bluuebunny/crossref_metadata_2025_split huggingface dataset:
Folie hystérique et hystérie virile
Authors: Douville Olivier 
Published: April 2014

Lier hystérie et féminité n’a pas été une opération diagnostique faite en tout temps et en tout lieu. L’hystérie masculine connue et reconnue avant la naissance de la psychiatrie, à la fin du XVIII e siècle, a été oubliée par Pinel pour ressurgir à la fin du XIX e siècle en étant alors largement confondue avec la névrose traumatique. Freud n’a pas cédé aux facilités qu’apportait une telle confusion. En effet, son travail sur une « Névrose démoniaque au XVII e siècle » explore et enrichit le lien entre hystérie masculine et complexe paternel. Plus encore, il voit le ressort ultime de l’hystérie masculine en un refus de la castration maternelle, ce qui mène à une comparaison avec les tableaux plus répandus de la névrose hystérique. La clinique de l’hystérie serait-elle sexuée ?
« Ma fille est hystérique »
Authors: de Rouvray Patricia 
Published: April 2014

Moments de travail analytique avec une enfant de 7 ans dont le symptôme est la provocation dite « hystérique ». La mise en mots de son rapport au père et la mise à distance de sa mère dans la cure nous indiquent le chemin de sa castration. Et démontrent le travail complexe de l’analyse d’enfant qui doit composer avec la structure des parents. Nous voyons comment l’enfant se sert de son symptôme pour interroger et mettre à jour celui de sa famille. Une des questions est de savoir si l’on peut parler de structure hystérique chez l’enfant ? Et quelle trace la cure pourra-t-elle laisser ?
Tumor necrosis factor (TNF)-α gene +489 polymorphisms: association with psoriatic arthritis
Authors: Murdaca G. , Puppo F. 
Published: April 2014

Objective of this work was to investigate the role of single nucleotide polymorphisms (SNPs) at position +489 of the tumor necrosis factor (TNF)-α gene in generic susceptibility and severity of psoriatic arthritis (PsA). Fifty-seven Caucasian PsA patients diagnosed according to CASPAR criteria and 155 healthy matched controls were studied. PASI score, DAS28 and Disability INdex HAQ were calculated. Genomic DNA was extracted from peripheral blood samples and SNPs +489 G&gt;A (rs 80267959) were amplified by PCR. The SNP +489 genotype was significantly associated with PsA susceptibility (p=0.0136) and severity of clinical and laboratory parameters (p values ranging from 0.016 to 2.908 x 10-12). The difference in severity was accounted for by the difference between the AA and GA genotypes with respect to the GG genotype. These findings suggest that TNF-α gene polymorphisms may influence PsA susceptibility and severity. Psoriatics arthritis (PsA) is a complex immunemediated disease that results from the interplay between multiple genetic and environmental factor [1]. Although the pathogenesis of PsA remains elusive, there is evidence that genetic factors may contribute to the etiology of the disease [2]. Is has been estimated that at least one third of the genetic contribution to PsA resides in the major histocompatibility complex (MHC) region [2]. The tumor necrosis factor (TNF)-α gene, which is located in the short arm of chromosome 6 in the MHC class III region between the HLA-B and HLA-DR genes, has been proposed as a major candidate gene in PsA [3]. This hypothesis is supported by studies which have found high serum, synovial fluid and synovial membrane TNF-α levels in patients with PsA [4,5]. Several single nucleotide polymorphisms (PNPs) have been identified in the TNF-α gene promoter [6]. In particular, two common polymorphisms, namely G to A substitutions at positions -238 and -308 have been studied in patients with PsA. However, association studies of these two TNF-α polymorphisms and genetic susceptibility to PsA have lead to conflicting results [7-12]. Previous studies have indicated the potential role of the SNP at +489 position in the first intron of the TNF-α gene in the susceptibility to some rheumatic autoimmune diseases like rheumatoid arthritis [13], systemic lupus erythematosus [14] and systemic sclerosis [15]. However, to our present knowledge, studies on the association of +489 polymorphism with PsA susceptibility and response to TNF-α inhibitors are not reported in the literature. Is this study we investigated the role of SNPs at +489 within the TNF-α gene in PsA susceptibility and severity.
Management of diabetes during natural emergencies
Authors: Baruah Mintu , Kumar K.V.S. 
Published: April 2014

AbstractDisaster preparedness is an important but often a neglected part in the management of chronic disorders. India is facing an epidemic of diabetes and the patients with diabetes are also exposed to the risk of natural disaster along with other members of the society. India faced many disasters in the past including the Bhopal gas leak, Gujarat earthquake and Andaman tsunami. These disasters exposed the lacunae in the disaster preparedness and lead to devastating health consequences. Previous research focused more on the immediate, traumatic aspects of the disasters and neglected the impact on chronic disorders. The experience of managing diabetes after Hurricane Katrina gave important insights into the short and long term consequences of a disaster. Our article provides information about the impact of disasters on diabetes, difficulties in the management and suggested measures at various levels to improve the disaster preparedness.
Assessment of quality of life of type 2 diabetes patients with newly diagnosed non alcoholic fatty liver disease using quality of life instrument for Indian diabetes patients
Authors: Roy Kuhu , Iyer Uma 
Published: April 2014

Abstract
Introduction: Non alcoholic fatty liver disease is emerging as a public health problem among type 2 diabetes mellitus patients. It has an impact on quality of life, which is meagrely explored. Aim: To assess quality of life of type 2 diabetes patients with newly diagnosed non alcoholic fatty liver disease. Materials and Methods: Confirmed cases of newly diagnosed non alcoholic fatty liver disease with type 2 diabetes mellitus (n = 55) were enrolled. Clinical, anthropometric and medical profiles were assessed. Quality of life was assessed with the help of quality of life instrument for Indian diabetes patients. Results: Weight (P = 0.005) and body mass index (P 0.008) in grade 3 hepatic steatosis were higher than grade 2 steatosis. Physical health deteriorated from grade 1 to grade 3 hepatic steatosis. The mean likert scores decreased significantly (P 0.000) from grade 2 to grade 3 and between grade 1 and grade 3 (P 0.0014) hepatic steatosis in the physical endurance domain. Perceptions regarding general health and treatment satisfaction revealed existing loopholes in the health system and one′s general attitude towards health. The dietary domain was marked with gross dissatisfaction amongst most with hepatic steatosis with a significant reduction in mean likert scale score between grade 1 and grade 2 (P 0.012) of hepatic steatosis. Conclusions: Modifiable domains of quality of life should be addressed as a core component of standard care in newly diagnosed non alcoholic fatty liver disease with type 2 diabetes mellitus to avert future cardiac and hepatic events.
Attitude of health care professionals about the diabetes from India
Authors: Kumar K.V.S. , Gupta A. , Kumar Amit 
Published: April 2014

Abstract
Background: Health care workers should have adequate knowledge and the correct attitude to deal with the diabetes. We conducted this study among nursing and medical students to assess their attitude regarding diabetes. Materials and Methods: This cross-sectional descriptive study was conducted on medical (Group 1, N = 50) and nursing (Group 2, N = 50) students. Data was collected using the Diabetes Attitude Scale questionnaire developed by the University of Michigan Diabetes Research and Training Centre. The scores identify the attitude regarding five key areas of diabetes, namely need for special training, seriousness of diabetes, value of tight control, psychosocial impact and patient autonomy. The data were analyzed with appropriate statistical tests using GraphPad Prism Software, version 6 (GraphPad Software, San Deigo, CA, USA). Results: The study participants consist of 100 students of which 27 were male and 73 were female with a mean age of 22.9 ± 3.3 year. The scores in any subscale did not differ between the medical and nursing students. The correlation analyzes revealed that seriousness of diabetes is increasing linearly with age (P = 0.0325) and all the five key areas of diabetes showed a significant correlation with the increasing duration of residency (P < 0.05). Conclusion: Increasing age and more exposure to formal education are the major determinants of an individual′s attitude toward diabetes. Our study attempts to highlights the need of education for all health care workers involved in the management of diabetes.
Burden of diabetes among various ethnic minorities in US and its implications
Authors: Mundra Vishal 
Published: April 2014

Abstract
Introduction: Diabetes is one of the major healthcare issues worldwide. The average prevalence of diabetes was 11.7% in adults between 20-79 years of age in the US in 2011. This is a brief review of diabetes etio-pathogenesis and prevalence amongst various ethnic groups in the US. Materials and Methods: A pubmed search was done using key words diabetes, minorities and prevalence on September 15 2013. Relevant studies were selected for further review. In addition, more information was obtained from CDC websites. Discussion: As per CDC fact sheet 2011, 11.3% of all US adults ≥20 years of age had diabetes. 7.1% of non-Hispanic Whites, 8.4% of Asian Americans, 11.8% of Hispanics, and 12.6% of African-Americans (non-Hispanic Blacks) had diabetes in adults ≥20 years of age. Overall, 26.9% of adults of ≥65 years of age had diabetes in 2010. Amongst Native Indians, the prevalence ranges from 5.5% in Alaska natives to 33.5% amongst natives in Arizona. For immigrant south Asian population to the US (India, Pakistan, Nepal, Bangladesh and Sri Lanka), the prevalence has been documented to be varying from 17% to 29%. The wide variation in prevalence of diabetes poses a tough challenge to confine the epidemic as the measures have to be tailored to the needs of different race and ethnic groups. Conclusion: As these ethnic groups continue to grow, management of diabetes in these minorities confers a major health issue in the US.
Therapy in type 2 diabetes: A logical empiricism - based approach
Authors: Kalra Sanjay , Gupta Yashdeep 
Published: April 2014

AbstractThere is ongoing debate about the relevance of the ‘guideline approach,” vis-a-vis the “pathophysiologic approach” in the management of diabetes. However, it is disheartening to note that both these stands neglects the most important people involved in diabetes management: The person with diabetes, the family, and the treating physician. We discuss a logical empiricism based approach for diabetes care in this brief communication.
Limited prosthesis wear in geriatric diabetic edentulous patients: A social morbidity
Authors: Rathee Manu , Tamrakar Amit 
Published: April 2014

AbstractTooth loss is a widespread geriatric healthcare issue. The problems with the complete denture wear in edentulous patients are compounded by the coexisting diabetes. The dryness of thin oral mucosa resultant from diabetes or as side effect of medications used for various advanced age health problems lead to restricted prosthesis wear. Impaired chewing ability and denture problems can cause isolation among geriatric population.
A reconstruction of sea surface temperature variability in the southeastern Gulf of Mexico from 1734 to 2008 C.E. using cross‐dated Sr/Ca records from the coral Siderastrea siderea
Authors: DeLong Kristine L. , Flannery Jennifer A. , Poore Richard Z. , Quinn Terrence M. , Maupin Christopher R. , Lin Ke , Shen Chuan‐Chou 
Published: April 2014

AbstractThis study uses skeletal variations in coral Sr/Ca from three Siderastrea siderea coral colonies within the Dry Tortugas National Park in the southeastern Gulf of Mexico (24°42′N, 82°48′W) to reconstruct monthly sea surface temperature (SST) variations from 1734 to 2008 Common Era (C.E.). Calibration and verification of the replicated coral Sr/Ca‐SST reconstruction with local, regional, and historical temperature records reveals that this proxy‐temperature relationship is stable back to 1879 C.E. The coral SST reconstruction contains robust interannual (~2.0°C) and multidecadal variability (~1.5°C) for the past 274 years, the latter of which does not covary with the Atlantic Multidecadal Oscillation. Winter SST extremes are more variable than summer SST extremes (±2.2°C versus ±1.6°C, 2σ) suggesting that Loop Current transport in the winter dominates variability on interannual and longer time scales. Summer SST maxima are increasing (+1.0°C for 274 years, σMC = ±0.5°C, 2σ), whereas winter SST minima contain no significant trend. Colder decades (~1.5°C) during the Little Ice Age (LIA) do not coincide with decades of sunspot minima. The coral SST reconstruction contains similar variability to temperature reconstructions from the northern Gulf of Mexico (planktic foraminifer Mg/Ca) and the Caribbean Sea (coral Sr/Ca) suggesting areal reductions in the Western Hemisphere Warm Pool during the LIA. Mean summer coral SST extremes post‐1985 C.E. (29.9°C) exceeds the long‐term summer average (29.2°C for 1734–2008 C.E.), yet the warming trend after 1985 C.E. (0.04°C for 24 years, σMC = ±0.5, 2σ) is not significant, whereas Caribbean coral Sr/Ca studies contain a warming trend for this interval.
Retroviruses in Human Gene Therapy
Authors: Pedersen Finn Skou , Bahrami Shervin , Duch Mogens 
Published: April 2014

Abstract

A retrovirus‐based gene transfer system consists of two components: the transfer vector, which harbours a foreign gene linked to elements needed for retroviral replication, and the packaging cell, which supplies the necessary retroviral proteins for transfer of the vector through a single round of viral replication. A hallmark of retroviral replication is the stable maintenance of the transferred gene(s) during cell division. The first type of transfer vectors used in gene therapy trials were derived from mouse retroviruses and referred to as retroviral vectors. Lentiviral vectors are derived from human immunodeficiency virus type 1 and exhibit distinct features that provide advantages in some settings. Retroviral and lentiviral vectors are being used in clinical trials for several diseases, including monogenic diseases and cancer. The clinical protocols include gene transfer
in vivo
as well as
ex vivo
, the latter being followed by installation of the genetically modified cells into the body.

Key Concepts:

The retroviral replication machinery leads to stable maintenance of a transferred gene.

The stable integration of retroviral vectors into a chromosome of the target cell may have adverse effects on neighbouring genes.

Retroviral gene transfer does not require the expression of retroviral genes in the target cell.

The term retroviral vector is used for a vector based on murine leukaemia virus.

The term lentiviral vector is used for a vector based on human immunodeficiency virus type 1.

Retroviral vectors allow gene transfer only to dividing cells, whereas lentiviral vectors target dividing as well as nondividing cells.

In clinical protocols using retroviral or lentiviral vectors, gene transfer may take place
ex vivo
or
in vivo
.

The selectivity of retroviral vectors for dividing cells has been exploited to target tumour cells.
Temperature Stress in Plants
Authors: Kai Hiroomi , Iba Koh 
Published: April 2014

Abstract

Temperature stress in plants is classified into three types depending on the stressor, which may be high, chilling or freezing temperature. Temperature‐stressed plants show low germination rates, growth retardation, reduced photosynthesis, and often die. The elucidation of mechanisms by which temperature stress causes disorders is important to reveal responses by which plants cope with adverse temperature conditions. However, plants respond to temperature stress by regulating membrane lipid composition, stress‐related transcription factors, metabolite synthesis and detoxification pathways. Such plant molecular responses to temperature stress will help establish genetic engineering techniques to produce temperature stress‐tolerant plants. Genetic engineering techniques have been applied to improve the adaptability of plants by altering temperature stress‐related gene expression in response to unfavourable temperature conditions. In this article, the authors focus on plant responses and adaptation to temperature stress and strategies for the genetic improvement of temperature stress tolerance in plants.

Key Concepts:

Plants cope with adverse temperature stress by altering molecular mechanisms involving proteins, antioxidants, metabolites, regulatory factors, other protectants and membrane lipids.

Thermotolerance is closely correlated with the production of toxic acrolein and methyl vinyl ketone from membrane trienoic fatty acids under heat stress, and it is possible to produce thermotolerant plants with reduced trienoic fatty acid contents.

Regulatory factors such as heat shock factors directly and/or indirectly induce accumulation of stress‐related gene products under high temperature conditions and contribute to thermotolerance.

Under high temperature conditions, several protectants, such as glycinebetaine which apparently stabilises photosystem II proteins, accumulate to protect proteins and photosystems in plants.

Antioxidants decrease levels of stress‐inducible reactive oxygen species, contributing to improved tolerance to cold as well as high temperature stress.
Crop Plants: Evolution
Authors: Hancock James F , Miller Allison J 
Published: April 2014

AbstractAgriculture arose independently in several locations across the world, beginning approximately 13 000 years ago in the Near East. All crop plants originated from wild plant populations. At the beginning of the domestication process, a number of changes began to appear in the genetic and physiological makeup of many crop species. Some of these changes were due to conscious selection such as increases in palatability and colour, but many of the others were the unconscious byproduct of planting and harvesting. Changes in crop species during domestication were gradual, likely taking thousands of years. Many of the traits associated with plant domestication are regulated by only a few genes, and in many cases these genes have pleiotropic effects, where they affect a number of traits simultaneously. Many of the genes associated with domestication are also clustered close together on the same chromosome. The process of domestication severely limited the amount of genetic variation in crop species.Key Concepts:The most potent force influencing variation in cultivated populations is artificial selection, a specialised case of directional selection with humans acting as the agents of selection.The morphology and physiology of crop species were gradually changed through both conscious and unconscious selection by humans.Many of the traits associated with plant domestication are regulated by only a few genes that are close together on chromosomes.A high percentage of crop species are polyploid, with more than one set of chromosomes.Agriculture probably first emerged in the hills above the Tigris River on the western edge of what is now called Iran approximately 13 000 years ago, but it also appeared independently in Mesoamerica, South America, China, Africa, Asia and Eastern North America.Until recently, it was thought that once humans began cultivation, selection for the domestication genes would be rapid; however, new archaeological evidence indicates that predomestication cultivation may have actually taken 1000 years.During the process of crop domestication, genetic variability was greatly restricted by the selection of a limited number of desirable individuals.
Cystic Fibrosis: Gene Therapy
Authors: Sumner‐Jones Stephanie G , Gill Deborah R 
Published: April 2014

AbstractCystic fibrosis (CF) is an autosomal recessive disease caused by mutations of theCFTRgene, which encodes a member of the adenosine triphosphate‐binding cassette superfamily of transmembrane proteins. CFTR normally acts as a cyclic adenosine monophosphate‐activated chloride channel and as a regulator of other ion channels. The main cause of morbidity and mortality is the effect of CFTR dysfunction on the lung, which reduces life expectancy of CF patients (current median approximately 40 years according to UK and US national patient registries). There has been some progress in the identification of pharmacological agents that can correct the CFTR defect in patients carrying some classes of mutation, but with nearly 2000 different disease‐causing mutations reported, gene therapy remains the most likely option for the amelioration of lung disease in the majority of CF sufferers. The progress achieved and the hurdles identified as a result of the clinical trials of gene therapy vectors in CF patients are reviewed.Key Concepts:CF is a monogenic recessive disease with an incidence of 1:2500 in populations of Caucasian descent in particular, caused by mutations in theCFTRgene.It is a life‐limiting condition and disease management involves a heavy therapeutic burden with no definitive cure.Disruption of theCFTRgene leads to incorrect or insufficient transport of chloride ions across the epithelial cells of the body with a range of consequences in different organs, crucially inadequate clearance of bacteria from the lungs due to ineffective mucociliary clearance, resulting in progressive fibrosis and clogging of the lung with mucus, and eventually respiratory failure.Discovery of the genetic basis for CF quickly led to evaluation of gene therapy as a therapeutic option, with a range of viral and nonviral vectors.Although the vectors tested showed some efficacy in terms of correcting the fundamental chloride transport defect, no CF gene therapy trial has so far been able to demonstrate long‐term clinical improvement.
DNA
Damage Response: From Tumourigenesis to Therapy
Authors: Bain Amanda L , Mastrocola Adam S , Tibbetts Randal S , Khanna Kum Kum 
Published: April 2014

Abstract

The
deoxyribonucleic acid (DNA)
damage response (DDR) pathway is a surveillance network, whereby lesions are eliminated from DNA to ensure genomic integrity. The DDR detects aberrant DNA and chromosomal structures and elicits a multifaceted response network to coordinate multiple cellular processes, including regulation of the cell cycle, DNA repair, replication and, under certain circumstances, the triggering of programmed cell death. However, when the DDR is dysregulated, genomic integrity is not ensured, which may lead to tumourigenesis. Paradoxically, although genomic instability is a hallmark of many cancers, many conventional cancer treatments elicit the generation of additional DNA damage to exploit inherent DDR faults present in tumour cells. In addition, new‐targeted DDR inhibitors are currently being developed to enhance therapeutic indexes, including those that are synthetically lethal in particular tumour cell types, providing exciting new therapeutic avenues for cancer treatment. The challenge is how to identify the patients most receptive to these treatments.

Key Concepts:

Genome stability is critical to prevent tumourigenesis.

Cell cycle checkpoints and DNA repair exist to prevent faulty genetic information from passing onto daughter cells.

Many cancer types exhibit defective DNA repair pathways.

DNA repair is an ideal therapeutic target for cancer.

Cancers exhibit multiple chromosomal alterations.

Inherited mutations in DNA repair genes can cause chromosomal instability disorders.