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The aim of this paper is to preserve the originality of the art form. The recent trends of consumerism, market and selling attitude have made this art a maidservant of the moneyed people. The selling of art and modifying it is not bad but it should not affect the creativity of the people. Due to the contemporary styles the real essence of this folk art is disappearing which in turn is also depleting the values associated with it. A serious thought is urgently required before the traditional creativity and values are drained out to nothing. NGO professionals, researchers, folk artists, and people concerned all should take concrete steps and the appropriate measures to retain this art in its originality because it’s a legacy being passed down from generations.

Previous studies have shown that common variants of the gene coding for FK506-binding protein 51 (FKBP5), a critical regulator of glucocorticoid sensitivity, affect vulnerability to stress-related disorders. In a previous report,FKBP5rs1360780 was identified as a functional variant because of its effect on gene methylation. Here we report evidence for a novel functionalFKBP5allele, rs3800373. This study assessed the association between rs3800373 and post-traumatic chronic pain in 1607 women and men from two ethnically diverse human cohorts. The molecular mechanism through which rs3800373 affects adverse outcomes was established viain silico,in vivo, andin vitroanalyses. The rs3800373 minor allele predicted worse adverse outcomes after trauma exposure, such that individuals with the minor (risk) allele developed more severe post-traumatic chronic musculoskeletal pain. Among these individuals, peritraumatic circulatingFKBP5expression levels increased as cortisol and glucocorticoid receptor (NR3C1) mRNA levels increased, consistent with increased glucocorticoid resistance. Bioinformatic,in vitro, and mutational analyses indicate that the rs3800373 minor allele reduces the binding of a stress- and pain-associated microRNA, miR-320a, toFKBP5via altering theFKBP5mRNA 3′UTR secondary structure (i.e., is a riboSNitch). This results in relatively greaterFKBP5translation, unchecked by miR-320a. Overall, these results identify an important gene–miRNA interaction influencing chronic pain risk in vulnerable individuals and suggest that exogenous methods to achieve targeted reduction in poststressFKBP5mRNA expression may constitute useful therapeutic strategies.SIGNIFICANCE STATEMENTFKBP5is a critical regulator of the stress response. Previous studies have shown that dysregulation of the expression of this gene plays a role in the pathogenesis of chronic pain development as well as a number of comorbid neuropsychiatric disorders. In the current study, we identified a functional allele (rs3800373) in the 3′UTR ofFKBP5that influences vulnerability to chronic post-traumatic pain in two ethnic cohorts. Using multiple complementary experimental approaches, we show that theFKBP5rs3800373 minor allele alters the secondary structure ofFKBP5mRNA, decreasing the binding of a stress- and pain-associated microRNA, miR-320a. This results in relatively greaterFKBP5translation, unchecked by miR-320a, increasing glucocorticoid resistance and increasing vulnerability to post-traumatic pain.

Previous studies have shown that common variants of the gene coding for FK506-binding protein 51 (FKBP5), a critical regulator of glucocorticoid sensitivity, affect vulnerability to stress-related disorders. In a previous report, FKBP5 rs1360780 was identified as a functional variant because of its effect on gene methylation. Here we report evidence for a novel functional FKBP5 allele, rs3800373. This study assessed the association between rs3800373 and post-traumatic chronic pain in 1607 women and men from two ethnically diverse human cohorts. The molecular mechanism through which rs3800373 affects adverse outcomes was established via in silico, in vivo, and in vitro analyses. The rs3800373 minor allele predicted worse adverse outcomes after trauma exposure, such that individuals with the minor (risk) allele developed more severe post-traumatic chronic musculoskeletal pain. Among these individuals, peritraumatic circulating FKBP5 expression levels increased as cortisol and glucocorticoid receptor (NR3C1) mRNA levels increased, consistent with increased glucocorticoid resistance. Bioinformatic, in vitro, and mutational analyses indicate that the rs3800373 minor allele reduces the binding of a stress- and pain-associated microRNA, miR-320a, to FKBP5 via altering the FKBP5 mRNA 3′UTR secondary structure (i.e., is a riboSNitch). This results in relatively greater FKBP5 translation, unchecked by miR-320a. Overall, these results identify an important gene–miRNA interaction influencing chronic pain risk in vulnerable individuals and suggest that exogenous methods to achieve targeted reduction in poststress FKBP5 mRNA expression may constitute useful therapeutic strategies. SIGNIFICANCE STATEMENT FKBP5 is a critical regulator of the stress response. Previous studies have shown that dysregulation of the expression of this gene plays a role in the pathogenesis of chronic pain development as well as a number of comorbid neuropsychiatric disorders. In the current study, we identified a functional allele (rs3800373) in the 3′UTR of FKBP5 that influences vulnerability to chronic post-traumatic pain in two ethnic cohorts. Using multiple complementary experimental approaches, we show that the FKBP5 rs3800373 minor allele alters the secondary structure of FKBP5 mRNA, decreasing the binding of a stress- and pain-associated microRNA, miR-320a. This results in relatively greater FKBP5 translation, unchecked by miR-320a, increasing glucocorticoid resistance and increasing vulnerability to post-traumatic pain.

Introduction A motor vehicle collision (MVC) is one of the most common life-threatening events experienced by individuals living in the USA. While most individuals recover following MVC, a significant proportion of individuals develop adverse post-traumatic sequelae such as post-traumatic stress disorder or persistent musculoskeletal pain. Adverse post-traumatic sequelae are common, morbid and costly public health problems in the USA and other industrialised countries. The pathogenesis of these disorders following MVC remains poorly understood. In the USA, available data suggest that African-Americans experience an increased burden of adverse post-traumatic sequelae after MVC compared to European Americans, but to date no studies examining the pathogenesis of these disorders among African-Americans experiencing MVC have been performed. Methods and analysis The African-American CRASH (AA CRASH) study is an NIH-funded, multicentre, prospective study that enrols African-Americans (n=900) who present to the emergency department (ED) within 24 hours of MVC. Participants are enrolled at 13 ED sites in the USA. Individuals who are admitted to the hospital or who report a fracture or tissue injury are excluded. Participants complete a detailed ED interview that includes an assessment of crash history, current post-traumatic symptoms and health status prior to the MVC. Blood samples are also collected in the ED using PAXgene DNA and PAXgene RNA tubes. Serial mixed-mode assessments 6 weeks, 6 months and 1 year after MVC include an assessment of adverse sequelae, general health status and health service utilisation. The results from this study will provide insights into the incidence and pathogenesis of persistent pain and other post-traumatic sequelae in African-Americans experiencing MVC. Ethics and dissemination AA CRASH has ethics approval in the USA, and the results will be published in a peer-reviewed journal.

We obtained recommendations for a graphical user interface (GUI) design for a new medical monitoring system. Data were obtained from 26 combat-experienced medics. Volunteers were briefed on the medical monitoring system. They then completed a questionnaire on background medical treatment experience, provided drawings on how and what information should be displayed on the GUI screens for use on a personal digital assistant, and participated in focus group sessions with four to seven medics per group to obtain group consensus on what information the GUI screens should contain. Detailed displays on seven screens provide the medical and situational awareness information medics need for triage decisions and for early processing of a casualty. The created GUI screens are a combination of object-based and text-based information using a color-coded system. Medics believed the information displayed with these GUI designs would improve treatment of casualties on the battlefield.

The Warfighter Physiological Status Monitoring (WPSM) system collects vital sign information and other event information. This information is sent wirelessly to a personal digital assistant (PDA) held by the medic. The primary purpose of this study was to determine what features should be included in the graphical user interface (GUI) of the WPSM system as it would appear on the Battlefield Medical Information System-Tactical (BMIS-T) PDA. To meet this objective, information was obtained from 26 experienced combat medics. A background questionnaire was administered to obtain information regarding the volunteers' medical experience, types of injuries and illnesses observed or treated, and how medical decisions such as triage assessments are made during combat. Secondly, these volunteers were asked to design individual GUI screens after being provided a briefing on what the WPSM system is. Finally, four focus groups of between 4 and 7 medics provided group consensus feedback on what the GUIs for the WPSM system should look like. Results from the volunteers' individual GUI designs and focus group sessions revealed most medics wanted a (1) geo-location screen, (2) a screen summarizing the medical status of the squad or platoon they were monitoring, (3) an individual patient screen, (4) a treatment and evacuation information screen, (5) an electronic Field Medical Card (FMC), and (6) a reference information screen.