bluuebunny/crossref_metadata_2025_split huggingface dataset:
Predication Drives Verb Cortical Signatures
Authors: Hernández Mireia , Fairhall Scott L. , Lenci Alessandro , Baroni Marco , Caramazza Alfonso 
Published: February 2014

Abstract
Verbs and nouns are fundamental units of language, but their neural instantiation remains poorly understood. Neuropsychological research has shown that nouns and verbs can be damaged independently of each other, and neuroimaging research has found that several brain regions respond differentially to the two word classes. However, the semantic–lexical properties of verbs and nouns that drive these effects remain unknown. Here we show that the most likely candidate is predication: a core lexical feature involved in binding constituent arguments (boy, candies) into a unified syntactic–semantic structure expressing a proposition (the boy likes the candies). We used functional neuroimaging to test whether the intrinsic “predication-building” function of verbs is what drives the verb–noun distinction in the brain. We first identified verb-preferring regions with a localizer experiment including verbs and nouns. Then, we examined whether these regions are sensitive to transitivity—an index measuring its tendency to select for a direct object. Transitivity is a verb-specific property lying at the core of its predication function. Neural activity in the left posterior middle temporal and inferior frontal gyri correlates with transitivity, indicating sensitivity to predication. This represents the first evidence that grammatical class preference in the brain is driven by a word's function to build predication structures.
On the Role of SST Forcing in the 2011 and 2012 Extreme U.S. Heat and Drought: A Study in Contrasts
Authors: Wang Hailan , Schubert Siegfried , Koster Randal , Ham Yoo-Geun , Suarez Max 
Published: February 2014

Abstract
This study compares the extreme heat and drought that developed over the United States in 2011 and 2012 with a focus on the role of sea surface temperature (SST) forcing. Experiments with the NASA Goddard Earth Observing System, version 5 (GEOS-5), atmospheric general circulation model show that the winter/spring response over the United States to the Pacific SST is remarkably similar for the two years despite substantial differences in the tropical Pacific SST. As such, the pronounced winter and early spring temperature differences between the two years (warmth confined to the south in 2011 and covering much of the continent in 2012) primarily reflect differences in the contributions from the Atlantic and Indian Oceans, with both acting to cool the east and upper Midwest during 2011, while during 2012 the Indian Ocean reinforced the Pacific-driven, continental-wide warming and the Atlantic played a less important role. During late spring and summer of 2011, the tropical Pacific SST forced a continued warming and drying over the southern United States, though considerably weaker than observed. Nevertheless, the observed 2011 anomalies fall well within the model’s intraensemble spread. In contrast, the observed rapid development of intense heat and drying over the central United States during June and July 2012 falls on the margins of the model’s intraensemble spread, with the response to the SST giving little indication that 2012 would produce record-breaking precipitation deficits and heat. A diagnosis of the 2012 observed circulation anomalies shows that the most extreme heat and drought was tied to the development of a stationary Rossby wave and an associated anomalous upper-tropospheric high maintained by weather transients.
Comparison of alternate scoring of variables on the performance of the frailty index
Authors: Peña Fernando G , Theou Olga , Wallace Lindsay , Brothers Thomas D , Gill Thomas M , Gahbauer Evelyne A , Kirkland Susan , Mitnitski Arnold , Rockwood Kenneth 
Published: February 2014

Abstract

Background
The frailty index (FI) is used to measure the health status of ageing individuals. An FI is constructed as the proportion of deficits present in an individual out of the total number of age-related health variables considered. The purpose of this study was to systematically assess whether dichotomizing deficits included in an FI affects the information value of the whole index.

Methods
Secondary analysis of three population-based longitudinal studies of community dwelling individuals: Nova Scotia Health Survey (NSHS, n = 3227 aged 18+), Survey of Health, Ageing and Retirement in Europe (SHARE, n = 37546 aged 50+), and Yale Precipitating Events Project (Yale-PEP, n = 754 aged 70+). For each dataset, we constructed two FIs from baseline data using the deficit accumulation approach. In each dataset, both FIs included the same variables (23 in NSHS, 70 in SHARE, 33 in Yale-PEP). One FI was constructed with only dichotomous values (marking presence or absence of a deficit); in the other FI, as many variables as possible were coded as ordinal (graded severity of a deficit). Participants in each study were followed for different durations (NSHS: 10 years, SHARE: 5 years, Yale PEP: 12 years).

Results
Within each dataset, the difference in mean scores between the ordinal and dichotomous-only FIs ranged from 0 to 1.5 deficits. Their ability to predict mortality was identical; their absolute difference in area under the ROC curve ranged from 0.00 to 0.02, and their absolute difference between Cox Hazard Ratios ranged from 0.001 to 0.009.

Conclusions
Analyses from three diverse datasets suggest that variables included in an FI can be coded either as dichotomous or ordinal, with negligible impact on the performance of the index in predicting mortality.
Estrogen receptor α-coupled Bmi1 regulation pathway in breast cancer and its clinical implications
Authors: Wang Huali , Liu Haijing , Li Xin , Zhao Jing , Zhang Hong , Mao Jingzhuo , Zou Yongxin , Zhang Hong , Zhang Shuang , Hou Wei , Hou Lin , McNutt Michael A , Zhang Bo 
Published: February 2014

Abstract

Background
Bmi1 has been identified as an important regulator in breast cancer, but its relationship with other signaling molecules such as ERα and HER2 is undetermined.

Methods
The expression of Bmi1 and its correlation with ERα, PR, Ki-67, HER2, p16INK4a, cyclin D1 and pRB was evaluated by immunohistochemistry in a collection of 92 cases of breast cancer and statistically analyzed. Stimulation of Bmi1 expression by ERα or 17β-estradiol (E2) was analyzed in cell lines including MCF-7, MDA-MB-231, ERα-restored MDA-MB-231 and ERα-knockdown MCF-7 cells. Luciferase reporter and chromatin immunoprecipitation assays were also performed.

Results
Immunostaining revealed strong correlation of Bmi1 and ERα expression status in breast cancer. Expression of Bmi1 was stimulated by 17β-estradiol in ERα-positive MCF-7 cells but not in ERα-negative MDA-MB-231 cells, while the expression of Bmi1 did not alter expression of ERα. As expected, stimulation of Bmi1 expression could also be achieved in ERα-restored MDA-MB-231 cells, and at the same time depletion of ERα decreased expression of Bmi1. The proximal promoter region of Bmi1 was transcriptionally activated with co-transfection of ERα in luciferase assays, and the interaction of the Bmi1 promoter with ERα was confirmed by chromatin immunoprecipitation. Moreover, in breast cancer tissues activation of the ERα-coupled Bmi1 pathway generally correlated with high levels of cyclin D1, while loss of its activity resulted in aberrant expression of p16INK4a and a high Ki-67 index, which implied a more aggressive phenotype of breast cancer.

Conclusions
Expression of Bmi1 is influenced by ERα, and the activity of the ERα-coupled Bmi1 signature impacts p16INK4a and cyclin D1 status and thus correlates with the tumor molecular subtype and biologic behavior. This demonstrates the important role which is played by ERα-coupled Bmi1 in human breast cancer.
Epidemiology and treatment outcomes of diabetic retinopathy in a diabetic population from Cameroon
Authors: Jingi Ahmadou M , Noubiap Jean Jacques N , Ellong Augustin , Bigna Jean Joel R , Mvogo Côme Ebana 
Published: February 2014

Abstract

Background
Diabetic retinopathy (DR) is the most common microvascular complication of diabetes. It can lead to significant visual loss. The aim of this study was to determine the frequency and clinical profile of diabetic retinopathy, and assess the outcomes of laser photocoagulation therapy in a diabetic population in Cameroon.

Methods
We carried out a prospective cohort study during 24 months in the Department of Ophthalmology of the Douala General Hospital, Cameroon. We included all diabetic patients who were referred from diabetes clinics for ophthalmologic evaluation. Data included type and duration of diabetes, visual acuity, intra-ocular pressure, results of fundoscopy and fluorescein angiography, and outcomes two months after treatment with laser photocoagulation.

Results
We included 407 patients; 88% had type 2 diabetes. Their mean duration of diabetes was 6.4 years (SD=6.6). Forty point three percent (164/407) of patients were found to have DR on fundoscopy. Of the 164 patients with DR, 63.4% (104/164) had non-proliferative and 36.6% (60/164) had proliferative DR. Diabetic maculopathy was found in 14.5% (59/407) of all participants, and 36% (59/164) of patients with DR. There was a strong correlation between the duration of diabetes and retinopathy status (p < 0.001, r = 0.9541). Overall, 17.4% (71/407) of patients were eligible for laser photocoagulation. Of these, 66.2% (47/71) were treated, and 78.7% (37/47) of treated patients came back for control two months later. Among these treated patients an improvement of the retinopathy was noted in 73% (27/37), no change in 16.2% (6/37) and a worsening in 10.8% (4/37). Severe proliferative DR was significantly associated with treatment failure (p < 0.001).

Conclusions
The frequency of DR may be high among diabetic patients in Cameroon. There was a good uptake of laser photocoagulation therapy among patients affected by DR in our setting, with good treatment outcomes. Interventions to prevent diabetes and increase the precocity of diagnosis and treatment of DR should be scaled up.
Treatment fidelity of brief motivational interviewing and health education in a randomized clinical trial to promote dental attendance of low-income mothers and children: Community-Based Intergenerational Oral Health Study “Baby Smiles”
Authors: Weinstein Philip , Milgrom Peter , Riedy Christine A , Mancl Lloyd A , Garson Gayle , Huebner Colleen E , Smolen Darlene , Sutherland Marilynn , Nykamp Ann 
Published: February 2014

Abstract

Background
Fidelity assessments are integral to intervention research but few published trials report these processes in detail. We included plans for fidelity monitoring in the design of a community-based intervention trial.

Methods
The study design was a randomized clinical trial of an intervention provided to low-income women to increase utilization of dental care during pregnancy (mother) or the postpartum (child) period. Group assignment followed a 2 × 2 factorial design in which participants were randomly assigned to receive either brief Motivational Interviewing (MI) or Health Education (HE) during pregnancy (prenatal) and then randomly reassigned to one of these groups for the postpartum intervention. The study setting was four county health departments in rural Oregon State, USA. Counseling was standardized using a step-by-step manual. Counselors were trained to criteria prior to delivering the intervention and fidelity monitoring continued throughout the implementation period based on audio recordings of counselor-participant sessions. The Yale Adherence and Competence Scale (YACS), modified for this study, was used to code the audio recordings of the counselors’ delivery of both the MI and HE interventions. Using Interclass Correlation Coefficients totaling the occurrences of specific MI counseling behaviors, ICC for prenatal was .93, for postpartum the ICC was .75. Participants provided a second source of fidelity data. As a second source of fidelity data, the participants completed the Feedback Questionnaire that included ratings of their satisfaction with the counselors at the completion of the prenatal and post-partum interventions.

Results
Coding indicated counselor adherence to MI protocol and variation among counselors in the use of MI skills in the MI condition. Almost no MI behaviors were found in the HE condition. Differences in the length of time to deliver intervention were found; as expected, the HE intervention took less time. There were no differences between the overall participants’ satisfaction ratings of the HE and MI sessions by individual counselor or overall (p > .05).

Conclusions
Trial design, protocol specification, training, and continuous supervision led to a high degree of treatment fidelity for the counseling interventions in this randomized clinical trial and will increase confidence in the interpretation of the trial findings.

Trial registration
ClinicalTrials.gov: NCT01120041
RETRACTED ARTICLE: Emodin enhances osteogenesis and inhibits adipogenesis
Authors: Yang Feng , Yuan Pu-wei , Hao Yang-Quan , Lu Zheng-Mao 
Published: February 2014

Abstract

Background
It has been suggested that the formation of osteoblasts in bone marrow is closely associated with adipogenesis, and the balance between osteogenesis and adipogenesis differentiation of MSCs (mesenchymal stem cells) is disrupted in osteoporosis. In order to improve the treatment of osteoporosis, available agents with roles of regulating the balance is highly desirable. Emodin is a natural anthraquinone derivative extracted from Chinese herbs, which have been used to treat bone diseases for thousands of years. However, the underlying molecular mechanisms of emodin in modulating osteogenesis and adipogenesis remain poorly understood.

Methods
The molecular mechanisms of emodin on the processes of osteogenesis and adipogenesis in ovariectomized mouse and BMSCs (bone marrow mesenchymal stem cells) have been studied. We have analyzed the effects of emodin in vivo and in vitro. Female ICR mice were assigned to three groups: sham group, ovariectomy group, emodin group. Efficacy was evaluated by H&E, immunohistochemical assay and Micro-CT. In vitro, we analyze the effect of emodin—at concentrations between 0.1 μM and 10 μM-on the processes of inducing osteogenesis and inhibiting adipogenesis in BMSCs by ALP, Oil red O staining, real time RT-PCR and western blot.

Results
As our experiment shows that emodin could increase the number of osteoblast, BMD (bone mineral density), BV/TV (trabecular bone volume fraction), Tb.N (trabecular number) and Conn.D (connectivity density) of OVX (ovariectomized) mice and decrease the bone marrow fat tissue and adipocytes. The genes and proteins expression of osteogenesis markers, such as Runx2, osterix, collagen type I, osteocalcin, or ALP were up-regulated. While, the genes and proteins involved in adipogenesis, PPARγ, C/EBPα and ap2 were down-regulated.

Conclusion
It proves that emodin inhibits adipocyte differentiation and enhances osteoblast differentiation from BMSCs.
Musculoskeletal disorder risk factors among nursing professionals in low resource settings: a cross-sectional study in Uganda
Authors: Munabi Ian G , Buwembo William , Kitara David L , Ochieng Joseph , Mwaka Erisa S 
Published: February 2014

Abstract

Background
Musculoskeletal disorders (MSD) constitute one of the main occupational hazards among health care workers. However, few epidemiological studies on work related MSD among nursing professionals have been carried out in Africa. The purpose of this study was to assess the work related musculoskeletal disorders and associated risk factors among nursing professionals in Uganda.

Methods
This was a cross-sectional study of MSD among 880 nursing professionals from five selected hospitals in Uganda. Data was collected using a questionnaire adapted from the Dutch Musculoskeletal and Nordic Musculoskeletal questionnaires. Descriptive (mean, standard deviation and percentages) and inferential (Chi square test and logistic regression analysis) statistics were used to analyse data. Alpha level was set at p < 0.05.

Results
A total of 741 completed questionnaires were analysed (response rate 85.4%). The average age of the respondents was 35.4 (SD 10.7) years and a majority were female (85.7%). The average working hours per week was 43.7 (SD 18.9 hours). The 12-month period-prevalence of MSD at anybody site was 80.8%. The most common site of MSD was the lower back (61.9%). Significant risk factors for reported MSD included often working in a slightly bent posture (adjOR 2.25, 95% CI 1.20-4.26), often working in a slightly twisted posture for long (adjOR 1.97, 95% CI 1.03-3.77), mental exhaustion (adjOR 2.05, 95% CI 1.17-3.5), being absent from the work station for more than 6 months due to illness or an accident (adjO|R, 4.35, 95% CI 1.44-13.08) and feeling rested after a break (adjOR 2.09, 95% CI 1.16-3.76).

Conclusions
Musculoskeletal disorders affect more than 80% of nursing professionals in Uganda with the most commonly, affected site being the lower back. Significant risk factors for MSD include; being absent from the work station for more than 6 months due to illness or an accident, working in awkward postures, pushing/pulling of heavy loads and mental exhaustion. There is a need for greater advocacy, better working conditions and adoption of strategies to reduce occupational injuries.
CD8+T cell–specific induction of NKG2D receptor by doxorubicin plus interleukin-12 and its contribution to CD8+T cell accumulation in tumors
Authors: Hu Jiemiao , Zhu Shiguo , Xia Xueqing , Zhang Liangfang , Kleinerman Eugenie S , Li Shulin 
Published: February 2014

Abstract

Background
Increased infiltration of CD8+T cells into tumors has a positive impact on survival. Our previous study showed that doxorubicin (Dox) plus interleukin-12 (IL-12) boosted the accumulation of CD8+T cells in tumors and had a greater antitumor effect than did either agent alone. The purpose of this study was to determine the impact of NKG2D expression on CD8+T cell infiltration and antitumor efficacy.

Methods
Tumor-bearing mice were administered Dox, IL-12 plasmid DNA, or both via intraperitoneal injection or intramuscular electroporation. The induction of NKG2D on CD8+T cells and other lymphocytes was analyzed via flow cytometry, and NKG2D-positive CD8+T cell–specific localization in tumors was determined by using immunofluorescence staining in various types of immune cell–depleted mice.

Results
The combination of Dox plus IL-12 specifically increased expression of NKG2D in CD8+T cells but not in other types of immune cells, including NK cells, which naturally express NKG2D. This induced NKG2D expression in CD8+T cells was associated with increased accumulation of CD8+T cells in murine tumors. Administration of NKG2D-blocking antibody or CD8+T cell–depletion antibody abrogated the NKG2D+CD8+T cell detection in tumors, whereas administration of NK cell–depletion antibody had no effect. Increased NKG2D expression in CD8+T cells was associated with increased antitumor efficacy in vivo.

Conclusion
We conclude that Dox plus IL-12 induces NKG2D in CD8+T cells in vivo and boosts NKG2D+CD8+T-dependent antitumor immune surveillance. This discovery reveals a novel mechanism for how chemoimmunotherapy synergistically promotes T cell–mediated antitumor immune surveillance.
cAMP signaling inhibits radiation-induced ATM phosphorylation leading to the augmentation of apoptosis in human lung cancer cells
Authors: Cho Eun-Ah , Kim Eui-Jun , Kwak Sahng-June , Juhnn Yong-Sung 
Published: February 2014

Abstract

Background
The ataxia–telangiectasia mutated (ATM) protein kinase plays a central role in coordinating the cellular response to radiation-induced DNA damage. cAMP signaling regulates various cellular responses including metabolism and gene expression. This study aimed to investigate the mechanism through which cAMP signaling regulates ATM activation and cellular responses to ionizing radiation in lung cancer cells.

Methods
Lung cancer cells were transfected with constitutively active stimulatory G protein (GαsQL), and irradiated with γ-rays. The phosphorylation of ATM and protein phosphatase 2A was analyzed by western blotting, and apoptosis was assessed by western blotting, flow cytometry, and TUNNEL staining. The promoter activity of NF-κB was determined by dual luciferase reporter assay. BALB/c mice were treated with forskolin to assess the effect in the lung tissue.

Results
Transient expression of GαsQL significantly inhibited radiation-induced ATM phosphorylation in H1299 human lung cancer cells. Treatment with okadaic acid or knock down of PP2A B56δ subunit abolished the inhibitory effect of Gαs on radiation-induced ATM phosphorylation. Expression of GαsQL increased phosphorylation of the B56δ and PP2A activity, and inhibition of PKA blocked Gαs-induced PP2A activation. GαsQL enhanced radiation-induced cleavage of caspase-3 and PARP and increased the number of early apoptotic cells. The radiation-induced apoptosis was increased by inhibition of NF-κB using PDTC or inhibition of ATM using KU55933 or siRNA against ATM. Pretreatment of BALB/c mice with forskolin stimulated phosphorylation of PP2A B56δ, inhibited the activation of ATM and NF-κB, and augmented radiation-induced apoptosis in the lung tissue. GαsQL expression decreased the nuclear levels of the p50 and p65 subunits and NF-κB-dependent activity after γ-ray irradiation in H1299 cells. Pretreatment with prostaglandin E2 or isoproterenol increased B56δ phosphorylation, decreased radiation-induced ATM phosphorylation and increased apoptosis.

Conclusions
cAMP signaling inhibits radiation-induced ATM activation by PKA-dependent activation of PP2A, and this signaling mechanism augments radiation-induced apoptosis by reducing ATM-dependent activation of NF-κB in lung cancer cells.
Combination therapy with ampicillin and azithromycin in an experimental pneumococcal pneumonia is bactericidal and effective in down regulating inflammation in mice
Authors: Majhi Arnab , Kundu Kiran , Adhikary Rana , Banerjee Madhubanti , Mahanti Sayantika , Basu Anirban , Bishayi Biswadev 
Published: February 2014

Abstract

Objectives
Emergence of multidrug resistance among Streptococcus pneumoniae (SP), has limited the available options used to treat infections caused by this organism. The objective of this study was to compare the role of monotherapy and combination therapy with ampicillin (AMP) and azithromycin (AZM) in eradicating bacterial burden and down regulating lung inflammation in a murine experimental pneumococcal infection model.

Methods
Balb/C mice were infected with 106 CFU of SP. Treatments with intravenous ampicillin (200 mg/kg) and azithromycin (50 mg/kg) either alone or in combination was initiated 18 h post infection, animals were sacrificed from 0 – 6 h after initiation of treatment. AMP and AZM were quantified in serum by microbiological assay. Levels of TNF-α, IFN-γ IL-6, and IL-10 in serum and in lungs, along with myeloperoxidase, inflammatory cell count in broncho alveolar lavage fluid, COX-2 and histopathological changes in lungs were estimated.

Results
Combination therapy down regulated lung inflammation and accelerated bacterial clearance. This approach also significantly decreased TNF-α, IFN-γ, IL-6 and increased IL-10 level in serum and lungs along with decreased myeloperoxidase, pulmonary vascular permeability, inflammatory cell numbers and COX-2 levels in lungs.

Conclusions
Combinatorial therapy resulted in comparable bactericidal activity against the multi-drug resistant isolate and may represent an alternative dosing strategy, which may help to alleviate problems with pneumococcal pneumonia.