlands around the lakes were positively related to the densities of periodic and equilibrium strategists. These results suggest that decreases in habitat connectivity, forested wetland buffers and water quality resulting from environmental manipulations may cause local extinction of certain fish taxa and accelerate the dominance of tolerant fishes in floodplain lakes.
Characterization of a Novel Rice Metallothionein Gene Promoter: Its Tissue Specificity and Heavy Metal Responsiveness
Authors: Dong Chun‐Juan , Wang Yun , Yu Shi‐Shi , Liu Jin‐Yuan 
Published: July 2010

Abstract The rice (Oryza sativa L.) metallothionein gene OsMT‐I‐4b has previously been identified as a type I MT gene. To elucidate the regulatory mechanism involved in its tissue specificity and abiotic induction, we isolated a 1 730 bp fragment of the OsMT‐I‐4b promoter region. Histochemical β‐glucuronidase (GUS) staining indicated a precise spacial and temporal expression pattern in transgenic Arabidopsis. Higher GUS activity was detected in the roots and the buds of flower stigmas, and relatively lower GUS staining in the shoots was restricted to the trichomes and hydathodes of leaves. No activity was observed in the stems and seeds. Additionally, in the root of transgenic plants, the promoter activity was highly upregulated by various environmental signals, such as abscisic acid, drought, dark, and heavy metals including Cu2+, Zn2+, Pb2+ and Al3+. Slight induction was observed in transgenic seedlings under salinity stress, or when treated with Co2+ and Cd2+. Promoter analysis of 5′‐deletions revealed that the region −583/−1 was sufficient to drive strong GUS expression in the roots but not in the shoots. Furthermore, deletion analysis indicated important promoter regions containing different metal‐responsive cis‐elements that were responsible for responding to different heavy metals. Collectively, these findings provided important insight into the transcriptional regulation mechanisms of the OsMT‐I‐4b promoter, and the results also gave us some implications for the potential application of this promoter in plant genetic engineering.
Aquaporin‐2 urinary excretion in preterm infants: relationship to diuresis and vasopressin
Authors: Iacobelli S. , Gouyon J.B. , Bonsante F. , Mastrofrancesco L. , Svelto M. , Valenti G. 
Published: July 2010

AbstractAims:  Few investigations have explored the urinary aquaporin‐2 (u‐AQP2) excretion pattern after birth in preterm infants with conflicting results regarding the correlation between u‐AQP2, urinary osmolality and vasopressin. The aims of this study were to evaluate u‐AQP2 excretion during the first week of life in preterm infants, to correlate u‐AQP2 with other markers of renal function and to investigate the relationship between u‐AQP2, urinary tonicity and arginine‐vasopressin in the immature kidney.Methods:  In infants born less than 33 weeks daily diuresis, u‐AQP2, urinary arginine‐vasopressin, urine and plasma tonicity, creatinine and electrolytes were measured through the first 7 days of life.Results:  Fifty‐five infants were evaluated. u‐AQP2 excretion showed the following profile: the highest u‐AQP2 levels were found on day 2 and values remained significantly higher until day 5 with respect to day 1. On day 6, u‐AQP2 levels significantly decreased to values closer to those found on day 1. u‐AQP2 excretion was not associated with arginine‐vasopressin while significant, but weak association was found with urinary tonicity (r = −0.20; −0.32 < r < −0.11; P < 0.05). u‐AQP2 excretion and creatinine clearance were significantly associated during the study period (r = 0.19; 0.08 < r < 0.29; P < 0.05). There was a strong association between totally u‐AQP2 excretion and diuresis over the week (r = 0.72; 0.66 < r < 0.76; P < 0.0001).Conclusion:  Significant variations occur in AQP2 expression levels during the first week of life in preterm infants. AQP2 does not seem to contribute to the urinary concentration ability after birth. Further investigations are required to elucidate the mechanisms underlying the strong association between diuresis and u‐AQP2 excretion in early postnatal life.
Hypothermia Reduces Brain Edema, Spontaneous Recurrent Seizure Attack, and Learning Memory Deficits in the Kainic Acid Treated Rats
Authors: Wang Yu , Liu Ping‐Ping , Li Liang‐yong , Zhang Hui‐Min , Li Tao 
Published: July 2010

SUMMARYAims:It is unknown whether hypothermia can disrupt the progress of epileptogenesis. The present study aimed to determine the effect of hypothermia on brain edema and epileptogenesis and to establish whether brain edema is associated with epileptogenesis after severe status epilepticus (SE).Methodology:Rats were injected with a single dose of Kainic acid (KA) to produce either chronic epileptic rats (rats with spontaneous recurrent seizure, SRS) or rats without spontaneous recurrent seizure (no‐SRS rats). A second KA injection was used to induce SE in SRS rats and in no‐SRS rats. The number of SRS was counted and the brain edema induced by SE was assessed by brain water content measurement. The cognitive function was assessed by the radial‐arm maze (RAM) test.Results:A second KA injection resulted in brain edema that was more severe in SRS rats than in no‐SRS rats. After second injection of KA, hypothermia treatment attenuated the KA induced brain edema and reduced the SRS attack in SRS rats. Additionally cognitive function was better in hypothermia‐treated SRS rats than in nomothermia treated SRS rats 1 month after the second KA injection.Conclusions:Hypothermia treatment immediately after SE not only exhibited protective effects against the chronic spontaneous recurrent convulsant seizures but also improved cognitive function. These antiepileptogenic properties of hypothermia may be related to its attenuating effect on brain edema induced by SE. They therefore suggest that brain edema may be involved in the progress of epileptogenesis.
Bony Avulsion of the Medial Head of Triceps Brachii
Authors: Barnes James R. , Atwal Navraj , Sarangi Partha 
Published: July 2010

We describe a 69-year-old patient who presented with an isolated avulsion fracture of the medial head of triceps brachii after a fall onto her elbow. As far as we are aware, this pattern of injury has not been previously described in the literature. Our patient had no functional deficit and was managed conservatively. She was referred for physiotherapy, and discharged once her pain subsequently subsided. Although the literature favours surgical management of similar injuries, we feel that our case shows that good results may still be achieved from conservative management.
Association of Chlamydia pneumoniae immunoglobulin G antibodies with the risk of lung cancer among non‐smoking women in Liaoning, China
Authors: Liu Zhuang , Su Meng , Yu Shi‐cheng , Yin Zhi‐hua , Zhou Bao‐sen 
Published: July 2010

AbstractThe role of Chlamydia pneumoniae in the cause of lung cancer is controversial. In this study, we investigated the association between C. pneumoniae immunoglobulin (Ig) G antibodies and risk of lung cancer among non‐smoking women. C. pneumoniae IgG antibody levels were compared between 192 adult Chinese women who met the diagnostic criteria of lung cancer and 90 healthy controls. C. pneumoniae IgG antibodies were tested with the use of an enzyme‐linked immunosorbent assay. The prevalence of C. pneumoniae IgG seropositivity was 61.98% of cases and 28.89% of controls (P < 0.05). According to the results of the multiple logistic analysis model, the odds ratios for C. pneumoniae IgG antibody seropositivity, body mass index, and educational levels were 3.919 (P < 0.001), 0.731 (P= 0.274), and 1.646 (P= 0.069), respectively. C. pneumoniae infection may be a risk factor for lung cancer.
Mitochondrial metabolism and diabetes
Authors: Kwak Soo Heon , Park Kyong Soo , Lee Ki‐Up , Lee Hong Kyu 
Published: July 2010

AbstractThe oversupply of calories and sedentary lifestyle has resulted in a rapid increase of diabetes prevalence worldwide. During the past two decades, lines of evidence suggest that mitochondrial dysfunction plays a key role in the pathophysiology of diabetes. Mitochondria are vital to most of the eukaryotic cells as they provide energy in the form of adenosine triphosphate by oxidative phosphorylation. In addition, mitochondrial function is an integral part of glucose‐stimulated insulin secretion in pancreatic β‐cells. In the present article, we will briefly review the major functions of mitochondria in regard to energy metabolism, and discuss the genetic and environmental factors causing mitochondrial dysfunction in diabetes. In addition, the pathophysiological role of mitochondrial dysfunction in insulin resistance and β‐cell dysfunction are discussed. We argue that mitochondrial dysfunction could be the central defect causing the abnormal glucose metabolism in the diabetic state. A deeper understanding of the role of mitochondria in diabetes will provide us with novel insights in the pathophysiology of diabetes. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00047.x, 2010)
Epidemiology, Diagnosis, and Antimicrobial Treatment of Acute Bacterial Meningitis
Authors: Brouwer Matthijs C. , Tunkel Allan R. , van de Beek Diederik 
Published: July 2010

SUMMARY
The epidemiology of bacterial meningitis has changed as a result of the widespread use of conjugate vaccines and preventive antimicrobial treatment of pregnant women. Given the significant morbidity and mortality associated with bacterial meningitis, accurate information is necessary regarding the important etiological agents and populations at risk to ascertain public health measures and ensure appropriate management. In this review, we describe the changing epidemiology of bacterial meningitis in the United States and throughout the world by reviewing the global changes in etiological agents followed by specific microorganism data on the impact of the development and widespread use of conjugate vaccines. We provide recommendations for empirical antimicrobial and adjunctive treatments for clinical subgroups and review available laboratory methods in making the etiological diagnosis of bacterial meningitis. Finally, we summarize risk factors, clinical features, and microbiological diagnostics for the specific bacteria causing this disease.
Role of Tumor Necrosis Factor Alpha in Disease Using a Mouse Model of Shiga Toxin-Mediated Renal Damage
Authors: Lentz Erin K. , Cherla Rama P. , Jaspers Valery , Weeks Bradley R. , Tesh Vernon L. 
Published: July 2010

ABSTRACT
Mice have been extensively employed as an animal model of renal damage caused by Shiga toxins. In this study, we examined the role of the proinflammatory cytokine tumor necrosis factor alpha (TNF-α) in the development of toxin-mediated renal disease in mice. Mice pretreated with TNF-α and challenged with Shiga toxin type 1 (Stx1) showed increased survival compared to that of mice treated with Stx1 alone. Conversely, mice treated with Stx1 before TNF-α administration succumbed more quickly than mice given Stx1 alone. Increased lethality in mice treated with Stx1 followed by TNF-α was associated with evidence of glomerular damage and the loss of renal function. No differences in renal histopathology were noted between animals treated with Stx1 alone and the TNF-α pretreatment group, although we noted a sparing of renal function when TNF-α was administered before toxin. Compared to that of treatment with Stx1 alone, treatment with TNF-α after toxin altered the renal cytokine profile so that the expression of proinflammatory cytokines TNF-α and interleukin-1β (IL-1β) increased, and the expression of the anti-inflammatory cytokine IL-10 decreased. Increased lethality in mice treated with Stx1 followed by TNF-α was associated with higher numbers of dUTP-biotin nick end labeling-positive renal tubule cells, suggesting that increased lethality involved enhanced apoptosis. These data suggest that the early administration of TNF-α is a candidate interventional strategy blocking disease progression, while TNF-α production after intoxication exacerbates disease.
Stereoelectronic interaction effects on the conformational properties of 5-methyl-5-aza-1,3-dithiacyclohexane and its analogous containing N, P, O, and Se atoms — A hybrid density functional theory (DFT), ab initio study, and natural bond orbital (NBO) analysis
Authors: Nori-Shargh Davood , Hassanzadeh Neda , Kosari Meisam , Rabieikarahroudi Parvin , Yahyaei Hooriye , Sharifi Sasan 
Published: July 2010

Natural bond orbital (NBO) analysis, hybrid density functional theory (hybrid DFT: B3LYP/6-311+G**//B3LYP/6-311+G**), and ab initio molecular orbital (MO: MP2/6-311+G**//B3LYP/6-311+G**) based methods were used to study the electronic delocalization energy (DE), dipole–dipole interactions, and steric repulsions on the conformational properties of 5-methyl-5-aza-1,3-dioxacyclohexane (1) (-phospha- (2), -arsena- (3)), 5-methyl-5-aza-1,3-dithiacyclohexane (4) (-phospha- (5), -arsena- (6)), and 5-methyl-5-aza-1,3-diselenacyclohexane (7) (-phospha- (8), -arsena- (9)). The MP2/6-311+G**//B3LYP/6-311+G** and B3LYP/6-311+G**//B3LYP/6-311+G** results revealed that the axial stereoisomers of compounds 1–9 are more stable than their equatorial stereoisomers. In this regard, the obtained results showed an egregious axial preference for compounds 1, 4, and 7. Importantly, the results showed that the energy differences between the axial and equatorial stereoisomers decrease from compounds 1 → 3, 4 → 6, and also, 7 → 9. The NBO analysis of donor–acceptor interactions revealed that the calculated DE for compounds 1–3 are –21.50, –7.84, and –4.38 kcal mol–1, respectively. The decrease of the calculated DE values from compound 1 to compound 3 could reasonably explain the decrease of the energy differences between the axial and equatorial stereoisomers from compound 1 to compound 3. The correlation between the DE, dipole–dipole interactions, structural parameters, and conformational behaviors of compounds 1–9 has been investigated.