Drosophila Larval Models of Invasive Tumorigenesis for In Vivo Studies on Tumour/Peripheral Host Tissue Interactions during Cancer Cachexia.

Cancer cachexia is a common deleterious paraneoplastic syndrome that represents an area of unmet clinical need, partly due to its poorly understood aetiology and complex multifactorial nature. We have interrogated multiple genetically defined larval Drosophila models of tumourigenesis against key features of human cancer cachexia. Our results indicate that cachectic tissue wasting is dependent on the genetic characteristics of the tumour and demonstrate that host malnutrition or tumour burden are not sufficient to drive wasting. We show that JAK/STAT and TNF-α/Egr signalling are elevated in cachectic muscle and promote tissue wasting. Furthermore, we introduce a dual driver system that allows independent genetic manipulation of tumour and host skeletal muscle. Overall, we present a novel Drosophila larval paradigm to study tumour/host tissue crosstalk in vivo, which may contribute to future research in cancer cachexia and impact the design of therapeutic approaches for this pathology.

Assessment of the different citation systems in the scientific publication of nursing authors from Spanish-speaking countries.

OBJECTIVE: To assess the distribution of citations of nursing authors in Spanish in Google Scholar as well as to compare the possible differences between this source and Web of Science and Scopus. METHOD: This is a descriptive cross-sectional study based on the citation systems offered by Google Scholar, Web of Science, and Scopus. RESULTS: Nursing researchers present a verified mean h-index of 7.82 in Academic Google. 74% of researchers belong to the academic field, compared to 26%, who are in health services. Most of them live in Spain (83%), followed by Colombia (12%), Mexico (4%), and Chile (1%). In Spain, the community with the largest number of researchers is Andalusia (41.5%), followed by Valencia (14.6%), and Madrid (7.3%). CONCLUSION: The Google Scholar citation system requires adjustments in its algorithm for selecting works and citations, and it should also allow some system of confirmation by authors. Nursing can have relatively low h-index values compared to other courses due to short research development.

Assessment of the different citation systems in the scientific publication of nursing authors from Spanish-speaking countries / Avaliação dos diferentes sistemas de citação na publicação científica de autores de enfermagem em espanhol / Evaluación de los diferentes sistemas de citación en la publicación científica de autores enfermeros en español

ABSTRACT Objective: To assess the distribution of citations of nursing authors in Spanish in Google Scholar as well as to compare the possible differences between this source and Web of Science and Scopus. Method: This is a descriptive cross-sectional study based on the citation systems offered by Google Scholar, Web of Science, and Scopus. Results: Nursing researchers present a verified mean h-index of 7.82 in Academic Google. 74% of researchers belong to the academic field, compared to 26%, who are in health services. Most of them live in Spain (83%), followed by Colombia (12%), Mexico (4%), and Chile (1%). In Spain, the community with the largest number of researchers is Andalusia (41.5%), followed by Valencia (14.6%), and Madrid (7.3%). Conclusion: The Google Scholar citation system requires adjustments in its algorithm for selecting works and citations, and it should also allow some system of confirmation by authors. Nursing can have relatively low h-index values compared to other courses due to short research development.

RESUMO Objetivo: Avaliar a distribuição de citações de autores de enfermagem em espanhol no Google Scholar, bem como comparar as possíveis diferenças entre esta fonte e Web of Science e Scopus. Método: Estudo descritivo transversal baseado nos sistemas de citação oferecidos pelo Google Scholar, Web of Science e Scopus. Resultados: Pesquisadores da área de enfermagem apresentam índice h médio verificado no Google Acadêmico de 7,82. 74% dos pesquisadores pertencem à área acadêmica, contra 26% que estão agrupados nos serviços de saúde. A maioria deles está localizada na Espanha (83%), seguida pela Colômbia (12%), México (4%) e Chile (1%). Na Espanha, a comunidade com maior número de pesquisadores é a Andaluzia (41,5%), seguida da Comunidade Valenciana (14,6%) e Madrid (7,3%). Conclusão: O sistema de citações do Google Scholar requer ajustes em seu algoritmo de seleção de obras e citações, devendo também permitir algum sistema de confirmação por parte dos autores. A enfermagem pode ter valores relativamente baixos do índice h em comparação com outras disciplinas devido ao curto desenvolvimento da pesquisa.

RESUMEN Objetivo: Evaluar la distribución de citas de autores enfermeros en español en Google Académico, así como comparar las posibles diferencias entre esta fuente y Web of Science y Scopus. Método: Estudio descriptivo transversal basado en los sistemas de citas ofrecidos por Google Académico, Web of Science y Scopus. Resultados: Los investigadores del área de enfermería presentan un índice h verificado medio de 7.82 en Google Académico. El 74% de los investigadores pertenece al ámbito académico, frente a un 26% que se aglutina en los servicios de salud. La mayoría de ellos se ubican en España (83%), seguido de Colombia (12%), Méjico (4%) y Chile (1%). En España, la comunidad que mayor número de investigadores aglutina es Andalucía (41,5%), seguida de la Comunidad Valencia (14,6%) y Madrid (7,3%). Conclusión: El sistema de citación de Google Académico precisa de ajustes en su algoritmo de selección de trabajos y citas, además debería permitir algún sistema de confirmación por parte de los autores. Enfermería puede tener valores relativamente bajos del índice h frente a otras disciplinas debido al breve desarrollo investigador.

The antimicrobial peptide defensin cooperates with tumour necrosis factor to drive tumour cell death in Drosophila.

Antimicrobial peptides (AMPs) are small cationic molecules best known as mediators of the innate defence against microbial infection. While in vitro and ex vivo evidence suggest AMPs' capacity to kill cancer cells, in vivo demonstration of an anti-tumour role of endogenous AMPs is lacking. Using a Drosophila model of tumourigenesis, we demonstrate a role for the AMP Defensin in the control of tumour progression. Our results reveal that Tumour Necrosis Factor mediates exposure of phosphatidylserine (PS), which makes tumour cells selectively sensitive to the action of Defensin remotely secreted from tracheal and fat tissues. Defensin binds tumour cells in PS-enriched areas, provoking cell death and tumour regression. Altogether, our results provide the first in vivo demonstration for a role of an endogenous AMP as an anti-cancer agent, as well as a mechanism that explains tumour cell sensitivity to the action of AMPs.

A Neuronal Relay Mediates a Nutrient Responsive Gut/Fat Body Axis Regulating Energy Homeostasis in Adult Drosophila.

The control of systemic metabolic homeostasis involves complex inter-tissue programs that coordinate energy production, storage, and consumption, to maintain organismal fitness upon environmental challenges. The mechanisms driving such programs are largely unknown. Here, we show that enteroendocrine cells in the adult Drosophila intestine respond to nutrients by secreting the hormone Bursicon α, which signals via its neuronal receptor DLgr2. Bursicon α/DLgr2 regulate energy metabolism through a neuronal relay leading to the restriction of glucagon-like, adipokinetic hormone (AKH) production by the corpora cardiaca and subsequent modulation of AKH receptor signaling within the adipose tissue. Impaired Bursicon α/DLgr2 signaling leads to exacerbated glucose oxidation and depletion of energy stores with consequent reduced organismal resistance to nutrient restrictive conditions. Altogether, our work reveals an intestinal/neuronal/adipose tissue inter-organ communication network that is essential to restrict the use of energy and that may provide insights into the physiopathology of endocrine-regulated metabolic homeostasis.

Estudio de prescripción de opioides mayores para el control del dolor en pacientes hospitalizados / Use of major opioids for control of pain in hospitalized patients

Objetivos: Analizar las características de prescripción de opioides mayores para el tratamiento del dolor en pacientes hospitalizados. Evaluar la influencia de las características epidemiológicas de la población, la prescripción por servicios clínicos, la eficacia de la analgesia pautada, la prescripción de fármacos concomitantes y los efectos adversos secundarios al tratamiento opioide. Material y métodos: Estudio descriptivo, retrospectivo realizado entre marzo y abril de 2016 en el Hospital Universitario Fundación Alcorcón. Se consideró el primer opioide prescrito durante la estancia hospitalaria, haciéndose un seguimiento durante los cinco primeros días de tratamiento o hasta la discontinuación de este. Se excluyeron pacientes con prescripción de opioides en procedimientos quirúrgicos exclusivamente, que no continuaron con el tratamiento de los mismos durante su ingreso. Las variables recogidas fueron: sociodemográficas, clínicas, servicio clínico, prescripción de opioides mayores y otros fármacos, valoración del dolor y efectos adversos. Resultados: Los opioides más prescritos fueron morfina y fentanilo. Fentanilo y oxicodona se prescribieron principalmente en dolor mixto, morfina en dolor nociceptivo y petidina en dolor visceral. Las vías de administración más usadas fueron intravenosa y epidural. La mayoría de los pacientes tomaron otros fármacos concomitantes, siendo el más frecuente paracetamol. Los principales servicios prescriptores fueron traumatología, oncología y medicina interna. Fentanilo se pautó principalmente en traumatología y medicina interna, morfina en traumatología y oncología, oxicodona en oncología y petidina en medicina interna. La unidad del dolor realizó seguimiento de la mitad de los pacientes, especialmente en pacientes quirúrgicos. La mayoría de los pacientes tenían registrado el valor de la escala numérica simple, siendo la media 2,7. Los efectos secundarios fueron leves, destacando náuseas, vómitos y estreñimiento. Discusión: El grado de analgesia conseguido con el tratamiento opioide fue satisfactorio, con un valor aceptable. Los efectos secundarios fueron porcentualmente leves, destacando las náuseas, los vómitos y el estreñimiento propios de los opioides. La prescripción de opioides mayores siguió el patrón habitual de utilización en el ámbito hospitalario. Este tipo de estudios permite conocer y comparar el uso de opioides entre servicios clínicos y hospitales, así como predecir necesidades y reconocer ineficiencias

Objectives: Analyze prescription characteristics of major opioids for treatment of pain in hospitalized patients, influence of the epidemiological characteristics of population, to evaluate prescription for clinical services, efficacy of the analgesia, prescription of concomitant drugs and adverse effects secondary to opioid treatment. Material and methods: A descriptive, retrospective study carried out between March and April 2016 at Alcorcón Foundation University Hospital. It was considered first opioid prescribed during hospital stay, being followed during first five days of treatment or until discontinuation of the same. Patients with opioid prescribing were excluded exclusively in surgical procedures, who did not continue their treatment during their admission. Variables included were sociodemographic, clinical, clinical service, prescription of major opioids and other drugs, pain assessment and adverse effects. Results: Most commonly prescribed opioids were morphine and fentanyl. Fentanyl and oxycodone were prescribed mainly in mixed pain, morphine in nociceptive pain and pethidine in visceral pain. Most commonly used routes of administration were intravenous and epidural. Most of the patients took other concomitant drugs, being the most frequent paracetamol. The main prescribing services were traumatology, oncology and internal medicine. Fentanyl was mainly based on traumatology and internal medicine, morphine in traumatology and oncology, oxycodone in oncology and pethidine in internal medicine. Pain unit monitored half of patients, especially in surgical patients. Majority of patients had value of the simple numerical scale, with the mean being 2.7. Side effects were mild, emphasizing nausea, vomiting and constipation. Discussion: Degree of analgesia obtained with opioid treatment was satisfactory, with an acceptable value. Side effects were mild, with prominent opioid nausea, vomiting and constipation. Prescription of major opioids followed the usual pattern of use in hospital setting. This type of study allows to know and compare use of opioids between clinical services and hospitals, as well as predicting needs and recognizing inefficiencies

Bursicon-α subunit modulates dLGR2 activity in the adult Drosophila melanogaster midgut independently to Bursicon-ß.

Bursicon is the main regulator of post molting and post eclosion processes during arthropod development. The active Bursicon hormone is a heterodimer of Burs-α and Burs-ß. However, adult midguts express Burs-α to regulate the intestinal stem cell niche. Here, we examined the potential expression and function of its heterodimeric partner, Burs-ß in the adult midgut. Unexpectedly, our evidence suggests that Burs-ß is not significantly expressed in the adult midgut. burs-ß mutants displayed the characteristic developmental defects but showed wild type-like adult midguts, thus uncoupling the developmental and adult phenotypes seen in burs-α mutants. Gain of function data and ex vivo experiments using a cAMP biosensor, demonstrated that Burs-α is sufficient to drive stem cell quiescence and to activate dLGR2 in the adult midgut. Our evidence suggests that the post developmental transactivation of dLGR2 in the adult midgut is mediated by Burs-α and that the ß subunit of Bursicon is dispensable for these activities.

Fluoroscopia y protección radiológica en tratamiento del dolor / Fluroscopy and radiation protection in pain management

La fluorosocopia es una técnica esencial para la realización de la mayoría de bloqueos en tratamiento del dolor pero, a pesar de utilizarse diariamente, un gran porcentaje de especialistas no ha recibido formación específica, según se describe en una encuesta realizada entre los encuestados de la especialidad (1). Con este artículo pretendemos exponer conceptos básicos de los tipos de radiación, sobre cómo se generan los rayos X y cómo podemos controlar la imagen que obtenemos en el monitor modificando diferentes parámetros como corriente o voltaje. También se describen los límites de dosis establecidos en la legislación española, cómo se puede monitorizar la radiación, las recomendaciones para reducir la exposición a rayos X y tratamos de insistir en la importancia de informar al paciente del uso de rayos X, lo cual raramente realizamos (AU)

The use of fluoroscopy is an essential tool for the practice of blocks and techniques in pain management. However and despite its frequent use, a large number of pain specialists have not received specific training, according to the study that we carried out among pain practitioners (1). In the present study we pretend to describe the basic principles of radiation, generation of X rays, and control of the monitor image using the, voltage or current. We also describe the dose limits established by Spanish law, how to monitor radiation, recommendations to reduce exposure to X rays and finally we insist on the importance to inform the patient about the use of X rays, since rarely it is done (AU)

mTORC1-mediated translational elongation limits intestinal tumour initiation and growth.

Inactivation of APC is a strongly predisposing event in the development of colorectal cancer, prompting the search for vulnerabilities specific to cells that have lost APC function. Signalling through the mTOR pathway is known to be required for epithelial cell proliferation and tumour growth, and the current paradigm suggests that a critical function of mTOR activity is to upregulate translational initiation through phosphorylation of 4EBP1 (refs 6, 7). This model predicts that the mTOR inhibitor rapamycin, which does not efficiently inhibit 4EBP1 (ref. 8), would be ineffective in limiting cancer progression in APC-deficient lesions. Here we show in mice that mTOR complex 1 (mTORC1) activity is absolutely required for the proliferation of Apc-deficient (but not wild-type) enterocytes, revealing an unexpected opportunity for therapeutic intervention. Although APC-deficient cells show the expected increases in protein synthesis, our study reveals that it is translation elongation, and not initiation, which is the rate-limiting component. Mechanistically, mTORC1-mediated inhibition of eEF2 kinase is required for the proliferation of APC-deficient cells. Importantly, treatment of established APC-deficient adenomas with rapamycin (which can target eEF2 through the mTORC1-S6K-eEF2K axis) causes tumour cells to undergo growth arrest and differentiation. Taken together, our data suggest that inhibition of translation elongation using existing, clinically approved drugs, such as the rapalogs, would provide clear therapeutic benefit for patients at high risk of developing colorectal cancer.

Local control of intestinal stem cell homeostasis by enteroendocrine cells in the adult Drosophila midgut.

BACKGROUND: Enteroendocrine cells populate gastrointestinal tissues and are known to translate local cues into systemic responses through the release of hormones into the bloodstream. RESULTS: Here we report a novel function of enteroendocrine cells acting as local regulators of intestinal stem cell (ISC) proliferation through modulation of the mesenchymal stem cell niche in the Drosophila midgut. This paracrine signaling acts to constrain ISC proliferation within the epithelial compartment. Mechanistically, midgut enteroendocrine cells secrete the neuroendocrine hormone Bursicon, which acts-beyond its known roles in development-as a paracrine factor on the visceral muscle (VM). Bursicon binding to its receptor, DLGR2, the ortholog of mammalian leucine-rich repeat-containing G protein-coupled receptors (LGR4-6), represses the production of the VM-derived EGF-like growth factor Vein through activation of cAMP. CONCLUSIONS: We therefore identify a novel paradigm in the regulation of ISC quiescence involving the conserved ligand/receptor Bursicon/DLGR2 and a previously unrecognized tissue-intrinsic role of enteroendocrine cells.

c-Src drives intestinal regeneration and transformation.

The non-receptor tyrosine kinase c-Src, hereafter referred to as Src, is overexpressed or activated in multiple human malignancies. There has been much speculation about the functional role of Src in colorectal cancer (CRC), with Src amplification and potential activating mutations in up to 20% of the human tumours, although this has never been addressed due to multiple redundant family members. Here, we have used the adult Drosophila and mouse intestinal epithelium as paradigms to define a role for Src during tissue homeostasis, damage-induced regeneration and hyperplasia. Through genetic gain and loss of function experiments, we demonstrate that Src is necessary and sufficient to drive intestinal stem cell (ISC) proliferation during tissue self-renewal, regeneration and tumourigenesis. Surprisingly, Src plays a non-redundant role in the mouse intestine, which cannot be substituted by the other family kinases Fyn and Yes. Mechanistically, we show that Src drives ISC proliferation through upregulation of EGFR and activation of Ras/MAPK and Stat3 signalling. Therefore, we demonstrate a novel essential role for Src in intestinal stem/progenitor cell proliferation and tumourigenesis initiation in vivo.

FAK acts as a suppressor of RTK-MAP kinase signalling in Drosophila melanogaster epithelia and human cancer cells.

Receptor Tyrosine Kinases (RTKs) and Focal Adhesion Kinase (FAK) regulate multiple signalling pathways, including mitogen-activated protein (MAP) kinase pathway. FAK interacts with several RTKs but little is known about how FAK regulates their downstream signalling. Here we investigated how FAK regulates signalling resulting from the overexpression of the RTKs RET and EGFR. FAK suppressed RTKs signalling in Drosophila melanogaster epithelia by impairing MAPK pathway. This regulation was also observed in MDA-MB-231 human breast cancer cells, suggesting it is a conserved phenomenon in humans. Mechanistically, FAK reduced receptor recycling into the plasma membrane, which resulted in lower MAPK activation. Conversely, increasing the membrane pool of the receptor increased MAPK pathway signalling. FAK is widely considered as a therapeutic target in cancer biology; however, it also has tumour suppressor properties in some contexts. Therefore, the FAK-mediated negative regulation of RTK/MAPK signalling described here may have potential implications in the designing of therapy strategies for RTK-driven tumours.

Transformed epithelia trigger non-tissue-autonomous tumor suppressor response by adipocytes via activation of Toll and Eiger/TNF signaling.

High tumor burden is associated with increased levels of circulating inflammatory cytokines that influence the pathophysiology of the tumor and its environment. The cellular and molecular events mediating the organismal response to a growing tumor are poorly understood. Here, we report a bidirectional crosstalk between epithelial tumors and the fat body-a peripheral immune tissue-in Drosophila. Tumors trigger a systemic immune response through activation of Eiger/TNF signaling, which leads to Toll pathway upregulation in adipocytes. Reciprocally, Toll elicits a non-tissue-autonomous program in adipocytes, which drives tumor cell death. Hemocytes play a critical role in this system by producing the ligands Spätzle and Eiger, which are required for Toll activation in the fat body and tumor cell death. Altogether, our results provide a paradigm for a long-range tumor suppression function of adipocytes in Drosophila, which may represent an evolutionarily conserved mechanism in the organismal response to solid tumors.

Reduced LIMK2 expression in colorectal cancer reflects its role in limiting stem cell proliferation.

OBJECTIVE: Colorectal cancer (CRC) is a major contributor to cancer mortality and morbidity. LIM kinase 2 (LIMK2) promotes tumour cell invasion and metastasis. The objectives of this study were to determine how LIMK2 expression is associated with CRC progression and patient outcome, and to use genetically modified Drosophila and mice to determine how LIMK2 deletion affects gastrointestinal stem cell regulation and tumour development. DESIGN: LIMK2 expression and activity were measured by immunostaining tumours from CRC-prone mice, human CRC cell lines and 650 human tumours. LIMK knockdown in Drosophila or Limk2 deletion in mice allowed for assessment of their contributions to gastrointestinal stem cell homeostasis and tumour development. RESULTS: LIMK2 expression was reduced in intestinal tumours of cancer-prone mice, as well as in human CRC cell lines and tumours. Reduced LIMK2 expression and substrate phosphorylation were associated with shorter patient survival. Genetic analysis in Drosophila midgut and intestinal epithelial cells isolated from genetically modified mice revealed a conserved role for LIMK2 in constraining gastrointestinal stem cell proliferation. Limk2 deletion increased colon tumour size in a colitis-associated colorectal mouse cancer model. CONCLUSIONS: This study revealed that LIMK2 expression and activity progressively decrease with advancing stage, and supports the hypothesis that there is selective pressure for reduced LIMK2 expression in CRC to relieve negative constraints imposed upon gastrointestinal stem cells.

p120 catenin is required for the stress response in Drosophila.

p120ctn is a ubiquitously expressed core component of cadherin junctions and essential for vertebrate development. Surprisingly, Drosophila p120ctn (dp120ctn) is dispensable for adherens junctions and development, which has discouraged Drosophila researchers from further pursuing the biological role of dp120ctn. Here we demonstrate that dp120ctn loss results in increased heat shock sensitivity and reduced animal lifespan, which are completely rescued by ectopic expression of a dp120ctn-GFP transgene. Transcriptomic analysis revealed multiple relish/NF-κB target genes differentially expressed upon loss of dp120ctn. Importantly, this aberrant gene expression was rescued by overexpression of dp120ctn-GFP or heterozygosity for relish. Our results uncover a novel role for dp120ctn in the regulation of animal stress response and immune signalling. This may represent an ancient role of p120ctn and can influence further studies in Drosophila and mammals.

Rac1 drives intestinal stem cell proliferation and regeneration.

Adult stem cells are responsible for maintaining the balance between cell proliferation and differentiation within self-renewing tissues. The molecular and cellular mechanisms mediating such balance are poorly understood. The production of reactive oxygen species (ROS) has emerged as an important mediator of stem cell homeostasis in various systems. Our recent work demonstrates that Rac1-dependent ROS production mediates intestinal stem cell (ISC) proliferation in mouse models of colorectal cancer (CRC). Here, we use the adult Drosophila midgut and the mouse small intestine to directly address the role of Rac1 in ISC proliferation and tissue regeneration in response to damage. Our results demonstrate that Rac1 is necessary and sufficient to drive ISC proliferation and regeneration in an ROS-dependent manner. Our data point to an evolutionarily conserved role of Rac1 in intestinal homeostasis and highlight the value of combining work in the mammalian and Drosophila intestine as paradigms to study stem cell biology.

ROS production and NF-κB activation triggered by RAC1 facilitate WNT-driven intestinal stem cell proliferation and colorectal cancer initiation.

The Adenomatous Polyposis Coli (APC) gene is mutated in the majority of colorectal cancers (CRCs). Loss of APC leads to constitutively active WNT signaling, hyperproliferation, and tumorigenesis. Identification of pathways that facilitate tumorigenesis after APC loss is important for therapeutic development. Here, we show that RAC1 is a critical mediator of tumorigenesis after APC loss. We find that RAC1 is required for expansion of the LGR5 intestinal stem cell (ISC) signature, progenitor hyperproliferation, and transformation. Mechanistically, RAC1-driven ROS and NF-κB signaling mediate these processes. Together, these data highlight that ROS production and NF-κB activation triggered by RAC1 are critical events in CRC initiation.

Non-autonomous crosstalk between the Jak/Stat and Egfr pathways mediates Apc1-driven intestinal stem cell hyperplasia in the Drosophila adult midgut.

Inactivating mutations within adenomatous polyposis coli (APC), a negative regulator of Wnt signaling, are responsible for most sporadic and hereditary forms of colorectal cancer (CRC). Here, we use the adult Drosophila midgut as a model system to investigate the molecular events that mediate intestinal hyperplasia following loss of Apc in the intestine. Our results indicate that the conserved Wnt target Myc and its binding partner Max are required for the initiation and maintenance of intestinal stem cell (ISC) hyperproliferation following Apc1 loss. Importantly, we find that loss of Apc1 leads to the production of the interleukin-like ligands Upd2/3 and the EGF-like Spitz in a Myc-dependent manner. Loss of Apc1 or high Wg in ISCs results in non-cell-autonomous upregulation of upd3 in enterocytes and subsequent activation of Jak/Stat signaling in ISCs. Crucially, knocking down Jak/Stat or Spitz/Egfr signaling suppresses Apc1-dependent ISC hyperproliferation. In summary, our results uncover a novel non-cell-autonomous interplay between Wnt/Myc, Egfr and Jak/Stat signaling in the regulation of intestinal hyperproliferation. Furthermore, we present evidence suggesting potential conservation in mouse models and human CRC. Therefore, the Drosophila adult midgut proves to be a powerful genetic system to identify novel mediators of APC phenotypes in the intestine.

Encuesta acerca de la utilización de fluoroscopia en el tratamiento del dolor. ¿Lo hacemos correctamente? / A survey on the use of fluoroscopy in the treatment of pain: Do we perform it correctly?

Objetivos. La fluoroscopia es una técnica que se utiliza habitualmente para procedimientos en tratamiento del dolor y de la que, a pesar de la importancia que tiene sobre la salud, se desconoce la forma de empleo entre los especialistas. Realizamos una encuesta nacional para evaluar su empleo. Material y métodos. Se diseñó y envió una encuesta de 15 preguntas relacionadas con el uso de la fluoroscopia en tratamiento del dolor a 105 Unidades de Diagnóstico y Tratamiento del Dolor en España, en 2008. Resultados. Se recibieron 63 encuestas con respuestas válidas (60%). La mayoría de los especialistas (66,6%) no habían recibido formación específica en fluoroscopia durante su residencia o en la formación en dolor. El 90% de los especialistas que respondieron realiza los procedimientos que requieren rayos x (Rx) en el quirófano. El 54,7% realiza menos de 10 procedimientos a la semana y solo un 12% realiza más de 20 procedimientos por semana. En relación con la protección radiológica, la mayoría no utiliza gafas protectoras (80%) y solo el 50% lleva guantes plomados. El 47% se coloca a menos de 0,5 m del paciente. La mayoría (76%) no informa acerca de la radiación ni lo incluye en el consentimiento (80%). Conclusiones. Existe una deficiente formación acerca del manejo de la fluoroscopia en el área de tratamiento del dolor y de ello se deriva que las medidas de protección radiológica adoptadas suelan ser insuficientes. Los tratamientos se suelen realizar en quirófano. Más de la mitad de los especialistas realizan menos de 10 procedimientos semanales con Rx. El control y seguimiento de los valores de radiación es insuficiente, así como la información y la protección ofrecida al paciente(AU)

Objectives. Fluoroscopy is technique that is commonly used for procedures in the treatment of pain, but despite its importance in healthcare, many specialists do not know how to use it. We conducted a national survey to evaluate its use. Material and methods. A questionnaire with 15 questions related to the use of fluoroscopy in the treatment of pain was designed and sent to 105 units that diagnosed and treated pain in Spain, in 2008. Results. A total of 63 (60%) questionnaires with valid responses were received. The majority of specialist (66.6%) had not received specific training on fluoroscopy or pain during their residency. Almost all (90%) of specialists who responded performed procedures that required X-rays in the operating theatre. Just over half (54.7%) performed less than 10 procedures a week, and only 12% performed more than 20 procedures per week. As regards radiation protection, the majority (80%) did not use protective glasses, and only 50% wore leaded gloves. Just under half (47%) were situated less than 0.5 metre from the patient. The majority (76%) did not inform about the radiation, nor was it mentioned in the informed consent (80%). Conclusions. There is a lack of information on the handling of the fluoroscope in the area of pain treatment, and this usually leads to the adoption of insufficient radiation protection measures. The treatments are usually performed in the operating theatre. More than half the specialists perform less 10 procedures per week with x-rays. The control and follow-up of radiation values is insufficient, as is the information and protection offered to the patient(AU)

Inducible progenitor-derived Wingless regulates adult midgut regeneration in Drosophila.

The ability to regenerate following stress is a hallmark of self-renewing tissues. However, little is known about how regeneration differs from homeostatic tissue maintenance. Here, we study the role and regulation of Wingless (Wg)/Wnt signalling during intestinal regeneration using the Drosophila adult midgut. We show that Wg is produced by the intestinal epithelial compartment upon damage or stress and it is exclusively required for intestinal stem cell (ISC) proliferation during tissue regeneration. Reducing Wg or downstream signalling components from the intestinal epithelium blocked tissue regeneration. Importantly, we demonstrate that Wg from the undifferentiated progenitor cell, the enteroblast, is required for Myc-dependent ISC proliferation during regeneration. Similar to young regenerating tissues, ageing intestines required Wg and Myc for ISC hyperproliferation. Unexpectedly, our results demonstrate that epithelial but not mesenchymal Wg is essential for ISC proliferation in response to damage, while neither source of the ligand is solely responsible for ISC maintenance and tissue self-renewal in unchallenged tissues. Therefore, fine-tuning Wnt results in optimal balance between the ability to respond to stress without negatively affecting organismal viability.