Prevalência de lesões por fricção em pacientes hospitalizados com câncer

Esse estudo objetivou identificar a prevalência de lesões por fricção (LF) em pacientes hospitalizados com câncer e avaliar os fatores demográficos e clínicos associados ao seu desenvolvimento. Estudo epidemiológico, de corte transversal, realizado no Instituto do Câncer do Estado de São Paulo Octavio Frias de Oliveira. Todos os pacientes adultos, internados entre 10 e 18 de abril de 2010, foram avaliados por meio de entrevista e exame físico. Utilizou-se o teste Qui-Quadrado para comparação das variáveis demográficas e clínicas entre pacientes com e sem LF. Foram avaliados 157 pacientes: cinco apresentaram nove LF, acarretando prevalência de 3,3%. Quanto às variáveis demográficas, houve diferença estatisticamente significativa somente para o número de filhos (p=0,027). Clinicamente, pacientes com LF apresentaram menores escores na escala de Karnofsky (p=0,031) e na Escala de Braden (p=0,026), além de comportamento pouco colaborativo (p=0,042). Esse estudo contribui para um melhor conhecimento acerca das LF em pacientes com câncer.

TCR-induced NF-kappaB activation: a crucial role for Carma1, Bcl10 and MALT1.

T-cell receptor (TCR) engagement induces the maturation of thymocytes and the activation and proliferation of peripheral T cells through signaling pathways that target several transcription factors. The transcription factor nuclear factor-κB (NF-κB) has an essential role in the activation of mature T cells but the signaling pathway leading from TCR stimulation to NF-κB activation is not well defined. Carma1, Bcl10 and MALT1 are recently identified proteins that have an important and previously unexpected role in antigen receptor-induced NF-κB activation and the control of lymphocyte proliferation. We believe that the recent advances in this field could stimulate research for the development of new immunomodulatory drugs and could lead to a better understanding of the molecular mechanisms underlying the formation of lymphomas and potentially of other immune disorders.

Estradiol and progesterone strongly inhibit the innate immune response of mononuclear cells in newborns.

Newborns are particularly susceptible to bacterial infections due to qualitative and quantitative deficiencies of the neonatal innate immune system. However, the mechanisms underlying these deficiencies are poorly understood. Given that fetuses are exposed to high concentrations of estradiol and progesterone during gestation and at time of delivery, we analyzed the effects of these hormones on the response of neonatal innate immune cells to endotoxin, bacterial lipopeptide, and Escherichia coli and group B Streptococcus, the two most common causes of early-onset neonatal sepsis. Here we show that at concentrations present in umbilical cord blood, estradiol and progesterone are as powerful as hydrocortisone for inhibition of cytokine production by cord blood mononuclear cells (CBMCs) and newborn monocytes. Interestingly, CBMCs and newborn monocytes are more sensitive to the effects of estradiol and progesterone than adult peripheral blood mononuclear cells and monocytes. This increased sensitivity is associated with higher expression levels of estrogen and membrane progesterone receptors but is independent of a downregulation of Toll-like receptor 2 (TLR2), TLR4, and myeloid differentiation primary response gene 88 in newborn cells. Estradiol and progesterone mediate their anti-inflammatory activity through inhibition of the NF-κB pathway but not the mitogen-activated protein kinase pathway in CBMCs. Altogether, these results suggest that elevated umbilical cord blood concentrations of estradiol and progesterone acting on mononuclear cells expressing high levels of steroid receptors contribute to impair innate immune responses in newborns. Therefore, intrauterine exposure to estradiol and progesterone may participate in increasing susceptibility to infection during the neonatal period.

Intraclass reliability of the Alberta Infant Motor Scale in the Brazilian version

This study had as its objective to analyze the intraclass reliability of the Alberta Infant Motor Scale (AIMS), in the Brazilian version, in preterm and term infants. It was a methodological study, conducted from November 2009 to April 2010, with 50 children receiving care in two public institutions in Fortaleza, Ceará, Brazil. Children were grouped according to gestational age as preterm and term, and evaluated by three evaluators in the communication laboratory of a public institution or at home. The intraclass correlation indices for the categories prone, supine, sitting and standing ranged from 0.553 to 0.952; most remained above 0.800, except for the standing category of the third evaluator, in which the index was 0.553. As for the total score and percentile, rates ranged from 0.843 to 0.954. The scale proved to be a reliable instrument for assessing gross motor performance of Brazilian children, particularly in Ceará, regardless of gestational age at birth.

Rouva Anna-Liisa Vaurola 18/9 1973

Kirje 18.9.1973

Administration of Il-18bp by Gene Therapy Reduces Inflammation and Prevents Joint Destruction by Downregulation of Mmp9 In Rat Aia: Role ff Mmp9 In Bone and Joint Destruction in Arthritis

Background and objectives Interleukin 18 (IL-18) is a pleiotropic cytokine involved in rheumatoid arthritis (RA) pathogenesis. This study was carried out to evaluate the effi cacy of IL-18 binding protein (IL-18BP) gene therapy in the rat adjuvant- induced arthritis (AIA) model and to decipher the mechanisms by which IL-18BP delivery lessens bone destruction.Materials and methods Arthritis was induced in female Lewis rat by Mycobacterium butyricum and the mRNA expression of IL-18 and IL-18BP was determined in the joints. In a preventive study, rats were divided into an adenovirus producing IL-18BP-Fc (AdmIL-18BP-Fc) group (n=8) and an adenovirus producing green fl uorescent protein (AdGFP) group (n=7). On day 8 after AIA induction, adenoviruses were injected. Clinical parameters were assessed. At day 18, during maximal arthritis, the rats were euthanized, ankles were collected and x-rays were performed. mRNA and protein were extracted from joints for analysis by quantitative reverse transcriptase-PCR, multiplex, Western blot and zymography.Results The authors observed a decrease in the (IL-18BP/ IL-18) ratio from day 7 to 45. Administration of AdmIL-18BPd-Fc decreased clinical parameters and prevented bone and joint destruction compared to AdGFP administration. IL-18BP delivery reduced the (receptor activator of nuclear factor κB ligand (RANKL)/osteoprotegerin (OPG)) ratio by 70%, the matrix metalloproteinase 9 (MMP9) level by 33% and the tartrate-resistant acid phosphatase (TRAP) level by 44% in the joint homogenates from AdmIL-18BPd-Fc compared to AdGFP treated rats.Conclusions In rat AIA, a decrease in the (IL-18BP/IL-18) ratio was observed. IL-18BP delivery prevented joint and bone destruction by downregulating MMP9, (RANKL/OPG) and TRAP, suggesting a potential benefi t of a similar therapy in RA.Abstract topics Towards novel therapeutic strategies.

Taloudellisen hyvinvoinnin lisääminen säästäväisen elämäntavan avulla

Puhe maalaisliiton valtakunnallisessa kekrijuhlassa Ylihärmässä 1.11.1953

Bulgarian kansantasavallan Kansalliskokouksen Puhemiehistön Puheenjohtajan Georgi Traikovin virallinen vierailu Suomeen 6.-11.6.1968 (Tasavallan Presidentin päivällispuhe Bulgarian presidentti Georgi Traikovin kunniaksi 6.6.1968)

Puhe

A Internacionalização de Empresas Portuguesas para Cabo Verde investimento directo e as estratégias competitivas

A presente investigação procura estudar a internacionalização das empresas portuguesas para Cabo Verde, através de investimento directo, e as estratégias competitivas que elas adoptaram. Na sequência da revisão da literatura, a fim de obter respostas para a pergunta de pesquisa, analisamos a internacionalização das empresas portuguesas, a sua evolução, o investimento português no estrangeiro, e a evolução dos fluxos do Investimento Directo Estrangeiro (IDE) em Cabo Verde, a partir de dados estatísticos recolhidos na literatura publicada. De seguida foram recolhidos dados primários, através da aplicação de dois questionários direccionados para o mercado cabo-verdiano (clientes) e empresas portuguesas que investiram em Cabo Verde. A amostra é constituída por 157 clientes, 77 do sexo feminino e 80 do sexo masculino, e a outra amostra é constituída por 10 empresas portuguesas que investiram em Cabo Verde através de Investimento Directo.

Myostatin augments muscle-specific ring finger protein-1 expression through an NF-kB independent mechanism in SMAD3 null muscle.

Smad (Sma and Mad-related protein) 2/3 are downstream signaling molecules for TGF-β and myostatin (Mstn). Recently, Mstn was shown to induce reactive oxygen species (ROS) in skeletal muscle via canonical Smad3, nuclear factor-κB, and TNF-α pathway. However, mice lacking Smad3 display skeletal muscle atrophy due to increased Mstn levels. Hence, our aims were first to investigate whether Mstn induced muscle atrophy in Smad3(-/-) mice by increasing ROS and second to delineate Smad3-independent signaling mechanism for Mstn-induced ROS. Herein we show that Smad3(-/-) mice have increased ROS levels in skeletal muscle, and inactivation of Mstn in these mice partially ablates the oxidative stress. Furthermore, ROS induction by Mstn in Smad3(-/-) muscle was not via nuclear factor-κB (p65) signaling but due to activated p38, ERK MAPK signaling and enhanced IL-6 levels. Consequently, TNF-α, nicotinamide adenine dinucleotide phosphate oxidase, and xanthine oxidase levels were up-regulated, which led to an increase in ROS production in Smad3(-/-) skeletal muscle. The exaggerated ROS in the Smad3(-/-) muscle potentiated binding of C/EBP homology protein transcription factor to MuRF1 promoter, resulting in enhanced MuRF1 levels leading to muscle atrophy.

Adenosine A2B receptor-mediated leukemia inhibitory factor release from astrocytes protects cortical neurons against excitotoxicity.

ABSTRACT: BACKGROUND: Neuroprotective and neurotrophic properties of leukemia inhibitory factor (LIF) have been widely reported. In the central nervous system (CNS), astrocytes are the major source for LIF, expression of which is enhanced following disturbances leading to neuronal damage. How astrocytic LIF expression is regulated, however, has remained an unanswered question. Since neuronal stress is associated with production of extracellular adenosine, we investigated whether LIF expression in astrocytes was mediated through adenosine receptor signaling. METHODS: Mouse cortical neuronal and astrocyte cultures from wild-type and adenosine A2B receptor knock-out animals, as well as adenosine receptor agonists/antagonists and various enzymatic inhibitors, were used to study LIF expression and release in astrocytes. When needed, a one-way analysis of variance (ANOVA) followed by Bonferroni post-hoc test was used for statistical analysis. RESULTS: We show here that glutamate-stressed cortical neurons induce LIF expression through activation of adenosine A2B receptor subtype in cultured astrocytes and require signaling of protein kinase C (PKC), mitogen-activated protein kinases (MAPKs: p38 and ERK1/2), and the nuclear transcription factor (NF)-κB. Moreover, LIF concentration in the supernatant in response to 5'-N-ethylcarboxamide (NECA) stimulation was directly correlated to de novo protein synthesis, suggesting that LIF release did not occur through a regulated release pathway. Immunocytochemistry experiments show that LIF-containing vesicles co-localize with clathrin and Rab11, but not with pHogrin, Chromogranin (Cg)A and CgB, suggesting that LIF might be secreted through recycling endosomes. We further show that pre-treatment with supernatants from NECA-treated astrocytes increased survival of cultured cortical neurons against glutamate, which was absent when the supernatants were pre-treated with an anti-LIF neutralizing antibody. CONCLUSIONS: Adenosine from glutamate-stressed neurons induces rapid LIF release in astrocytes. This rapid release of LIF promotes the survival of cortical neurons against excitotoxicity.

Um Sistema de Gestão Portuária baseada na Tecnologia Workflow

A crescente complexidade da gestão portuária, a rápida evolução dos meios tecnológicos aliada à enorme demanda que os sistemas de informação têm no seio das organizações como ferramenta de suporte á execução de diferentes processos, faz com que haja uma enorme pressão na procura de novas soluções para um problema colocado já inúmeras vezes: como conceber sistemas, que desenvolvidas e disponibilizadas no mais curto espaço de tempo, sejam impulsionadores de mudanças efectivas nos processos de negócio. No contexto de uma empresa de gestão portuária em que tipicamente há diferentes entidades implicadas nos processos de negócio conceber tais sistemas é um enorme desafio. Neste trabalho pretendemos seguir uma nova abordagem para um Sistema de Gestão Portuária utilizando Tecnologias que permitem implementar a automatização de processos – Sistemas de Gestão de Workflow.