Methods for prenatal assessment of fetal cardiac function

Fetal cardiac function is increasingly recognized as a marker of disease severity and prognosis in selected fetal conditions. Magnetic resonance imaging (MRI) has been used in experimental (animal) fetal cardiology but the lack of a noninvasive fetal electrocardiogram (ECG) to trigger image acquisition remains a major limiting factor precluding its application in humans. Fetal medicine specialists are therefore limited to ultrasound to evaluate human fetal cardiac function. In this review, we aim to provide a complete overview of the different ultrasound techniques that can be used for fetal cardiac function assessment and we discuss their (theoretical) strengths and shortcomings. Conventional methods include M-mode assessment of ventricular contractility and Doppler assessment of the precordial veins and cardiac output (CO). More recent techniques such as the measurement of the myocardial performance index (MPI), myocardial motion analysis with tissue Doppler, speckle tracking and three-dimensional (3D) ultrasound techniques are also discussed. Copyright © 2009 John Wiley & Sons, Ltd.     

Fetal therapy: practical ethical considerations

Progress in prenatal diagnosis can lead to the diagnosis of severe fetal abnormalities for which natural history anticipates a fatal outcome or the development of severe disability despite optimal postnatal care. Intrauterine therapy can be offered in these selected cases. Prenatal diagnosis is the only field of medicine in which termination is an option in the management of severe diseases. Fetal therapy has therefore developed as an alternative to fatalist expectant prenatal management as well as to termination of pregnancy (TOP). There are few standards of fetal care that have gone beyond the stage of equipoise and even fewer have been established based on appropriate studies comparing pre- and postnatal care. Several ethical questions are being raised as fetal surgery develops, including basic Hippocratic principles of patients' autonomy and doctors' duty of competence moving the boundaries between experimental surgery, therapeutic innovation and standard care. In addition, the technical success of a fetal intervention can only rarely fully predict the postnatal outcome. Managing uncertainty regarding long-term morbidity and the possibility for fetal therapy to change the risk of perinatal death into that of severe handicap remains a critical factor affecting women's choice for TOP as an alternative to fetal therapy. Copyright © 2011 John Wiley & Sons, Ltd.     

The nuchal translucency and the fetal heart: a literature review

In this overview the current knowledge of the relationship between an increased nuchal translucency (NT) measurement and fetal heart structure and function in chromosomally normal fetuses is reviewed. Relevant pathophysiological theories behind the increased NT are discussed. Fetuses with an increased NT have an increased risk for congenital heart disease (CHD) with no particular bias for one form of CHD over another. This risk increases with increasing NT measurement. Although the NT measurement is only a modestly effective screening tool for all CHD when used alone, it may indeed be effective in identifying specific CHD “likely to benefit” from prenatal diagnosis. The combination of an increased NT, tricuspid regurgitation and an abnormal ductus venosus (DV) Doppler flow profile, is a strong marker for CHD. A fetal echocardiogram should be performed at 20 weeks' gestation in fetuses with an NT ≥ 95th percentile but < 99th percentile. When the NT measurement is ≥ 99th percentile, or when tricuspid regurgitation and/or an abnormal DV flow pattern is found along with the increased NT, an earlier echocardiogram is indicated, followed by a repeat scan at around 20 weeks' gestation. The resultant increased demand for early fetal echocardiography and sonographers with this special expertise needs to be planned and provided for. Copyright © 2009 John Wiley & Sons, Ltd.     

Oxidative stress-mediated cardiac mast cell degranulation

Pulmonary mast cell degranulation is a well-characterized response to diesel exhaust exposure. A primary constituent of fossil fuel combustion is sulfur dioxide (SO₂). SO₂ was shown to induce mast cell degranulation in an immortalized cell line secondary to induction of intracellular oxidative stress; however, it is not known whether SO₂-induced oxidative stress directly triggers the activation of cardiac mast cells. Accordingly, this study sought to determine whether Na₂SO₃ induces degranulation of cardiac mast cells, and furthermore whether cardiac mast cell activation may be prevented by inhibition of oxidative stress. To this end, cardiac mast cells were isolated from epicardial surface of the heart and incubated with increasing concentrations of Na₂SO₃ (0, 0.5, or 5 mM). Antioxidant compounds targeting different mechanisms of free radical generation, including ebselen, diphenyleneiodonium (DPI), or α-tocopherol, were incubated with 5 mM of Na₂SO₃ in order to determine their efficacy in preventing mast cell degranulation. Na₂SO₃ induced a significant concentration-dependent histamine release from cardiac mast cells ranging from 8.87% to 18.86%, which was prevented by ebselen. No effect was observed with DPI and α-tocopherol under these conditions. In conclusion, these findings indicate that SO₂ is capable of producing cardiac mast cell degranulation in vitro; however, the variable effectiveness of the three antioxidants evaluated is indicative of a multifactorial mechanism mediating SO₂-induced cardiac mast cell degranulation. The particular effectiveness of ebselen in preventing mast cell degranulation may be related to its multiple mechanisms of preventing oxidative stress.     

Mutagenic and carcinogenic effects of cadmium†

There is limited evidence to suggest that certain compounds of cadmium may be mildly mutagenic. Some compounds of cadmium have given rise to fibrosarcoma and rhabdomyosarcoma following subcutaneous or intramuscular injection in the rat and also to interstitial cell tumours of the testis as a sequel to cellular damage and testicular atrophy. Cadmium chloride aerosol inhalation has induced a high incidence of dose‐related lung cancer in the rat. Epidemiological observations suggest that mortality from prostatic and possibly from lung cancer has been increased in cadmium workers who had experienced the very high levels of cadmium, mainly as oxide dust or fume, which existed in the past. The more recent epidemiological studies have not added further evidence in support of the carcinogenic role of cadmium.     

Pooled Analysis of Two Swedish Case-Control Studies on the Use of Mobile and Cordless Telephones and the Risk of Brain Tumours Diagnosed During 1997–2003

Here we present the pooled analysis of 2 case–control studies on the association of brain tumours with mobile phone use. Use of analogue cellular phones increased the risk for acoustic neuroma by 5%, 95% confidence interval (CI) = 2-9% per 100 hrs of use. The risk increased for astrocytoma grade III—IV with latency period with highest estimates using >10-year time period from first use of these phone types. The risk increased per one year of use of analogue phones by 10%, 95% CI = 6-14%, digital phones by 11%, 95% CI = 6-16%, and cordless phones by 8%, 95% CI = 5-12%. For all studied phone types OR for brain tumours, mainly acoustic neuroma and malignant brain tumours, increased with latency period, especially for astrocytoma grade III—IV.     

PM2.5对小鼠和H9C2细胞心肌肥大相关因子mRNA表达的影响

用采自太原市4个不同季节的细颗粒物(PM_(2.5))对小鼠心肌细胞H9C2进行染毒后,采用荧光定量PCR技术检测心肌肥大相关因子ANP和TGF-β的mRNA水平.采用浓度分别为0、1、3、10μg·mL~(-1)的冬季PM_(2.5)处理H9C2细胞后,检测心肌肥大相关因子ANP、β-MHC、MMP2和MMP9的mRNA水平.之后分别选取4周龄、4月龄、10月龄C57BL/6雌性小鼠作为实验模型,采用咽后壁滴注的方法用3 mg·kg~(-1) PM_(2.5)暴露4周.采用苏木素-伊红染色(HE)对小鼠心脏组织病理切片进行观察,并检测ANP和β-MHC的mRNA水平.结果发现,与对照组相比,冬季PM_(2.5)诱导H9C2细胞中ANP和TGF-β的mRNA水平升高最为显著;其中,当冬季PM_(2.5)染毒浓度较高时可诱导ANP、β-MHC、MMP2和MMP9的mRNA水平均显著升高.经PM_(2.5)暴露4周后,幼年和老年小鼠心肌细胞核质比显著降低.老年小鼠心脏组织中ANP和β-MHC的mRNA表达水平显著上升.实验表明,冬季PM_(2.5)诱导心肌肥大标志物表达改变的效应要强于其他季节,且有一定的剂量效应关系,而老年小鼠对PM_(2.5)诱导的心肌肥大效应最为敏感.