bluuebunny/crossref_metadata_2025_split huggingface dataset:
BRIEFE UND TAGEBUCHBLÄTTER VON GRÄFIN C***: CLOTILDE VON STOCKHAUSEN'S DIARY COMES BACK TO LIGHT
Authors: Sayer John 
Published: January 2018

ABSTRACTMisconceptions surrounded the missing diary of Clotilde von Stockhausen, admired by Reichskanzler von Bülow but overlooked thereafter, until a copy was identified in 2016 and another later emerged during the Google digitalisation of Austrian National Library nineteenth‐century holdings. The fictions around the diary and von Bülow's interest are now explained and dispelled. The diary is introduced as a fine example of literature in miniature, beautifully written, using images from the natural world, a searching but witty record and exploration of personal feelings and reflections contrasting with outward appearances. What is known of the diary's composition and publication is discussed, and the diary is set against Clotilde's family background and high‐society prominence as an ambassador's wife at critical moments in Paris and Vienna.
Shining LIGHT on the metabolic role of the cytokine TNFSF14 and the implications on hepatic IL‐6 production
Authors: Saunders Bernadette M , Rudnicka Caroline , Filipovska Aleksandra , Davies Stefan , Ward Natalie , Hricova Jana , Schlaich Markus P , Matthews Vance B 
Published: January 2018

AbstractThe cytokine Tumor Necrosis Factor Superfamily member 14, TNFSF14 (or LIGHT), is a controversial player in numerous diseases. We investigated the role of endogenously expressed TNFSF14 in diet‐induced obesity in vivo. Firstly, we studied the effects of Tnfsf14 ablation on the development of obesity, glucose intolerance, insulin resistance, steatosis, tissue inflammation, and mitochondrial respiration in the liver. Secondly, we examined the role of TNFSF14 expression in hematopoietic cells on obesity and insulin sensitivity. Male Tnfsf14 knockout (KO) and wild type mice were fed chow or high fat diet (HFD) for 12 weeks and were assessed for weight gain, glucose intolerance, insulin resistance, hepatosteatosis, mitochondrial dysfunction, and cytokine expression. Wild‐type mice were also reconstituted with bone marrow cells from Tnfsf14 knockout mice and were fed chow or HFD for 12 weeks. These mice were examined for weight gain and insulin resistance. HFD fed mice had elevated circulating levels of serum TNFSF14. Liver and white adipose tissue are potential sources of this elevated TNFSF14. Tnfsf14 deficient mice displayed increased obesity, glucose intolerance, insulin resistance, hepatosteatosis, and mitochondrial dysfunction compared to control mice on a HFD. Hepatic cytokine profiling pointed to a potential novel role of decreased IL‐6 in the metabolic disturbances in obesogenic Tnfsf14 knockout mice. Bone marrow cells from Tnfsf14 deficient mice appeared to promote diet‐induced obesity, insulin resistance and reduced FGF21 levels in white adipose tissue and liver. Our novel data suggest that Tnfsf14 ablation exacerbates parameters of the metabolic syndrome under high fat feeding conditions and provides evidence to support the development of TNFSF14 agonists as potential therapeutics in diet‐induced obesity.
LncRNA‐RP11‐714G18.1 suppresses vascular cell migration via directly targeting LRP2BP
Authors: Zhang Yuan , Zheng Lei , Xu Bang‐Ming , Tang Wai‐Ho , Ye Zhi‐Dong , Huang Chuan , Ma Xin , Zhao Jing‐Jing , Guo Feng‐Xia , Kang Chun‐Min , Lu Jing‐Bo , Xiu Jian‐Cheng , Li Pan , Xu Yuan‐Jun , Xiao Lei , Wu Qian , Hu Yan‐Wei , Wang Qian 
Published: January 2018

AbstractAtherosclerotic cardiovascular disease is considered as the leading cause of mortality and morbidity worldwide. Accumulating evidence supports an important role for long noncoding RNA (lncRNA) in the pathogenesis of atherosclerosis. Nevertheless, the role of lncRNA in atherosclerosis‐associated vascular dysfunction and the underlying mechanism remain elusive. Here, using microarray analysis, we identified a novel lncRNA RP11‐714G18.1 with significant reduced expression in human advanced atherosclerotic plaque tissues. We demonstrated in both human vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) that RP11‐714G18.1 impaired cell migration, reduced the adhesion of ECs to monocytes, suppressed the neoangiogenesis, decreased apoptosis of VSMCs and promoted nitric oxide production. Mechanistically, RP11‐714G18.1 could directly bind to its nearby gene LRP2BP and increased the expression of LRP2BP. Moreover, we showed that RP11‐714G18.1 impaired cell migration through LRP2BP‐mediated downregulation of matrix metalloproteinase (MMP)1 in both ECs and VSMCs. In atherosclerotic patients, the serum levels of LRP2BP were positively correlated with high‐density lipoprotein cholesterol, but negatively correlated with cardiac troponin I. Our study suggests that RP11‐714G18.1 may play an athero‐protective role by inhibiting vascular cell migration via RP11‐714G18.1/LRP2BP/MMP1 signaling pathway, and targeting the pathway may provide new therapeutic approaches for atherosclerosis.
Developing a flexible, high‐efficiency Agrobacterium‐mediated sorghum transformation system with broad application
Authors: Che Ping , Anand Ajith , Wu Emily , Sander Jeffry D. , Simon Marissa K. , Zhu Weiwei , Sigmund Amy L. , Zastrow‐Hayes Gina , Miller Michael , Liu Donglong , Lawit Shai J. , Zhao Zuo‐Yu , Albertsen Marc C. , Jones Todd J. 
Published: January 2018

SummarySorghum is the fifth most widely planted cereal crop in the world and is commonly cultivated in arid and semi‐arid regions such as Africa. Despite its importance as a food source, sorghum genetic improvement through transgenic approaches has been limited because of an inefficient transformation system. Here, we report a ternary vector (also known as cohabitating vector) system using a recently described pVIR accessory plasmid that facilitates efficient Agrobacterium‐mediated transformation of sorghum. We report regeneration frequencies ranging from 6% to 29% in Tx430 using different selectable markers and single copy, backbone free ‘quality events’ ranging from 45% to 66% of the total events produced. Furthermore, we successfully applied this ternary system to develop transformation protocols for popular but recalcitrant African varieties including Macia, Malisor 84‐7 and Tegemeo. In addition, we report the use of this technology to develop the first stable CRISPR/Cas9‐mediated gene knockouts in Tx430.
Oxidative stress impairs myocyte autophagy, resulting in myocyte hypertrophy
Authors: Wang Jia‐Pu , Chi Rui‐Fang , Wang Ke , Ma Teng , Guo Xiao‐Fei , Zhang Xiao‐Li , Li Bao , Qin Fu‐Zhong , Han Xue‐Bin , Fan Bian‐Ai 
Published: January 2018

New Findings
What is the central question of this study?
Does oxidative stress induce impairment of autophagy that results in myocyte hypertrophy early after pressure overload?

What is the main finding and its importance?
In cultured myocytes, hydrogen peroxide decreased autophagy and increased hypertrophy, and inhibition of autophagy enhanced myocyte hypertrophy. In rats with early myocardial hypertrophy after pressure overload, myocyte autophagy was progressively decreased. The antioxidant N‐acetyl‐cysteine or the superoxide dismutase mimic tempol prevented the decrease of myocyte autophagy and attenuated myocyte hypertrophy early after pressure overload. These findings suggest that oxidative stress impairs myocyte autophagy that results in myocyte hypertrophy.

AbstractInsufficient or excessive myocyte autophagy is associated with left ventricular (LV) hypertrophy. Reactive oxygen species mediate myocyte hypertrophy in vitro and pressure overload‐induced LV hypertrophy in vivo. In the present study, we tested the hypothesis that oxidative stress induces an impairment of autophagy that results in myocyte hypertrophy. H9C2 cardiomyocytes pretreated with the autophagy inhibitor 3‐methyladenine were exposed to 10 and 50 μm hydrogen peroxide (H2O2) for 48 h. Male Sprague–Dawley rats underwent abdominal aortic constriction (AAC) or sham operation. The animals were killed 24, 48 or 72 h after surgery. In a separate group, the AAC and sham‐operated rats randomly received the antioxidant N‐acetyl‐cysteine or the superoxide dismutase mimic tempol for 72 h. In H9C2 cardiomyocytes, H2O2 decreased the ratio of microtubule‐associated protein light chain 3 (LC3) II to LC3 I and increased P62 and phosphorylated ERK (p‐ERK) proteins and myocyte surface area. 3‐Methyladenine further increased H2O2‐induced p‐ERK expression. In rats after AAC, the heart to body weight ratio was progressively increased, the LC3 II/I ratio was progressively decreased, p62 and p‐ERK expression was increased, and expression of Beclin1, Atg5 and Atg12 was decreased. N‐Acetyl‐cysteine or tempol prevented the decreases in the LC3 II/I ratio and Beclin1 and Atg5 expression and attenuated the increases in LV wall thickness, myocyte diameter and brain natriuretic peptide expression in AAC rats. In conclusion, oxidative stress decreases Beclin1 and Atg5 expression that results in impairment of autophagy, leading to myocyte hypertrophy. These findings suggest that antioxidants or restoration of autophagy might be of value in the prevention of early myocardial hypertrophy after pressure overload.
Targeted Synthesis and Characterization of a Gene Cluster Encoding NAD(P)H-Dependent 3α-, 3β-, and 12α-Hydroxysteroid Dehydrogenases from Eggerthella CAG:298, a Gut Metagenomic Sequence
Authors: Mythen Sean M. , Devendran Saravanan , Méndez-García Celia , Cann Isaac , Ridlon Jason M. 
Published: January 2018

ABSTRACT

Gut metagenomic sequences provide a rich source of microbial genes, the majority of which are annotated by homology or unknown. Genes and gene pathways that encode enzymes catalyzing biotransformation of host bile acids are important to identify in gut metagenomic sequences due to the importance of bile acids in gut microbiome structure and host physiology. Hydroxysteroid dehydrogenases (HSDHs) are pyridine nucleotide-dependent enzymes with stereospecificity and regiospecificity for bile acid and steroid hydroxyl groups. HSDHs have been identified in several protein families, including medium-chain and short-chain dehydrogenase/reductase families as well as the aldo-keto reductase family. These protein families are large and contain diverse functionalities, making prediction of HSDH-encoding genes difficult and necessitating biochemical characterization. We located a gene cluster in
Eggerthella
sp. CAG:298 predicted to encode three HSDHs (CDD59473, CDD59474, and CDD59475) and synthesized the genes for heterologous expression in
Escherichia coli
. We then screened bile acid substrates against the purified recombinant enzymes. CDD59475 is a novel 12α-HSDH, and we determined that CDD59474 (3α-HSDH) and CDD59473 (3β-HSDH) constitute novel enzymes in an iso-bile acid pathway. Phylogenetic analysis of these HSDHs with other gut bacterial HSDHs and closest homologues in the database revealed predictable clustering of HSDHs by function and identified several likely HSDH sequences from bacteria isolated or sequenced from diverse mammalian and avian gut samples.

IMPORTANCE
Bacterial HSDHs have the potential to significantly alter the physicochemical properties of bile acids, with implications for increased/decreased toxicity for gut bacteria and the host. The generation of oxo-bile acids is known to inhibit host enzymes involved in glucocorticoid metabolism and may alter signaling through nuclear receptors such as farnesoid X receptor and G-protein-coupled receptor TGR5. Biochemical or similar approaches are required to fill in many gaps in our ability to link a particular enzymatic function with a nucleic acid or amino acid sequence. In this regard, we have identified a novel 12α-HSDH and a novel set of genes encoding an iso-bile acid pathway (3α-HSDH and 3β-HSDH) involved in epimerization and detoxification of harmful secondary bile acids.
Cooperative Immune Suppression by Escherichia coli and Shigella Effector Proteins
Authors: de Jong Maarten F. , Alto Neal M. 
Published: January 2018

ABSTRACT

The enteric attaching and effacing (A/E) pathogens enterohemorrhagic
Escherichia coli
(EHEC) and enteropathogenic
E. coli
(EPEC) and the invasive pathogens enteroinvasive
E. coli
(EIEC) and
Shigella
encode type III secretion systems (T3SS) used to inject effector proteins into human host cells during infection. Among these are a group of effectors required for NF-κB-mediated host immune evasion. Recent studies have identified several effector proteins from A/E pathogens and EIEC/
Shigella
that are involved in suppression of NF-κB and have uncovered their cellular and molecular functions. A novel mechanism among these effectors from both groups of pathogens is to coordinate effector function during infection. This cooperativity among effector proteins explains how bacterial pathogens are able to effectively suppress innate immune defense mechanisms in response to diverse classes of immune receptor signaling complexes (RSCs) stimulated during infection.
Direct Manipulation of T Lymphocytes by Proteins of Gastrointestinal Bacterial Pathogens
Authors: Cassady-Cain Robin L. , Hope Jayne C. , Stevens Mark P. 
Published: January 2018

ABSTRACTGastrointestinal bacterial infection represents a significant threat to human health, as well as a burden on food animal production and welfare. Although there is advanced knowledge about the molecular mechanisms underlying pathogenesis, including the development of immune responses to these pathogens, gaps in knowledge persist. It is well established that gastrointestinal bacterial pathogens produce a myriad of proteins that affect the development and effectiveness of innate immune responses. However, relatively few proteins that directly affect lymphocytes responsible for humoral or cell-mediated immunity and memory have been identified. Here, we review factors produced by gastrointestinal bacterial pathogens that have direct T cell interactions and what is known about their functions and mechanisms of action. T cell-interacting bacterial proteins that have been identified to date mainly target three major T cell responses: activation and expansion, chemotaxis, or apoptosis. Further, the requirement for more focused studies to identify and understand additional mechanisms used by bacteria to directly affect the T cell immune response and how these may contribute to pathogenesis is highlighted. Increased knowledge in this area will help to drive development of better interventions in prevention and treatment of gastrointestinal bacterial infection.
Natural and Artificial Strategies To Control the Conjugative Transmission of Plasmids
Authors: Getino María , de la Cruz Fernando 
Published: January 2018

ABSTRACT
Conjugative plasmids are the main carriers of transmissible antibiotic resistance (AbR) genes. For that reason, strategies to control plasmid transmission have been proposed as potential solutions to prevent AbR dissemination. Natural mechanisms that bacteria employ as defense barriers against invading genomes, such as restriction-modification or CRISPR-Cas systems, could be exploited to control conjugation. Besides, conjugative plasmids themselves display mechanisms to minimize their associated burden or to compete with related or unrelated plasmids. Thus, FinOP systems, composed of FinO repressor protein and FinP antisense RNA, aid plasmids to regulate their own transfer; exclusion systems avoid conjugative transfer of related plasmids to the same recipient bacteria; and fertility inhibition systems block transmission of unrelated plasmids from the same donor cell. Artificial strategies have also been designed to control bacterial conjugation. For instance, intrabodies against R388 relaxase expressed in recipient cells inhibit plasmid R388 conjugative transfer; pIII protein of bacteriophage M13 inhibits plasmid F transmission by obstructing conjugative pili; and unsaturated fatty acids prevent transfer of clinically relevant plasmids in different hosts, promoting plasmid extinction in bacterial populations. Overall, a number of exogenous and endogenous factors have an effect on the sophisticated process of bacterial conjugation. This review puts them together in an effort to offer a wide picture and inform research to control plasmid transmission, focusing on Gram-negative bacteria.
Therapists’ experiences with a new treatment combining physical exercise and dietary therapy (the PED-t) for eating disorders: an interview study in a randomised controlled trial at the Norwegian School of Sport Sciences
Authors: Bakland Maria , Sundgot-Borgen Jorunn , Wynn Rolf , Rosenvinge Jan H , Stornæs Annett Victoria , Pettersen Gunn 
Published: January 2018

ObjectivesThe aim of the current study is to explore how therapists running a guided physical exercise and dietary therapy programme (PED-t) experience their contribution to the treatment of patients with bulimia nervosa and binge eating disorder.MethodsTen therapists running the PED-t were semistructurally interviewed and the transcribed interviews were analysed using a systematic text condensation approach.SettingThe study was run within the context of a randomised controlled trial at the Norwegian School of Sport Sciences.ResultsThe therapists experienced their knowledge about physical exercise and nutrition as important and useful, and that they could share their knowledge with the patients in different ways and with confidence in their own role. They also believed that their knowledge could serve as tools for the patients’ post-treatment recovery and management of their daily lives. Moreover, the therapists put much effort in adjusting their teaching to fit each individual participant. Finally, they reported their personal qualities as important to build trust and therapeutic alliance.ConclusionsThe terms ‘clinical confidence’ and ‘alliance’ may stand out as the overarching ‘metacategories’ covering the experiences revealed in this study. The clinical implication is that new groups of professionals may have an important role in the treatment of eating disorders.Trial registration numberNCTO2079935; Results.
Affective stimuli in behavioural interventions soliciting for health check-up services and the service users’ socioeconomic statuses: a study at Japanesepachinkoparlours
Authors: Kondo Naoki , Ishikawa Yoshiki 
Published: January 2018

Editor’s noteThe study reported in this article examines a health intervention that uses gendered stereotypes of the nursing profession and suggestive uniforms that play on women’s sexuality to encourage people to engage in health checkups. The intervention was not under the control of the authors and the study was approved by an institutional research ethics board. TheJournal of Epidemiology & Community Healthcondemns the use of sexism, gender and professional stereotypes and other forms of discriminatory or exploitative behaviour for any purpose, including health promotion programs. In light of concerns raised about this paper (see eLetters with this paper), we are conducting an audit of our review process and will put in place measures to ensure that the material we publish condemns sexism, racism and other forms of discrimination and embodies principles of inclusion and non-discrimination.BackgroundSocioeconomically vulnerable people are likely to have more health risks because of inadequate behaviour choices related to chronic social stresses. Brain science suggests that stress causes cognitively biased automatic decision making, preferring instant stress relief and pleasure (eg, smoking, alcohol use and drug abuse) as opposed to reflectively seeking health-maintenance services (eg, health check-ups). As such, hedonic stimuli that nudge people towards preventive actions could reduce health behaviour disparities. The purpose of this intervention study was to test this hypothesis.MethodsAn instant health check-up service company had 320 health check-up sessions atpachinko(Japanese gambling) parlours; 1721 persons in intervention sessions and 6507 persons in control sessions received the service. The stimuli the company used in the intervention sessions were young women wearing mildly erotic nurse costumes, who solicited the pachinko players for health check-up services. We compared the prevalence of socioeconomically vulnerable individuals between the intervention and control sessions, adjusting for individual-level and parlour-level potential confounders.ResultsEven adjusting for health risks and within-parlour clustering, the intervention sessions gathered more socioeconomically vulnerable customers than the regular sessions. Compared with control sessions, in intervention sessions the adjusted prevalence ratios were 1.15 (95% CI 0.99 to 1.35) for not having a job (vs having a job) and 1.36 (95% CI 1.00 to 1.86) for holders of National Health Insurance (which includes more socially vulnerable people than other insurance programmes).ConclusionThe results supported our hypothesis. Offering health check-up opportunities equipped with ‘tricks’ that nudge people to act might be effective for anyone but is potentially more valuable for socially vulnerable people. Ethical discussions are needed to further consider the use of erotic stimuli and other essential drivers of human behaviour.
Risk factors for survival in patients with von Hippel-Lindau disease
Authors: Wang Jiang-Yi , Peng Shuang-He , Li Teng , Ning Xiang-Hui , Liu Sheng-Jie , Hong Bao-An , Liu Jia-Yuan , Wu Peng-Jie , Zhou Bo-Wen , Zhou Jing-Cheng , Qi Nie-Nie , Peng Xiang , Zhang Jiu-Feng , Ma Kai-Fang , Cai Lin , Gong Kan 
Published: January 2018

BackgroundHistorically, von Hippel-Lindau (VHL) disease is characterised by a poor survival. Although genotype–phenotype correlation has been described in many studies, the risk factors for VHL survival remain unclear. This study aims to evaluate the median survival of Chinese patients with VHL disease and explore whether VHL survival is influenced by genetic and clinical factors.MethodsIn this retrospective study, we recruited 340 patients from 127 VHL families. Kaplan-Meier plot and Cox regression model were used to evaluate the median survival and assess how survival was influenced by birth year, birth order, sex, family history, mutation type, onset age and first presenting symptom.ResultsThe estimated median life expectancy for Chinese patients with VHL disease was 62 years. Patients with early-onset age, positive family history and truncating mutation types had poorer overall and VHL-related survival. Patients with haemangioblastoma as their first presenting symptom were related to a higher risk of death from central nervous system haemangioblastoma than those with abdominal lesions (HR 8.84, 95% CI 2.04 to 38.37, P=0.004).ConclusionsThis largest VHL survival analysis indicates that onset age, family history, mutation type and first presenting symptom have an effect on the survival of patients with VHL disease, which is helpful to genetic counselling and clinical decision-making.