bluuebunny/crossref_metadata_2025_split huggingface dataset:
Controls of Global Snow under a Changed Climate
Authors: Kapnick Sarah B. , Delworth Thomas L. 
Published: February 2013

AbstractThis study assesses the ability of a newly developed high-resolution coupled model from the Geophysical Fluid Dynamics Laboratory to simulate the cold-season hydroclimate in the present climate and examines its response to climate change forcing. Output is assessed from a 280-yr control simulation that is based on 1990 atmospheric composition and an idealized 140-yr future simulation in which atmospheric carbon dioxide increases at 1% yr−1 until doubling in year 70 and then remains constant. When compared with a low-resolution model, the high-resolution model is found to better represent the geographic distribution of snow variables in the present climate. In response to idealized radiative forcing changes, both models produce similar global-scale responses in which global-mean temperature and total precipitation increase while snowfall decreases. Zonally, snowfall tends to decrease in the low to midlatitudes and increase in the mid- to high latitudes. At the regional scale, the high- and low-resolution models sometimes diverge in the sign of projected snowfall changes; the high-resolution model exhibits future increases in a few select high-altitude regions, notably the northwestern Himalaya region and small regions in the Andes and southwestern Yukon, Canada. Despite such local signals, there is an almost universal reduction in snowfall as a percent of total precipitation in both models. By using a simple multivariate model, temperature is shown to drive these trends by decreasing snowfall almost everywhere while precipitation increases snowfall in the high altitudes and mid- to high latitudes. Mountainous regions of snowfall increases in the high-resolution model exhibit a unique dominance of the positive contribution from precipitation over temperature.
Curcumin Inhibits UV Radiation–Induced Skin Cancer in SKH‐1 Mice
Authors: Phillips Jeffrey , Moore‐Medlin Tara , Sonavane Kunal , Ekshyyan Oleksandr , McLarty Jerry , Nathan Cherie‐Ann O. 
Published: February 2013

ObjectiveAs skin cancer incidence increases, research has focused on novel chemopreventive agents that inhibit tumor formation. In prior experimentation, curcumin, a naturally occurring food substance and anticarcinogenic agent, inhibited cutaneous squamous cell carcinoma xenograft growth. We hypothesize curcumin will inhibit UVB radiation–induced skin cancer growth in mice, approximating a human chemopreventive model.Study DesignRandomized experimental animal and laboratory study.SettingLouisiana State University Health Sciences Center‐Shreveport, Louisiana.Subjects and MethodsSKH‐1 mice were pretreated with oral or topical curcumin or oral or topical control (n = 11/group) for 14 days. Mice received UVB radiation 3 times weekly for 24 weeks or were not radiated. Number of tumors formed and time to tumor onset for each mouse were recorded through tumor harvest after week 24. Tumor multiplicity and time to tumor onset were compared.ResultsTime to tumor onset was significantly shorter in control mice compared to mice receiving either oral (P =. 025) or topical (P =. 015) curcumin. A significant difference in the average number of tumors formed per mouse was seen, as fewer tumors were formed in the oral curcumin (P =. 01) and topical curcumin (P =. 01) groups, compared with respective controls. No significant difference in average number of tumors per mouse was seen between oral and topical curcumin (P =. 56), suggesting that both routes were equally effective.ConclusionCurcumin appears to inhibit skin cancer formation and prolong time to tumor onset when administered by either an oral or topical route. These data suggest that curcumin may have chemopreventive potential against skin cancer, necessitating future experimentation with human subjects.
Clinical Phenomenology and Mortality in Charles Bonnet Syndrome
Authors: Lapid Maria I. , Burton M. Caroline , Chang Megan T. , Rummans Teresa A. , Cha Stephen S. , Leavitt Jacqueline A. , Boeve Bradley F. 
Published: February 2013

Background/Aim: Despite existing diagnostic criteria for Charles Bonnet syndrome (CBS), clinical manifestations vary greatly. We examined the clinical course and mortality of patients diagnosed with CBS. Methods: We conducted a retrospective chart review of patients with CBS. We collected demographic and clinical information and medical burden scores. Kaplan-Meier mortality curves were compared using log-rank test. Cox proportional hazard model was used for multivariate analysis and hazard ratio (HR). Mortality was compared to expected mortality from Minnesota population. Results: Seventy-seven patients with CBS had a mean age of 79.5 (standard deviation ± 13.0) and were predominantly Caucasian (97%) and female (73%). In all, 20 (26%) subsequently developed a dementia syndrome, most often Lewy body. A total of 46 (60%) deaths occurred with an average follow-up time of 33.0 months. Characteristics associated with mortality included older age (75-84 [HR 3.34, P = .029], >85 [HR 4.58, P = .007]) and renal disease (HR 3.39 with 95% confidence interval 1.31-8.80, P = .012). Medical burden scores were not associated with overall mortality. Mortality was high compared to Minnesota population ( P < .0001). Conclusions: A large proportion of patients with CBS developed dementia, and there was a high mortality rate associated with older age and renal disease. Medical burden was not associated with mortality.
Hepatic effects of ketamine administration for 2 weeks in rats
Authors: Kalkan Y. , Tomak Y. , Altuner D. , Tumkaya L. , Bostan H. , Yilmaz A. , Unal D. , Kara A. , Turan A. 
Published: February 2013

The aim of the present study was to investigate the long-term and high-dose application of ketamine on the liver by employing histologic and biochemical methods. A total of 30 male rats were randomly assigned to control and four treatment groups ( n: 6). Saline for control group and different doses of ketamine for four treatment groups (40, 60, 80 and 100 mg kg−1) were administered intraperitoneal twice a day for 2 weeks. Immunohistological staining, light and electron microscopy were used to study tissue specimens. Histopathological changes were more severe and diverse in groups 80 and 100 mg kg−1 day−1, and the least significant change was observed in groups 40 and 60 mg kg−1 day−1. The most important ultrastructural changes were seen in mitochondria and in the rough endoplasmic reticulum. The immunoreactivity of calcineurin was determined as different. Prolonged use of ketamine caused hepatocellualar toxicity and histological changes in hepatocytes in a dose-dependent manner in all experimental groups.
Early Weight-Bearing After Percutaneous Reduction and Screw Fixation for Low-Energy Lisfranc Injury
Authors: Wagner Emilio , Ortiz Cristian , Villalón Ignacio E. , Keller Andrés , Wagner Pablo 
Published: February 2013

Background: Anatomic restoration and postoperative rehabilitation of displaced fracture-dislocations of the tarsometatarsal junction of the foot are essential. Our objective was to report percutaneous reduction and screw fixation results in low-energy Lisfranc fracture dislocation injuries that were treated with early weight-bearing and rehabilitation. Methods: We retrospectively evaluated patients with low-energy Lisfranc injuries who underwent surgery between May 2007 and April 2011. The study reviewed 22 patients (12 men and 10 women) with an average age of 36.2 years (range, 16-50 years) and an average follow-up of 33.2 months (range, 12-50 months). We report the mechanism of trauma; quality of reduction in the postoperative digital radiographs; subjective satisfaction; AOFAS score; time required to return to work, recreational activities, and low-impact sports; and complications. Postoperatively, all of the patients were instructed to be non-weight-bearing for 3 weeks, and the stitches were removed after 2 weeks. At the third postoperative week, the patients were encouraged to bear weight as tolerated. Results: Quality of reduction was anatomic or near anatomic in 100% of cases. The subjective satisfaction reported by patients was very good, with complete satisfaction in 20 of them (90.9%). The AOFAS average was 94 points (range, 90-100 points). Average return to work was at 7 weeks (range, 6-9 weeks), recreational activities 7.2 weeks (range, 6-9 weeks), training for low-impact sports 7.6 weeks (range, 7-8 weeks), and symptom-free sport activities 12.4 weeks (range, 11-13 weeks). Conclusion: In this selected group of patients with low-energy Lisfranc fracture dislocation, anatomic or near-anatomic reduction can be achieved with percutaneous reduction and screw fixation. Early weight-bearing is possible in these patients, and early return to regular activities and low-impact sport can be expected. Level of Evidence: Level IV, retrospective case series.
Listening and Representation
Authors: Herrick Rebekah 
Published: February 2013

AbstractPolicy representation requires legislators to advance the interests of their constituents. As a consequence, much research on representation examines the congruence between constituents' preferences and legislators' behaviors. This article argues it is more realistic to think of policy representation as listening—a process—than congruence—an outcome. Listening involves legislators monitoring constituent interests and using that information in making decisions. Using data from a survey of state legislators in 26 states, this research finds that monitoring contributes to using constituent information and offers a measure of listening based on these two behaviors. Furthermore, it finds that compared with the decisions of others, the decisions (measured as cosponsoring gay, lesbian, and bisexual [GLB] issue legislation) of legislators who listen are more strongly influenced by district preferences (measured as district votes on same-sex marriage ballot initiatives). This suggests that listening contributes to representation.
Botulinum toxin-A for the treatment of overactive bladder: UK contributions
Authors: Seth JH , Dowson C , Khan MS , Panicker JN , Fowler CJ , Dasgupta P , Sahai A 
Published: February 2013

Background: Botulinum toxin-A (BoNT/A) is now established second-line management for refractory overactive bladder (OAB) and recognised in many incontinence guidelines and pathways. For those with neurogenic detrusor overactivity secondary to spinal cord injury or multiple sclerosis, the toxin is currently licensed in certain parts of the world, including the UK. It is an effective treatment in those in whom antimuscarinics and conservative measures have failed who have symptoms of OAB and or detrusor overactivity (DO). Methods: Treatment can be given in an outpatient setting and can be administered under local anaesthesia. Its efficacy lasts for between six and 12 months. Results: It has an acceptable safety profile with the biggest risk being urinary tract infection and difficulty emptying the bladder, necessitating clean intermittent self-catheterisation (CISC). Medium-term follow-up suggests repeated injections are also safe and efficacious. Conclusions: The mechanism of action of the toxin is more complicated than originally thought, and it seems likely that it affects motor and sensory nerves of the bladder. In the last 10 years much of the progress of this treatment from early experimental trials to mainstream clinical use, and a better understanding of how it works in the bladder, are as a result of research conducted in the UK. This review summarises the significant and substantial evidence for BoNT/A to treat refractory OAB from UK centres.
GmGBP1, a homolog of human ski interacting protein in soybean, regulates flowering and stress tolerance in Arabidopsis
Authors: Zhang Yanwei , Zhao Lin , Li Haiyan , Gao Yang , Li Yongguang , Wu Xiaoxia , Teng Weili , Han Yingpeng , Zhao Xue , Li Wenbin 
Published: February 2013

Abstract

Background

SKIP is a transcription cofactor in many eukaryotes. It can regulate plant stress tolerance in rice and Arabidopsis. But the homolog of SKIP protein in soybean has been not reported up to now.

Results
In this study, the expression patterns of soybean GAMYB binding protein gene (GmGBP1) encoding a homolog of SKIP protein were analyzed in soybean under abiotic stresses and different day lengths. The expression of GmGBP1 was induced by polyethyleneglycol 6000, NaCl, gibberellin, abscisic acid and heat stress. GmGBP1 had transcriptional activity in C-terminal. GmGBP1 could interact with R2R3 domain of GmGAMYB1 in SKIP domain to take part in gibberellin flowering pathway. In long-day (16 h-light) condition, transgenic Arabidopsis with the ectopic overexpression of GmGBP1 exhibited earlier flowering and less number of rosette leaves; Suppression of AtSKIP in Arabidopsis resulted in growth arrest, flowering delay and down-regulation of many flowering-related genes (CONSTANS, FLOWERING LOCUS T, LEAFY); Arabidopsis myb33 mutant plants with ectopic overexpression of GmGBP1 showed the same flowering phenotype with wild type. In short-day (8 h-light) condition, transgenic Arabidopsis plants with GmGBP1 flowered later and showed a higher level of FLOWERING LOCUS C compared with wild type. When treated with abiotic stresses, transgenic Arabidopsis with the ectopic overexpression of GmGBP1 enhanced the tolerances to heat and drought stresses but reduced the tolerance to high salinity, and affected the expressions of several stress-related genes.

Conclusions
In Arabidopsis, GmGBP1 might positively regulate the flowering time by affecting CONSTANS, FLOWERING LOCUS T, LEAFY and GAMYB directly or indirectly in photoperiodic and gibberellin pathways in LDs, but GmGBP1 might represse flowering by affecting FLOWERING LOCUS C and SHORT VEGETATIVE PHASE in autonomous pathway in SDs. GmGBP1 might regulate the activity of ROS-eliminating to improve the resistance to heat and drought but reduce the high-salinity tolerance.
Risk of type 2 diabetes according to traditional and emerging anthropometric indices in Spain, a Mediterranean country with high prevalence of obesity: results from a large-scale prospective cohort study
Authors: Huerta José María , Tormo María-José , Chirlaque María-Dolores , Gavrila Diana , Amiano Pilar , Arriola Larraitz , Ardanaz Eva , Rodríguez Laudina , Sánchez María-José , Mendez Michelle , Salmerón Diego , Barricarte Aurelio , Burgui Rosana , Dorronsoro Miren , Larrañaga Nerea , Molina-Montes Esther , Moreno-Iribas Conchi , Quirós José Ramón , Toledo Estefanía , Travier Noémie , González Carlos A , Navarro Carmen 
Published: February 2013

Abstract

Background
Obesity is a major risk factor for type 2 diabetes mellitus (T2DM). A proper anthropometric characterisation of T2DM risk is essential for disease prevention and clinical risk assessement.

Methods
Longitudinal study in 37 733 participants (63% women) of the Spanish EPIC (European Prospective Investigation into Cancer and Nutrition) cohort without prevalent diabetes. Detailed questionnaire information was collected at baseline and anthropometric data gathered following standard procedures. A total of 2513 verified incident T2DM cases occurred after 12.1 years of mean follow-up. Multivariable Cox regression was used to calculate hazard ratios of T2DM by levels of anthropometric variables.

Results
Overall and central obesity were independently associated with T2DM risk. BMI showed the strongest association with T2DM in men whereas waist-related indices were stronger independent predictors in women. Waist-to-height ratio revealed the largest area under the ROC curve in men and women, with optimal cut-offs at 0.60 and 0.58, respectively. The most discriminative waist circumference (WC) cut-off values were 99.4 cm in men and 90.4 cm in women. Absolute risk of T2DM was higher in men than women for any combination of age, BMI and WC categories, and remained low in normal-waist women. The population risk of T2DM attributable to obesity was 17% in men and 31% in women.

Conclusions
Diabetes risk was associated with higher overall and central obesity indices even at normal BMI and WC values. The measurement of waist circumference in the clinical setting is strongly recommended for the evaluation of future T2DM risk in women.
Pharmacological, antioxidant, genotoxic studies and modulation of rat splenocyte functions by Cyperus rotundus extracts
Authors: Soumaya Kilani-Jaziri , Dhekra Mhalla , Fadwa Châbane , Zied Ghedira , Ilef Limem , Kamel Ghedira , Leila Chekir-Ghedira 
Published: February 2013

Abstract

Background

Cyperus rotundus Linn. (Cyperaceae) is a Tunisian medicinal plant used in folkloric (traditional) medicine to treat stomach disorders and inflammatory diseases. The present study explored the analgesic, anti-inflammatory and genotoxic activities of extracts from the aerial parts of C. rotundus. The antioxidant capacity and the modulation of splenocyte functions by these extracts were also investigated in mice. The phytochemical analysis was carried out using standard methods.

Methods
Aqueous, ethyl acetate, methanol and TOF-enriched extracts (300, 150, and 50 μg/ml) were evaluated for their analgesic and anti-inflammatory activities. 4, 2, and 1 mg/ml of each extract were tested to investigate their effect on lipid peroxidation. The genotoxic study was monitored by measuring the structural chromosome aberrations of mice treated with 300 mg/kg of extract. The proliferation of lymphocytes in the absence and presence of mitogens was assessed at a concentration range 1–1000 μg/ml.

Results
The tested extracts were able to decrease the mouse ear oedema induced by xylene. Furthermore, it was shown that the same extracts reduced the number of abdominal contractions caused by acetic acid in mice, revealing the peripheral analgesic activity of these extracts. It is worth noting that mice treated with doses up to 300 mg/kg b.w. of Cyperus rotundus extracts did not exhibit any toxicity. The tested extracts significantly enhance lymphocyte proliferation at 1 mg/ml.

Conclusions
It appears that C. rotundus extracts contain potent components such as flavonoids that may potentially be useful for modulating the immune cell functions, provoking analgesic, anti-inflammatory and antioxidant effects.
Cytosolic Ca2+ shifts as early markers of cytotoxicity
Authors: Wyrsch Philippe , Blenn Christian , Pesch Theresa , Beneke Sascha , Althaus Felix R 
Published: February 2013

Abstract
The determination of the cytotoxic potential of new and so far unknown compounds as well as their metabolites is fundamental in risk assessment. A variety of strategic endpoints have been defined to describe toxin-cell interactions, leading to prediction of cell fate. They involve measurement of metabolic endpoints, bio-energetic parameters or morphological cell modifications. Here, we evaluated alterations of the free cytosolic Ca2+ homeostasis using the Fluo-4 dye and compared results with the metabolic cell viability assay Alamar Blue. We investigated a panel of toxins (As2O3, gossypol, H2O2, staurosporine, and titanium(IV)-salane complexes) in four different mammalian cell lines covering three different species (human, mouse, and African green monkey). All tested compounds induced an increase in free cytosolic Ca2+ within the first 5 s after toxin application. Cytosolic Ca2+ shifts occurred independently of the chemical structure in all tested cell systems and were persistent up to 3 h. The linear increase of free cytosolic Ca2+ within the first 5 s of drug treatment correlates with the EC25 and EC75 values obtained in Alamar Blue assays one day after toxin exposure. Moreover, a rise of cytosolic Ca2+ was detectable independent of induced cell death mode as assessed by caspase and poly(ADP-ribose) polymerase (PARP) activity in HeLa versus MCF-7 cells at very low concentrations. In conclusion, a cytotoxicity assay based on Ca2+ shifts has a low limit of detection (LOD), is less time consuming (at least 24 times faster) compared to the cell viability assay Alamar Blue and is suitable for high-troughput-screening (HTS).
Toll-like receptor 4 mediates microglial activation and production of inflammatory mediators in neonatal rat brain following hypoxia: role of TLR4 in hypoxic microglia
Authors: Yao Linli , Kan Enci Mary , Lu Jia , Hao Aijun , Dheen S Thameem , Kaur Charanjit , Ling Eng-Ang 
Published: February 2013

AbstractBackgroundHypoxia induces microglial activation which causes damage to the developing brain. Microglia derived inflammatory mediators may contribute to this process. Toll-like receptor 4 (TLR4) has been reported to induce microglial activation and cytokines production in brain injuries; however, its role in hypoxic injury remains uncertain. We investigate here TLR4 expression and its roles in neuroinflammation in neonatal rats following hypoxic injury.MethodsOne day old Wistar rats were subjected to hypoxia for 2 h. Primary cultured microglia and BV-2 cells were subjected to hypoxia for different durations. TLR4 expression in microglia was determined by RT-PCR, western blot and immunofluorescence staining. Small interfering RNA (siRNA) transfection and antibody neutralization were employed to downregulate TLR4 in BV-2 and primary culture. mRNA and protein expression of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and inducible nitric oxide synthase (iNOS) was assessed. Reactive oxygen species (ROS), nitric oxide (NO) and NF-κB levels were determined by flow cytometry, colorimetric and ELISA assays respectively. Hypoxia-inducible factor-1 alpha (HIF-1α) mRNA and protein expression was quantified and where necessary, the protein expression was depleted by antibody neutralization.In vivoinhibition of TLR4 with CLI-095 injection was carried out followed by investigation of inflammatory mediators expression via double immunofluorescence staining.ResultsTLR4 immunofluorescence and protein expression in the corpus callosum and cerebellum in neonatal microglia were markedly enhanced post-hypoxia.In vitro, TLR4 protein expression was significantly increased in both primary microglia and BV-2 cells post-hypoxia. TLR4 neutralization in primary cultured microglia attenuated the hypoxia-induced expression of TNF-α, IL-1β and iNOS. siRNA knockdown of TLR4 reduced hypoxia-induced upregulation of TNF-α, IL-1β, iNOS, ROS and NO in BV-2 cells. TLR4 downregulation-mediated inhibition of inflammatory cytokines in primary microglia and BV-2 cells was accompanied by the suppression of NF-κB activation. Furthermore, HIF-1α antibody neutralization attenuated the increase of TLR4 expression in hypoxic BV-2 cells. TLR4 inhibitionin vivoattenuated the immunoexpression of TNF-α, IL-1β and iNOS on microglia post-hypoxia.ConclusionActivated microglia TLR4 expression mediated neuroinflammation via a NF-κB signaling pathway in response to hypoxia. Hence, microglia TLR4 presents as a potential therapeutic target for neonatal hypoxia brain injuries.