bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of sedation on visual sensations in patients undergoing cataract surgery under topical anaesthesia: a prospective randomized masked trial
Authors: Venkatakrishnan Jaichandran V. , Kumar Chandra M. , Ratra Vineet , Viswanathan Jagadeesh , Jeyaraman Vijay A. , Ragavendera Thennarasu 
Published: September 2011

Abstract.Purpose:  The main aim of the study was to determine whether intravenous sedation with midazolam reduces the ability of patients to see during cataract surgery performed under topical anaesthesia. We also sought to determine the effects of sedation on patient’s level of disturbance to the microscope light and visualization of surgical instruments and on the overall of experience of the patients during surgery.Methods:  A total of 78 patients, aged 40–75 years, were randomly divided into two groups: Group S, (sedation) who received intravenous midazolam 0.015 mg/kg, and Group NS, (no sedation) who did not receive midazolam. Patients with history of anxiety, those with history of intraocular surgery and those with severe chronic obstructive pulmonary disease were excluded. Topical anaesthesia was achieved by the application of 2% xylocaine gel over the conjunctiva. A blinded observer interviewed all the patients 30 min after the surgery using a standard questionnaire.Results:  Significant number of patients (25.6%) in Group NS was disturbed a lot because of the microscope light compared to Group S (5.1%), p = 0.021. Also, statistically significant number of patients in Group S (48.7%) compared to Group NS (20.5%) was not sure about the images perceived during surgery and were unable to recollect them after the surgery, p = 0.008, and 12.8% of the patients in Group NS reported the visual experience as frightening compared to 2.6% of patients in Group S, p = 0.239.Conclusion:  Our study confirms that intravenous midazolam reduces both the ability to see and recall intraoperative visual images in patients undergoing cataract surgery under topical anaesthesia.
Active Trachoma Is Associated with Increased Conjunctival Expression ofIL17Aand Profibrotic Cytokines
Authors: Burton Matthew J. , Ramadhani Athumani , Weiss Helen A. , Hu Victor , Massae Patrick , Burr Sarah E. , Shangali Wahida , Holland Martin J. , Mabey David C. W. , Bailey Robin L. 
Published: September 2011

ABSTRACTThe immunological basis of scarring trachoma is not well understood. It is unclear whether it is driven primarily through cell-mediated adaptive or epithelial-cell-derived innate responses. The purpose of this study was to investigate the expression of the inflammatory and fibrogenic mediators which may be involved. We conducted a cross-sectional survey of children living in an untreated trachoma-endemic community in Tanzania. The children were examined for signs of trachoma, and swabs were collected for bacteriological culture and RNA and DNA isolation.Chlamydia trachomatiswas detected by the Amplicor PCR test. The expression of the following genes was measured by quantitative reverse transcription-PCR (RT-PCR):S100A7,IL1B,IL17A,IL23A,CXCL5,CCL18,TLR2,NLRP3,KLRD1,CTGF, andMMP9. Four hundred seventy children under the age of 10 years were included. Follicular trachoma (TF) was detected in 65 children (14%),C. trachomatiswas detected in 25 (5%), and bacterial pathogens were cultured in 161 (34%). TF was associated with significantly increased expression ofS100A7,IL17A,CCL18,CXCL5, andCTGF.Expression was increased further in the presence of papillary inflammation. Nonchlamydial bacterial infection was associated with increased expression ofIL17A,CXCL5,CCL18, andKLRD1.IL17Aexpression was associated with increased expression ofS100A7,CXCL5,CCL18,KLRD1, andCTGF.These data are consistent with a role for IL-17A in orchestrating the proinflammatory response in trachoma. Its activity may be promoted either as part of the cell-mediated response or through innate pathways. It may drive a range of proinflammatory factors leading to excessive tissue damage and repair involving fibrosis.
Complete Genomic Sequence of the Equol-Producing Bacterium Eggerthella sp. Strain YY7918, Isolated from Adult Human Intestine
Authors: Yokoyama Shin-ichiro , Oshima Kenshiro , Nomura Izumi , Hattori Masahira , Suzuki Tohru 
Published: September 2011

ABSTRACT

Eggerthella
sp. strain YY7918 was isolated from the intestinal flora of a healthy human. It metabolizes daidzein (a soybean isoflavonoid) and produces
S
-equol, which has stronger estrogenic activities than daidzein. Here, we report the finished and annotated genomic sequence of this organism.
Complete Genome Sequence of the Ureolytic Streptococcus salivarius Strain 57.I
Authors: Geng Jianing , Huang Szu-Chuan , Li Shuangli , Hu Songnian , Chen Yi-Ywan M. 
Published: September 2011

ABSTRACT

Streptococcus salivarius
57.I is one of the most abundant and highly ureolytic bacteria in the human mouth. It can utilize urea as the sole nitrogen source via the activity of urease. Complete genome sequencing of
S. salivarius
57.I revealed a chromosome and a phage which are absent in strain SK126.
Genome Sequence of Lactobacillus salivarius NIAS840, Isolated from Chicken Intestine
Authors: Ham Jun-Sang , Kim Hyoun-Wook , Seol Kuk-Hwan , Jang Aera , Jeong Seok-Geun , Oh Mi-Hwa , Kim Dong-Hun , Kang Dae-Kyung , Kim Geun-Bae , Cha Chang-Jun 
Published: September 2011

ABSTRACT

Lactobacillus salivarius
is a well-known lactic acid bacterium to which increasing attention has been paid recently for use as probiotics for humans and animals.
L. salivarius
NIAS840 was first isolated from broiler chicken feces, displaying antimicrobial activities against multidrug-resistant
Staphylococcus aureus
and
Salmonella enterica
serovar Typhimurium. Here, we report the genome sequence of
L. salivarius
NIAS840 (2,046,557 bp) including a small plasmid and two megaplasmids.
Genome Sequence of Agrobacterium tumefaciens Strain F2, a Bioflocculant-Producing Bacterium
Authors: Li Ang , Geng Jianing , Cui Di , Shu Chang , Zhang Si , Yang Jixian , Xing Jie , Wang Jinna , Ma Fang , Hu Songnian 
Published: September 2011

ABSTRACT

Agrobacterium tumefaciens
F2 is an efficient bioflocculant-producing bacterium. But the genes related to the metabolic pathway of bioflocculant biosynthesis in strain F2 are unknown. We present the draft genome of
A. tumefaciens
F2. It could provide further insight into the biosynthetic mechanism of polysaccharide-like bioflocculant in strain F2.
Whole-Genome Sequence of the Xylanase-Producing Mesoflavibacter zeaxanthinifaciens Strain S86
Authors: Oh Chulhong , Heo Soo-Jin , De Zoysa Mahanama , Affan Abu , Jung Won-Kyo , Park Heung-Sik , Lee Youngdeuk , Lee Jehee , Yoon Kon-Tak , Kang Do-Hyung 
Published: September 2011

ABSTRACT

We isolated
Mesoflavibacter zeaxanthinifaciens
S86 as xylanase-producing bacteria from seawater sampled in Micronesia. Analysis of the
M. zeaxanthinifaciens
genome revealed that it contains a single circular chromosome of 3,704,661 bp with 3,249 putative open reading frames.
Complete Genome Sequence of a Nonculturable Methanococcus maripaludis Strain Extracted in a Metagenomic Survey of Petroleum Reservoir Fluids
Authors: Wang Xiaoyi , Greenfield Paul , Li Dongmei , Hendry Philip , Volk Herbert , Sutherland Tara D. 
Published: September 2011

ABSTRACT

Extraction of genome sequences from metagenomic data is crucial for reconstructing the metabolism of microbial communities that cannot be mimicked in the laboratory. A complete
Methanococcus maripaludis
genome was generated from metagenomic data derived from a thermophilic subsurface oil reservoir.
M. maripaludis
is a hydrogenotrophic methanogenic species that is common in mesophilic saline environments. Comparison of the genome from the thermophilic, subsurface environment with the genome of the type species will provide insight into the adaptation of a methanogenic genome to an oil reservoir environment.
International medical graduates in the USA: a qualitative study on perceptions of physician migration: Table 1
Authors: Chen P G , Nunez-Smith M , Berg D , Gozu A , Rulisa S , Curry L A 
Published: September 2011

ObjectivesPhysician migration from low-income to high-income nations is a global concern. Despite the centrality of understanding the perspectives of international medical graduates (IMGs) who have experienced migration to understanding the causes and consequences of this phenomenon, empirical literature is limited. The authors sought to characterise the experiences of IMGs from limited resource nations currently practicing primary care in the USA, with a focus on their perspectives on physician migration.DesignThe authors conducted a qualitative study utilising in-depth, in-person interviews and a standardised interview guide. The sample comprised a diverse, purposeful sample of IMGs (n=25) from limited resource nations (defined as having ≤2 physicians per 1000 population).ResultsAnalyses revealed four recurrent and unifying themes reflecting the perspectives of IMGs in the USA on physician migration: (1) decisions to migrate were pragmatic decisions made in the context of individual circumstance; (2) the act of migration ultimately affected participants' ability to return home in multiple, unpredictable ways; (3) the ongoing process of acclimation was coupled with inherent conflicts surrounding the decision to remain in the USA; and (4) the effects of policies in both the home country and in the USA occurred at multiple levels.ConclusionThe perspectives of IMGs who have migrated to the USA are an important addition to the ongoing discussion surrounding the global health workforce. Our findings highlight the effects of workforce policies which are often developed and discussed in abstraction, but have real, measurable impacts on the lives of individuals. Future efforts to address physician migration will need to acknowledge the immediate needs of the health workforce as well as the long-term needs of individuals within health systems.
Self-diagnosis of influenza during a pandemic: a cross-sectional survey
Authors: Jutel Annemarie , Baker Michael G , Stanley James , Huang Q Sue , Bandaranayake Don 
Published: September 2011

BackgroundSelf-diagnosis of influenza is an important component of pandemic control and management as it may support self-management practices and reduce visits to healthcare facilities, thus helping contain viral spread. However, little is known about the accuracy of self-diagnosis of influenza, particularly during pandemics.MethodsWe used cross-sectional survey data to correlate self-diagnosis of influenza with serological evidence of 2009 pandemic influenza A(H1N1) infection (haemagglutination inhibition titres of ≥1:40) and to determine what symptoms were more likely to be present in accurate self-diagnosis. The sera and risk factor data were collected for the national A(H1N1) seroprevalence survey from November 2009 to March 2010, 3 months after the first pandemic wave in New Zealand (NZ).ResultsThe samples consisted of 318 children, 413 adults and 423 healthcare workers. The likelihood of being seropositive was no different in those who believed they had influenza from those who believed they did not have influenza in all groups. Among adults, 23.3% (95% CI 11.9% to 34.7%) of those who reported having had influenza were seropositive for H1N1, but among those reporting no influenza, 21.3% (95% CI 13% to 29.7%) were also seropositive. Those meeting NZ surveillance or Ministry of Health influenza case definitions were more likely to believe they had the flu (surveillance data adult sample OR 27.1, 95% CI 13.6 to 53.6), but these symptom profiles were not associated with a higher likelihood of H1N1 seropositivity (surveillance data adult sample OR 0.93, 95% CI 0.5 to 1.7).ConclusionsSelf-diagnosis does not accurately predict influenza seropositivity. The symptoms promoted by many public health campaigns are linked with self-diagnosis of influenza but not with seropositivity. These findings raise challenges for public health initiatives that depend on accurate self-diagnosis by members of the public and appropriate self-management action.
Unfolded Protein Response Signaling and MAP Kinase Pathways Underlie Pathogenesis of Arsenic-Induced Cutaneous Inflammation
Authors: Li Changzhao , Xu Jianmin , Li Fugui , Chaudhary Sandeep C. , Weng Zhiping , Wen Jianming , Elmets Craig A. , Ahsan Habibul , Athar Mohammad 
Published: September 2011

Abstract
Arsenic exposure through drinking water is a major global public health problem and is associated with an enhanced risk of various cancers including skin cancer. In human skin, arsenic induces precancerous melanosis and keratosis, which may progress to basal cell and squamous cell carcinoma. However, the mechanism by which these pathophysiologic alterations occur remains elusive. In this study, we showed that subchronic arsenic exposure to SKH-1 mice induced unfolded protein response (UPR) signaling regulated by proteins, inositol-requiring enzyme-1 (IRE1), PKR-like endoplasmic reticulum kinase (PERK) and activating transcription factor 6 (ATF6). Arsenic activated all three UPR regulatory proteins in the skin. Arsenic induced IRE1 phosphorylation which resulted in augmented splicing of X-box binding protein 1 (XBP-1) leading to its migration to the nucleus, and also enhanced transcriptional activation of downstream target proteins. Hyperphosphorylation of PERK which induces eukaryotic translation initial factor 2α (eIF2α) in a phosphorylation-dependent manner enhanced translation of ATF4, in addition to augmenting proteolytic activation of ATF6 in arsenic-treated skin. A similar increase in the expression of CHOP was observed. Enhanced XBP-1s, ATF4, and ATF6 regulated downstream chaperones GRP94 and GRP78. In addition, arsenic induced inflammation-related p38/MAPKAPK-2 MAPK signaling and alterations in Th-1/Th-2/Th-17 cytokines/chemokines and their receptors. Antioxidant N-acetyl cysteine blocked arsenic-induced reactive oxygen species, with a concomitant attenuation of UPR and mitogen-activated protein kinase (MAPK) signaling and proinflammatory cytokine/chemokine signatures. Our results identify novel pathways involved in the pathogenesis of arsenic-med iated cutaneous inflammation which may also be related to enhanced cancer risk in arsenic exposed cohorts. Cancer Prev Res; 4(12); 2101–9. ©2011 AACR.
Bitter Melon Extract Impairs Prostate Cancer Cell-Cycle Progression and Delays Prostatic Intraepithelial Neoplasia in TRAMP Model
Authors: Ru Peng , Steele Robert , Nerurkar Pratibha V. , Phillips Nancy , Ray Ratna B. 
Published: September 2011

Abstract
Prostate cancer remains the second leading cause of cancer deaths among American men. Earlier diagnosis increases survival rate in patients. However, treatments for advanced disease are limited to hormone ablation techniques and palliative care. Thus, new methods of treatment and prevention are necessary for inhibiting disease progression to a hormone refractory state. One of the approaches to control prostate cancer is prevention through diet, which inhibits one or more neoplastic events and reduces the cancer risk. For centuries, Ayurveda has recommended the use of bitter melon (Momordica charantia) as a functional food to prevent and treat human health related issues. In this study, we have initially used human prostate cancer cells, PC3 and LNCaP, as an in vitro model to assess the efficacy of bitter melon extract (BME) as an anticancer agent. We observed that prostate cancer cells treated with BME accumulate during the S phase of the cell cycle and modulate cyclin D1, cyclin E, and p21 expression. Treatment of prostate cancer cells with BME enhanced Bax expression and induced PARP cleavage. Oral gavage of BME, as a dietary compound, delayed the progression to high-grade prostatic intraepithelial neoplasia in TRAMP (transgenic adenocarcinoma of mouse prostate) mice (31%). Prostate tissue from BME-fed mice displayed approximately 51% reduction of proliferating cell nuclear antigen expression. Together, our results suggest for the first time that oral administration of BME inhibits prostate cancer progression in TRAMP mice by interfering cell-cycle progression and proliferation. Cancer Prev Res; 4(12); 2122–30. ©2011 AACR.
Peroxisome Proliferator-Activated Receptor Pathway Gene Polymorphism Associated With Extent of Coronary Artery Disease in Patients With Type 2 Diabetes in the Bypass Angioplasty Revascularization Investigation 2 Diabetes Trial
Authors: Cresci Sharon , Wu Jun , Province Michael A. , Spertus John A. , Steffes Michael , McGill Janet B. , Alderman Edwin L. , Brooks Maria Mori , Kelsey Sheryl F. , Frye Robert L. , Bach Richard G. 
Published: September 2011

Background—
Coronary artery disease (CAD) is the major cause of death in patients with type 2 diabetes mellitus. Although demographic and clinical factors associated with extent of CAD in patients with diabetes mellitus have been described, genetic factors have not. We hypothesized that genetic variation in peroxisome proliferator-activated receptor (PPAR) pathway genes, important in diabetes mellitus and atherosclerosis, would be associated with extent of CAD in patients with diabetes mellitus.

Methods and Results—

We genotyped 1043 patients (702 white, 175 blacks) from the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) genetic cohort for 3351 variants in 223 PPAR pathway genes using a custom targeted-genotyping array. Angiographic end points were determined by a core laboratory. In whites, a single variant (rs1503298) in
TLL1
was significantly (
P
=5.5×10
−6
) associated with extent of CAD, defined as number of lesions with percent diameter stenosis ≥20%, after stringent Bonferroni correction for all 3351 single nucleotide polymorphisms. This association was validated in the diabetic subgroups of 2 independent cohorts, the Translational Research Investigating Underlying Disparities in Acute Myocardial Infarction Patients' Health Status (TRIUMPH) post–myocardial infarction registry and the prospective Family Heart Study (FHS) of individuals at risk for CAD.
TLL1
rs1503298 was also significantly associated with extent of severe CAD (≥70% diameter stenosis;
P
=3.7×10
−2
) and myocardial jeopardy index (
P
=8.7×10
−4
). In general linear regression modeling,
TLL1
rs1503298 explained more variance of extent of CAD than the previously determined clinical factors.

Conclusions—

We identified a variant in a single PPAR pathway gene,
TLL1
, that is associated with the extent of CAD independently of clinical predictors, specifically in patients with type 2 diabetes mellitus and CAD.

Clinical Trial Registration—

URL:
http://www.clinicaltrials.gov
. Unique identifier: NCT00006305.
Anticoagulation With the Oral Direct Thrombin Inhibitor Dabigatran Does Not Enlarge Hematoma Volume in Experimental Intracerebral Hemorrhage
Authors: Lauer Arne , Cianchetti Flor A. , Van Cott Elizabeth M. , Schlunk Frieder , Schulz Elena , Pfeilschifter Waltraud , Steinmetz Helmuth , Schaffer Chris B. , Lo Eng H. , Foerch Christian 
Published: September 2011

Background—
The direct thrombin inhibitor dabigatran etexilate (DE) may constitute a future replacement of vitamin K antagonists for long-term anticoagulation. Whereas warfarin pretreatment is associated with greater hematoma expansion after intracerebral hemorrhage (ICH), it remains unclear what effect direct thrombin inhibitors would have. Using different experimental models of ICH, this study compared hematoma volume among DE-treated mice, warfarin-treated mice, and controls.

Methods and Results—

CD-1 mice were fed with DE or warfarin. Sham-treated mice served as controls. At the time point of ICH induction, DE mice revealed an increased activated partial thromboplastin time compared with controls (mean±SD 46.1±5.0 versus 18.0±1.5 seconds;
P
=0.022), whereas warfarin pretreatment resulted in a prothrombin time prolongation (51.4±17.9 versus 10.4±0.3 seconds;
P
<0.001). Twenty-four hours after collagenase-induced ICH formation, hematoma volume was 3.8±2.9 μL in controls, 4.8±2.7 μL in DE mice, and 14.5±11.8 μL in warfarin mice (n=16; Welch ANOVA between-group differences
P
=0.007; posthoc analysis with the Dunnett method: DE versus controls,
P
=0.899; warfarin versus controls,
P
<0.001; DE versus warfarin,
P
=0.001). In addition, a model of laser-induced cerebral microhemorrhage was applied, and the distances that red blood cells and blood plasma were pushed into the brain were quantified. Warfarin mice showed enlarged red blood cell and blood plasma diameters compared to controls, but no difference was found between DE mice and controls.

Conclusions—
In contrast with warfarin, pretreatment with DE did not increase hematoma volume in 2 different experimental models of ICH. In terms of safety, this observation may represent a potential advantage of anticoagulation with DE over warfarin.
Further Investigation of the Impact of Idealized Continents and SST Distributions on the Northern Hemisphere Storm Tracks
Authors: Saulière Jérôme , Brayshaw David James , Hoskins Brian , Blackburn Michael 
Published: September 2011

Abstract
Building on previous studies of the basic ingredients of the North Atlantic storm track (examining land–sea contrast, orography, and SST), this article investigates the impact of Eurasian topography and Pacific SST anomalies on North Pacific and Atlantic storm tracks through a hierarchy of atmospheric GCM simulations using idealized boundary conditions in the Hadley Centre HadGAM1 atmospheric circulation model.
The Himalaya–Tibet mountain complex is found to play a crucial role in shaping the North Pacific storm track. The northward deflection of the westerly flow around northern Tibet generates an extensive pool of very cold air in the northeastern tip of the Asian continent, which strengthens the meridional temperature gradient and favors baroclinic growth in the western Pacific. The Kuroshio SST front is also instrumental in strengthening the Pacific storm track through its impact on near-surface baroclinicity, while the warm waters around Indonesia tend to weaken it through the impact on baroclinicity of stationary Rossby waves propagating poleward from the convective heating regions.
Three mechanisms by which the Atlantic storm track may be affected by changes in the boundary conditions upstream of the Rockies are discussed. In the model configuration used here, stationary Rossby waves emanating from Tibet appear to weaken the North Atlantic storm track substantially, whereas those generated over the cold waters off Peru appear to strengthen it. Changes in eddy-driven surface winds over the Pacific generally appear to modify the flow over the Rocky Mountains, leading to consistent modifications in the Atlantic storm track. The evidence for each of these mechanisms is, however, ultimately equivocal in these simulations.