78 resultados para Premature Rupture


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Thrombotic events are being increasingly recognized during the neonatal period. An infant girl was born at 29 weeks' gestation after a pregnancy complicated by twin-to-twin transfusion syndrome. After an initial uncomplicated clinical course, her oxygen requirement increased, which was interpreted as an early sign of bronchopulmonary dysplasia. At 3 weeks of age, she suddenly collapsed and died of severe pulmonary hypertension. At autopsy, multiple pulmonary artery emboli and several older renal vein thromboses were found. Results of genetic analyses of the infant and her family were negative for thrombophilia. Although embolism represents a frequent emergency in adults, fatal pulmonary embolism has never, to our knowledge, been described for premature infants. This case suggests that thrombotic events are underdiagnosed and that additional studies are needed to define infants at risk and optimal treatment strategies.

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In recent years, enamel matrix derivative (EMD) has garnered much interest in the dental field for its apparent bioactivity that stimulates regeneration of periodontal tissues including periodontal ligament, cementum and alveolar bone. Despite its widespread use, the underlying cellular mechanisms remain unclear and an understanding of its biological interactions could identify new strategies for tissue engineering. Previous in vitro research has demonstrated that EMD promotes premature osteoblast clustering at early time points. The aim of the present study was to evaluate the influence of cell clustering on vital osteoblast cell-cell communication and adhesion molecules, connexin 43 (cx43) and N-cadherin (N-cad) as assessed by immunofluorescence imaging, real-time PCR and Western blot analysis. In addition, differentiation markers of osteoblasts were quantified using alkaline phosphatase, osteocalcin and von Kossa staining. EMD significantly increased the expression of connexin 43 and N-cadherin at early time points ranging from 2 to 5 days. Protein expression was localized to cell membranes when compared to control groups. Alkaline phosphatase activity was also significantly increased on EMD-coated samples at 3, 5 and 7 days post seeding. Interestingly, higher activity was localized to cell cluster regions. There was a 3 fold increase in osteocalcin and bone sialoprotein mRNA levels for osteoblasts cultured on EMD-coated culture dishes. Moreover, EMD significantly increased extracellular mineral deposition in cell clusters as assessed through von Kossa staining at 5, 7, 10 and 14 days post seeding. We conclude that EMD up-regulates the expression of vital osteoblast cell-cell communication and adhesion molecules, which enhances the differentiation and mineralization activity of osteoblasts. These findings provide further support for the clinical evidence that EMD increases the speed and quality of new bone formation in vivo.

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Neonatal sepsis causes high mortality and morbidity in preterm infants, but less is known regarding the long-term outcome after sepsis. This study aimed to determine the impact of sepsis on neurodevelopment at 2 years' corrected age in extremely preterm infants.

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A steady rise in mortality from abdominal aortic aneurysm (AAA) was reported in the 1980s and 1990 s, although this is now declining rapidly. Reasons for the recent decline in mortality from AAA rupture are investigated here.

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Twenty-five years have passed since the first randomised controlled trial began its recruitment for screening for abdominal aortic aneurysm (AAA) in men aged 65 and above. Since this and other randomised trials, all launched in the late 80s and 90s of the last century, the epidemiologic profile of abdominal aortic aneurysm may have changed. The trials reported an AAA prevalence in the range of 4-7% for men aged 65 years or more. AAA-related mortality was significantly improved by screening, and after 13 years, the largest trial showed a benefit for all-cause mortality. Screening also was shown to be cost-effective. Today, there are studies showing a substantial decrease of AAA prevalence to sometimes less than 2% in men aged ≥ 65 years and there is evidence that the incidence of ruptured aneurysm and mortality from AAA is also declining. This decline preceded the implementation of screening programmes but may be due to a change in risk factor management. The prevalence of smoking has decreased and there has been improvement in the control of hypertension and a rising use of statins for cardiovascular risk prevention. Additionally, there is a shift of the burden to the older age group of ≥ 75 years. Such radical changes may influence screening policy and it is worth reflecting on the optimum age of screening - it might be better to screen at ages >65 years - or rescreening 5 to 10 years after the first screen.