Intrauterine diagnosis of heterotaxy syndrome

Background Heterotaxy syndrome, including right isomerism and left isomerism, is characterized by an abnormal symmetry of the viscera and veins and is frequently associated with complex cardiac anomalies. We sought to define the feasibility of in utero diagnosis and the postnatal outcome. Methods Patients with heterotaxy syndrome were identified from 579 fetal echocardiograms performed from January 1994 to December 1998. The diagnosis was made on the basis of the fetal echocardiographic findings and was confirmed with autopsy or postnatal evaluation. Results A total of 25 fetuses with right isomerism and 4 with left isomerism constitute the study population. The pregnancies of 7 fetuses (6 right and 1 left isomerism) were terminated before the 24th gestational week and subjected to autopsy. Twelve fetuses (10 right and 2 left isomerism) were lost to follow-up. Nine with right isomerism and 1 with left isomerism were delivered and underwent palliation. Among them, 5 patients (56%) with right isomerism died and more than half of the deaths occurred during infancy. The major cardiac anomalies detected and confirmed with postnatal evaluation or autopsy in fetuses with right isomerism were total anomalous pulmonary venous connection (6/15; 40%), common atrium (15/15; 100%), complete atrioventricular canal (15/15; 100%), double outlet right ventricle (15/15; 100%), and pulmonary stenosis (11/15; 73%). The major cardiac anomalies in fetuses with left isomerism were interruption of inferior vena cava (2/2; 100%), common atrium (1/2; 50%), and complete atrioventricular canal (1/2; 50%). Undetected lesions with fetal echocardiogram were abnormal pulmonary venous return to systemic veins in 1 case (sensitivity, 83%; 5/6; and specificity, 90%; 9/10) and outflow obstruction in 1 case (sensitivity, 91%; 11/12; and specificity, 67%; 2/3). Different patterns of rhythm disturbances were identified: supraventricular tachycardia in 1 case with right isomerism and sinus bradycardia with junctional rhythm in 3 cases with left isomerism (2 of them lost to follow-up). After birth, another 2 patients with right isomerism had supraventricular tachycardia, and 1 with left isomerism had sinus bradycardia develop at age 2 years. Conclusion Heterotaxy syndrome is usually detected in fetuses with the sonographic cardiac abnormalities. Visualization of the pulmonary venous return and outflow obstruction and characterization of the rhythm disturbances are feasible. However, in spite of prenatal diagnosis, the prognosis remains poor. (Am Heart J 2002;143:1002-8.)     

Effects of sera from burn patients on human hepatocytic viscoelasticity

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Effects of heparin on hepatic regeneration and function after partial hepatectomy in rats

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Cardiac Fas-Dependent and Mitochondria-Dependent Apoptotic Pathways in a Transgenic Mouse Model of Huntington’s Disease

Huntington’s disease is an autosomal dominant neurodegenerative disease caused by a CAG repeat expansion in the huntingtin gene. Heart disease is the second leading cause of death in patients with Huntington’s disease. This study was to evaluate whether cardiac Fas-dependent and mitochondria-dependent apoptotic pathways are activated in transgenic mice with Huntington’s disease. Sixteen Huntington’s disease transgenic mice (HD) and sixteen wild-type (WT) littermates were studied at 10.5 weeks of age. The cardiac characteristics, myocardial architecture, and two major apoptotic pathways in the excised left ventricle from mice were measured by histopathological analysis, Western blotting, and TUNEL assays. The whole heart weight and the left ventricular weight decreased significantly in the HD group, as compared to the WT group. Abnormal myocardial architecture, enlarged interstitial spaces, and more cardiac TUNEL-positive cells were observed in the HD group. The key components of Fas-dependent apoptosis (TNF-alpha, TNFR1, Fas ligand, Fas death receptors, FADD, activated caspase-8, and activated caspase-3) and the key components of mitochondria-dependent apoptosis (Bax, Bax-to-Bcl-2 ratio, cytosolic cytochrome c, activated caspase-9, and activated caspase-3) increased significantly in the hearts of the HD group. Cardiac Fas-dependent and mitochondria-dependent apoptotic pathways were activated in transgenic mice with Huntington’s disease, which might provide one of possible mechanisms to explain why patients with Huntington’s disease will develop heart failure.     

Imaging the Impact of Nox4 in Cycling Hypoxia-mediated U87 Glioblastoma Invasion and Infiltration

Purpose

We determined the impact of the cycling hypoxia tumor microenvironment on tumor cell invasion and infiltration in U87 human glioblastoma cells and investigated the underlying mechanisms using molecular bio-techniques and imaging.

Procedures

The invasive phenotype of U87 cells and xenografts exposed to experimentally imposed cycling hypoxic stress in vitro and in vivo was determined by the matrigel invasion assay in vitro and dual optical reporter gene imaging in vivo. RNAi-knockdown technology was utilized to study the role of the NADPH oxidase subunit 4 (Nox4) on cycling hypoxia-mediated tumor invasion.

Results

Cycling hypoxic stress significantly promoted tumor invasion in vitro and in vivo. However, Nox4 knockdown inhibited this effect. Nox4-generated reactive oxygen species (ROS) are required for cycling hypoxia-induced invasive potential in U87 cells through the activation of NF-??B- and ERK-mediated stimulation of MMP-9.

Conclusions

Cycling hypoxia-induced ROS via Nox4 should be considered for therapeutic targeting of tumor cell invasion and infiltration in glioblastoma.     

Caregiver self‐efficacy for managing behavioural problems of older people with dementia in Taiwan correlates with care receivers’ behavioural problems

Aims and objective. To investigate the relationship between family caregivers’ self‐efficacy for managing behavioural problems of older people with dementia and their behavioural problems in Taiwan. Background. Older people with dementia commonly have at least one behavioural problem, which caregivers complain is difficult to handle. To provide interventions that can help caregivers more effectively manage the behavioural problems of care receivers with dementia, caregivers’ self‐efficacy on managing behavioural problems must be assessed. However, it is not clear yet how these behavioural problems of older people with dementia may influence caregivers’ self‐efficacy for managing behavioural problems. Design. A prospective, correlational study. Method. Eighty dyads of older people with dementia and their family caregivers were recruited from neurological clinics of a medical centre in Taiwan. Care receivers were assessed for behavioural problems using the Chinese version of Cohen‐Mansfield Agitation Inventory, community form. Caregivers’ self‐efficacy for managing care receivers’ agitation was measured by the research team‐developed Agitation Management Self‐Efficacy Scale. Results. Caregiver self‐efficacy for managing behavioural problems was significantly and positively associated with more caregiver education, greater duration of caregiving and with care receivers’ less physically non‐aggressive behaviours. When caregiver characteristics were controlled for in hierarchical regression analysis, physically non‐aggressive behaviours explained 6% of the variance in caregiver self‐efficacy. Conclusions. Results of this study contradict the general belief that physically aggressive behaviours of elders with dementia are more difficult for family caregivers to handle than other behavioural problems. Clinicians need to address physically non‐aggressive problem behaviours. Relevance to clinical practice. Nurses could assess older patients with dementia for physically non‐aggressive behaviours and train less educated caregivers to improve their self‐efficacy for managing problem behaviours, thus enhancing the quality of life for both caregivers and care receivers.     

Grade changes in peer influence on adolescent cigarette smoking: a comparison of two measures

The effects of peer influence on adolescent cigarette smoking were investigated in longitudinal study of 309 white, middle-class subjects in the 8th and 11th grades. Subjects provided data on their smoking behavior, the proportion of their friends who smoked, and the identity of their best friend. Data from the person named as best friend was used to measure peer smoking, rather than the adolescent's perceptions of the friend's smoking. Peer influence was defined as the difference between the subject's smoking behavior and that of their best friend. This definition (PI1) minimized the confounding of peer influence with selective association. The effects of peer influence on change in smoking behavior were found to be stronger for 8th than 11th graders and for boys than girls. When the proportion of friends who smoke (PI2) was used as the measure of peer influence, the effects of peer influence were stronger for 11th than 8th graders. The relative merits of the two measures are discussed, and the argument is made that the difference between friend and adolescent smoking is a more appropriate measure of peer influence than the proportion of friends who smoke.