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OBJECTIVE: Synovial fluid (SF) plays an important role in the maintenance of articular cartilage. SF is a dynamic reservoir of proteins derived from cartilage and synovial tissue; thus, its composition may serve as a biomarker that reflects the health and pathophysiological condition of the joint. The purpose of the current study was to evaluate the osteoarthritic synovial fluid (OASF) and transforming growth factor-ß1 (TGF-ß1) activity in articular chondrocytes catabolic and inflammatory responses. DESIGN: Chondrocytes were seeded at passage 2 and cultured for 72 hours under different conditions. Human chondrocytes were subjected to OASF while rat chondrocytes were subjected to either healthy synovial fluid (rSF) or TGF-ß1 and then assigned for cell viability analysis. In addition, the effects of OASF and TGF-ß1 on chondrocytes metalloprotease (MMP)-3 and MMP-13 and interleukin-18 (IL-18) expression were evaluated by immunocytochemistry, ELISA, and reverse transcriptase-polymerase chain reaction. RESULTS: SF from osteoarthritic patients significantly induced MMP-3, MMP-13, and IL-18 receptor expression in chondrocytes. To put in evidence the inflammatory activity of OASF, healthy chondrocytes from rat were cultured with TGF-ß1. In the presence of TGF-ß1 these cells started to express MMP-3, MMP-13, and IL-18 genes and attached to each other forming a chondrocyte aggregated structure. Healthy SF was able to maintain a typical monolayer of rounded chondrocytes with no inflammatory response. CONCLUSION: In summary, these observations demonstrated that TGF-ß1, one of the components of OASF, has a dual effect, acting in chondrocyte maintenance and also inducing inflammatory and catabolic properties of these cells.

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Connective-tissue growth factor (CTGF/CCN2) is a matricellular-secreted protein involved in complex processes such as wound healing, angiogenesis, fibrosis and metastasis, in the regulation of cell proliferation, migration and extracellular matrix remodeling. Glioblastoma (GBM) is the major malignant primary brain tumor and its adaptation to the central nervous system microenvironment requires the production and remodeling of the extracellular matrix. Previously, we published an in vitro approach to test if neurons can influence the expression of the GBM extracellular matrix. We demonstrated that neurons remodeled glioma cell laminin. The present study shows that neurons are also able to modulate CTGF expression in GBM. CTGF immnoreactivity and mRNA levels in GBM cells are dramatically decreased when these cells are co-cultured with neonatal neurons. As proof of particular neuron effects, neonatal neurons co-cultured onto GBM cells also inhibit the reporter luciferase activity under control of the CTGF promoter, suggesting inhibition at the transcription level. This inhibition seems to be contact-mediated, since conditioned media from embryonic or neonatal neurons do not affect CTGF expression in GBM cells. Furthermore, the inhibition of CTGF expression in GBM/neuronal co-cultures seems to affect the two main signaling pathways related to CTGF. We observed inhibition of TGFß luciferase reporter assay; however phopho-SMAD2 levels did not change in these co-cultures. In addition levels of phospho-p44/42 MAPK were decreased in co-cultured GBM cells. Finally, in transwell migration assay, CTGF siRNA transfected GBM cells or GBM cells co-cultured with neurons showed a decrease in the migration rate compared to controls. Previous data regarding laminin and these results demonstrating that CTGF is down-regulated in GBM cells co-cultured with neonatal neurons points out an interesting view in the understanding of the tumor and cerebral microenvironment interactions and could open up new strategies as well as suggest a new target in GBM control.

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O objetivo deste estudo foi descrever a ocorrência de flebite, infiltração e extravasamento em recém-nascidos internados na unidade de terapia intensiva neonatal de uma maternidade pública do Rio de Janeiro. Trata-se de um estudo quantitativo descritivo com 36 recém-nascidos em uso de terapia intravenosa e com indicação de remoção do dispositivo intravenoso periférico. Foram avaliados 50 sítios de punção imediatamente após a remoção de cateteres periféricos originando uma média de 1,40 punções venosas por neonato. As complicações foram responsáveis por 48% da remoção dos cateteres, antes da alta do tratamento, com predomínio de infiltração (79,2%), seguida por flebite (16,7%) e extravasamento (4,2%). A fim de se evitar os agravos e promover a segurança dos recém-nascidos submetidos à terapia intravenosa, a equipe de enfermagem deve avaliar periodicamente o acesso venoso periférico e obter conhecimento acerca das intervenções necessárias quando detectados sinais de complicações.

This study aimed to describe phlebitis, infiltration and extravasation events in newborn infants hospitalized at the neonatal intensive care unit of a public maternity in Rio de Janeiro, Brazil. A quantitative and descriptive study was carried out, involving 36 newborns under intravenous therapy and indicated for the removal of the peripheral intravenous device. Fifty puncture sites were assessed immediately after the peripheral catheter removal, resulting in an average 1.40 punctures per infant. Complications were responsible for 48% of catheter removals before discharge from treatment, predominantly infiltration (79.2%), followed by phlebitis (16.7%) and extravasation (4.2%). To avoid aggravations and enhance the security of newborns submitted to intravenous therapy, the nursing team should periodically assess the peripheral venous access and gain knowledge on interventions needed when signs of complications are detected.

El objetivo de este estudio fue describir la ocurrencia de flebitis, infiltración y extravasamiento en recién nacidos internados en la unidad de terapia intensiva neonatal de una maternidad pública de Rio de Janeiro. Se trata de un estudio cuantitativo descriptivo con 36 recién nacidos en uso de terapia intravenosa y con indicación de remoción del dispositivo intravenoso periférico. Fueron evaluados 50 sitios de punción inmediatamente después de la remoción de catéteres periféricos originando una media de 1,40 punciones venosas por neonato. Las complicaciones fueron responsables por 48% de las remociones de los catéteres, antes del alta del tratamiento, con predominio de infiltraciones (79,2%), seguida por flebitis (16,7%) e extravasamiento (4,2%). Con el fin de evitar los lesiones y promover la seguridad de los recién nacidos sometidos a terapia intravenosa, el equipo de enfermería debe evaluar periódicamente el acceso venoso periférico y obtener conocimiento acerca de las intervenciones necesarias cuando detectadas señales de complicaciones.

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A implementação da terapia intravenosa no recém-nascido é complexa e desafiadora. Objetivou-se identificar as veias periféricas de escolha, para a punção venosa, no recém-nascido e descrever os critérios adotados pela equipe de enfermagem na escolha desses vasos. O cenário foi uma Unidade de Terapia Intensiva Neonatal do Rio de Janeiro, Brasil. Foram entrevistados dez profissionais de enfermagem de maio a junho de 2007. A análise temática originou as categorias: “Escolha da veia periférica em RN: prioridades da equipe de enfermagem” e “Critérios adotados e dificuldades enfrentadas na escolha das veias para punção venosa periférica”. As veias do arco dorsal da mão foram as de primeira escolha e as epicranianas as de última escolha. Os critérios de escolha foram visualização, facilidade, durabilidade e fármaco infundido. As dificuldades enfrentadas para a realização terapia intravenosa no recém-nascido foram o desgaste da rede venosa e a dor advinda das múltiplas punções.

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Thyroid hormones (THs) are essential for brain development, where they regulate gliogenesis, myelination, cell proliferation and protein synthesis. Hypothyroidism severely affects neuronal growth and establishment of synaptic connections. Triiodothyronine (T3), the biologically active form of TH, has a central function in these activities. So, Myosin-Va (Myo-Va), a molecular motor protein involved in vesicle and RNA transport, is a good candidate as a target for T3 regulation. Here, we analyzed Myo-Va expression in euthyroid and hypothyroid adult rat brains and synaptosomes. We observed a reduction of Myo-Va expression in cultured neural cells from newborn hypothyroid rat brain, while immunocytochemical experiments showed a punctate distribution of this protein in the cytoplasm of cells. Particularly, Myo-Va co-localized with microtubules in neurites, especially in their varicosities. Myo-Va immunostaining was stronger in astrocytes and neurons of controls when compared with hypothyroid brains. In addition, supplementation of astrocyte cultures with T3 led to increased expression of Myo-Va in cells from both euthyroid and hypothyroid animals, suggesting that T3 modulates Myo-Va expression in neural cells both in vivo and in vitro. We have further analyzed Myo-Va expression in U373 cells, a human glioblastoma line, and found the same punctate cytoplasmic protein localization. As in normal neural cells, this expression was also increased by T3, suggesting that the modulatory mechanism exerted by T3 over Myo-Va remains active on astrocyte tumor cells. These data, coupled with the observation that Myo-Va is severely affected in hypothyroidism, support the hypothesis that T3 activity regulates neural motor protein expression, taking Myo-Va as a model. As a consequence, reduced T3 activity could supposedly affect axonal transport and synaptic function, and could therefore explain disturbances seen in the hypothyroid brain.

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