135 research outputs found
Inelastic neutron scattering study of the H2 interaction with carbon-supported Pt and Pd catalysts
How do the graphenic domains terminate in activated carbons and carbon-supported metal catalysts?
Dynamics of Reactive Species and Reactant-Induced Reconstruction of Pt Clusters in Pt/Al2O3 Catalysts
Infección de macrófagos con virus encefalitis saint louis: efecto sobre el fenotipo celular y la apoptosis (Programa: enfermedades transmisibles y emergentes).
El Virus Encefalitis Saint Louis (VESL)es un virus neurotrópico que puede provocar en humanos encefalitis, meningitis y cefalea febril. Estudios epidemiológicos demostraron la circulación del virus en Argentina, reportándose el primer brote de encefalitis en Sud-América en Córdoba en el 2005. Los macrófagos tienen un rol muy importante en la patogénesis de las infecciones virales. Estas células son permisivas para la replicación y reservorio viral. Reconocen a los virus mediante receptores de reconocimiento de patrones, incluidos los receptores Toll-like, lo que genera la producción de moléculas antivirales y citoquinas pro-inflamatorias. Los macrófagos expresan diferentes fenotipos según el microambiente tisular y el estímulo externo. Se reconocen los macrófagos activados clásicamente (M1) que liberan citoquinas pro-inflamatorias y los macrófagos activados alternativamente (M2) que producen IL-10 y factor transformante del crecimiento. Como parte de la respuesta del macrófago a la infección viral, prolifera, se diferencia y muere. La apoptosis es un mecanismo de muerte que limita la actividad del macrófago activado. La interacción virus-macrófago ha sido analizada con numerosos tipos de virus. Sin embargo, existe escasa información sobre el impacto de VESL sobre la respuesta inmune innata. La emergencia de esta virosis en nuestro medio amerita abordar distintos aspectos de la respuesta inmune en esta infección. Este proyecto tiene como objetivo estudiar la interacción VESL-macrófago para esclarecer el rol del fenotipo celular y su relación con la depuración viral. Además, analizar la naturaleza y el tenor de los inmunomoduladores liberados y el papel de la apoptosis de los macrófagos en esta infección
Prevalence of pathogenetic MC4R mutations in Italian children with early onset obesity, tall stature and familial history of obesity.
BackgroundMelanocortin-4-receptor (MC4R) mutations represent the most frequent genetic cause of non-syndromic early onset obesity. Children carrying MC4R mutations seem to show a particular phenotype characterized by early onset, severe obesity and high stature. To verify whether MC4R mutations are associated with this particular phenotype in the Italian pediatric population, we decided to screen the MC4R gene in a group of obese children selected on the basis of their phenotype.MethodsTo perform this study, a multicentric approach was designed. Particularly, to be enrolled in the study subjects needed to meet the following criteria: Body mass index ≥ 3 deviation scores according to age and sex, familiar history of obesity (at least one parent obese), obesity onset before the 10 years old, height ≥ 2 deviation scores. The coding region of MC4R gene was screened in 240 obese children (mean age 8.3 ± 3.1, mean BMI 30.8 ± 5.4) and in 200 controls (mean age 8.1 ± 2.8; mean BMI 14.2 ± 2.5).ResultsThree mutations have been found in five obese children. The S127L (C380T), found in three unrelated children, had been described and functionally characterized previously. The Q307X (C919T) and the Y332H (T994C) mutations were found in two patients. Functional studies showed that only Q307X impaired protein function.ConclusionThe low prevalence of MC4R mutations (1.6%) in this group of obese children selected according to the obesity degree, the tall stature and the family history of obesity was similar to the prevalence observed in previous screenings performed in obese adults and in not phenotypically selected obese children
Infección de macrófagos con virus encefalitis saint louis: efecto sobre el fenotipo celular y la apoptosis (Programa: enfermedades transmisibles y emergentes)
El Virus Encefalitis Saint Louis (VESL)es un virus neurotrópico que puede provocar en humanos encefalitis, meningitis y cefalea febril. Estudios epidemiológicos demostraron la circulación del virus en Argentina, reportándose el primer brote de encefalitis en Sud-América en Córdoba en el 2005. Los macrófagos tienen un rol muy importante en la patogénesis de las infecciones virales. Estas células son permisivas para la replicación y reservorio viral. Reconocen a los virus mediante receptores de reconocimiento de patrones, incluidos los receptores Toll-like, lo que genera la producción de moléculas antivirales y citoquinas pro-inflamatorias. Los macrófagos expresan diferentes fenotipos según el microambiente tisular y el estímulo externo. Se reconocen los macrófagos activados clásicamente (M1) que liberan citoquinas pro-inflamatorias y los macrófagos activados alternativamente (M2) que producen IL-10 y factor transformante del crecimiento. Como parte de la respuesta del macrófago a la infección viral, prolifera, se diferencia y muere. La apoptosis es un mecanismo de muerte que limita la actividad del macrófago activado. La interacción virus-macrófago ha sido analizada con numerosos tipos de virus. Sin embargo, existe escasa información sobre el impacto de VESL sobre la respuesta inmune innata. La emergencia de esta virosis en nuestro medio amerita abordar distintos aspectos de la respuesta inmune en esta infección. Este proyecto tiene como objetivo estudiar la interacción VESL-macrófago para esclarecer el rol del fenotipo celular y su relación con la depuración viral. Además, analizar la naturaleza y el tenor de los inmunomoduladores liberados y el papel de la apoptosis de los macrófagos en esta infección.Fil: Caula, Cinthya. Universidad Católica de Córdoba. Facultad de Ciencias Químicas; ArgentinaFil: Cooke, Paula María. Universidad Católica de Córdoba. Facultad de Ciencias Químicas; ArgentinaFil: Orsilles, Miguel Ángel. Universidad Católica de Córdoba. Facultad de Ciencias Químicas; Argentin
An unexpected, mild phenotype of glucocorticoid resistance associated with glucocorticoid receptor gene mutation case report and review of the literature
BACKGROUND: Glucocorticoid resistance is a rare, sporadic or familial condition caused by mutation of the gene encoding the glucocorticoid receptor (GR). Clinically it is characterized by symptoms developed due to local, tissue-specific, or generalized partial insensitivity to glucocorticoids. CASE PRESENTATION: A 31-year-old woman was evaluated because of infertility at the Endocrine Unit of the 2nd Department of Medicine, Semmelweis University. During her laboratory investigations, elevated serum and salivary cortisol were observed which failed to be suppressed after administration of 1 mg dexamethasone. 24 h urinary cortisol was increased, but a normal midnight serum cortisol was detected suggesting a maintained circadian rhythm. Plasma dehydroepiandrosterone-sulfate and androstendione levels were also elevated. Repeated plasma ACTH measurements indicated slightly elevated or normal values. Bone mineral density was normal. All laboratory results confirmed the diagnosis of glucocorticoid resistance. Genetic counseling followed by Sanger sequencing of the coding region of the gene encoding human glucocorticoid receptor was performed and a missense mutation (Arg714Gln, R714Q) in a heterozygous form was detected. Following family screening, the same mutation was found in her clinically-healthy 35-year-old sister who had no fertility problems.This variant was not detected in more than 60 patients and controls tested either for glucocorticoid resistance or Cushing's syndrome in our Laboratory and it was absent in Exome Variant Server, HumanGene Mutation Database and ExAC databases. CONCLUSIONS: Our case fulfils the diagnostic criteria of glucocorticoid resistance, also named Chrousos syndrome. The glucocorticoid receptor gene mutation detected in our patient has been already reported in a 2-year-old child with hypoglycaemia, hypokalaemia, hypertension and premature puberty. These distinct phenotypes may suggest that other factors may modify the functional consequences of the R714Q variant of GR
Psychological treatments and psychotherapies in the neurorehabilitation of pain. Evidences and recommendations from the italian consensus conference on pain in neurorehabilitation
BACKGROUND:
It is increasingly recognized that treating pain is crucial for effective care within neurological rehabilitation in the setting of the neurological rehabilitation. The Italian Consensus Conference on Pain in Neurorehabilitation was constituted with the purpose identifying best practices for us in this context. Along with drug therapies and physical interventions, psychological treatments have been proven to be some of the most valuable tools that can be used within a multidisciplinary approach for fostering a reduction in pain intensity. However, there is a need to elucidate what forms of psychotherapy could be effectively matched with the specific pathologies that are typically addressed by neurorehabilitation teams.
OBJECTIVES:
To extensively assess the available evidence which supports the use of psychological therapies for pain reduction in neurological diseases.
METHODS:
A systematic review of the studies evaluating the effect of psychotherapies on pain intensity in neurological disorders was performed through an electronic search using PUBMED, EMBASE, and the Cochrane Database of Systematic Reviews. Based on the level of evidence of the included studies, recommendations were outlined separately for the different conditions.
RESULTS:
The literature search yielded 2352 results and the final database included 400 articles. The overall strength of the recommendations was medium/low. The different forms of psychological interventions, including Cognitive-Behavioral Therapy, cognitive or behavioral techniques, Mindfulness, hypnosis, Acceptance and Commitment Therapy (ACT), Brief Interpersonal Therapy, virtual reality interventions, various forms of biofeedback and mirror therapy were found to be effective for pain reduction in pathologies such as musculoskeletal pain, fibromyalgia, Complex Regional Pain Syndrome, Central Post-Stroke pain, Phantom Limb Pain, pain secondary to Spinal Cord Injury, multiple sclerosis and other debilitating syndromes, diabetic neuropathy, Medically Unexplained Symptoms, migraine and headache.
CONCLUSIONS:
Psychological interventions and psychotherapies are safe and effective treatments that can be used within an integrated approach for patients undergoing neurological rehabilitation for pain. The different interventions can be specifically selected depending on the disease being treated. A table of evidence and recommendations from the Italian Consensus Conference on Pain in Neurorehabilitation is also provided in the final part of the pape
Patients with usual vulvar intraepithelial neoplasia-related vulvar cancer have an increased risk of cervical abnormalities
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81890.pdf (publisher's version ) (Closed access)BACKGROUND: Vulvar squamous cell carcinoma (SCC) originates the following two pathways, related to differentiated (d) vulvar intraepithelial neoplasia (VIN) or to human papillomavirus (HPV)-related usual (u) VIN. Multicentric HPV infections (cervix, vagina and vulva) are common. We hypothesise that patients with a uVIN-related vulvar SCC more often have cervical high-grade squamous intraepithelial lesions (HSILs) compared with women with dVIN-related vulvar SCC. METHODS: All vulvar SCCs (201) were classified to be dVIN- (n=164) or uVIN related (n=37). Data with regard to the smear history and cervical histology were retrieved from PALGA, the nationwide Netherlands database of histo- and cytopathology. For HSIL cervical smears of which histology was taken, HPV DNA analysis on both the vulvar and cervical specimens was performed. RESULTS: At least one smear was available in 145 (72%) of the 201 patients. Patients with a uVIN-related vulvar SCC more often had an HSIL compared with patients with a dVIN-related SCC (35 vs 2%, P<0.001). A total of 10 of the 13 HSILs were histologically assessed and identical HPV types were found in the vulva and cervix. CONCLUSION: These data emphasise the necessity to differentiate between dVIN- and uVIN-related vulvar tumours and to examine the entire lower female ano-genital tract once an uVIN-related lesion is found
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