Parental depression was assessed using the Beck Depression Inventory (BDI) in  families with children with autism and/or intellectual disability (ID), and in  control families. Mothers with children with autism had higher depression scores (mean = .) than mothers of children with ID without autism (mean = .), who in turn, had higher depression scores than fathers of children with autism (mean = .), fathers of children with ID without autism (mean = .), and control mothers (mean = .) and fathers (mean = .). Forty-five per cent of mothers with children with ID without autism and % of mothers with children with autism had elevated depression scores (BDI > ), compared to -% in the other groups. Single mothers of children with disabilities were found to be more vulnerable to severe depression than mothers living with a partner.

The Edinburgh Postnatal Depression Scale (EPDS) was designed to be used by community health workers to screen for postnatal depression. We report data from a population-based sample of 1655 women who completed the EPDS at 2 months and 3 months postpartum. A total of 128 women were interviewed with the Montgomery Asberg Depression Rating Scale (MADRS) and assessed according to DSM-III-R criteria for major depression. A cut-off score of 11.5 on the EPDS identified all but two women with major depression, giving it a sensitivity of 96%, a specificity of 49% and a positive predictive value of 59%. This study supports the validity of the EPDS shown in earlier studies, and indicates that the scale is a useful screening instrument for identifying postnatal depression in primary health care in Sweden.

The SoC theory is valuable in understanding individual differences in psychological adaptation in parents of children with ID.

Well-being of parents with a child with ID is dependent upon the interplay of risk and protective factors and research needs to address these variables simultaneously.

Families with children with ID differ from control families in that the parents are less involved in paid work and have lower levels of well-being. A positive relation between involvement in paid work and well-being was found.

BackgroundAmyotrophic lateral sclerosis (ALS) is a rare disease in Taiwan; thus, estimation of ALS mortality is difficult. We evaluated factors associated with ALS survival in Taiwan.MethodsThe study enrolled 1149 Taiwanese with a primary diagnosis of ALS during 1999–2008. Follow-up information was available for all patients; mean (SD) duration of follow-up was 2.91 (2.62) years. Medical interventions, including noninvasive positive pressure ventilation (NIPPV), tracheotomy, gastrostomy, and riluzole, were included in time-dependent survival analysis.ResultsOf the 1149 ALS patients, 438 (38.12%) died during follow-up. Mortality in the first year was 16%, which was 13 times (95% CI 11.1–15.2) the age- and sex-standardized rate of the general population in Taiwan. The average annual crude mortality rate was 13.1% (person-years). Factors significantly associated with increased mortality were male sex, advanced age, rural residence, lower economic status, no tracheotomy, and no riluzole treatment. Significant predictors of long-term versus average survival were younger age at diagnosis, being a dependent or receiving social welfare, and NIPPV support. Significant predictors of short-term versus average survival were older age, being employed, no tracheotomy, and no riluzole use.ConclusionsThe results support the use of riluzole to improve ALS survival. Patients who received riluzole and underwent tracheotomy had the best survival.

Eosinophil cationic protein (ECP) is currently used as a biomarker for airway inflammation. It is a heparin-binding ribonuclease released by activated eosinophils. Its cytotoxicity toward cancer cell lines is blocked by heparin. The objective of this study was to locate the heparin binding site of ECP by sitedirected mutagenesis and construction of a synthetic peptide derived from this region. Synthetic heparin with >5 monosaccharide units showed strong inhibition of ECP binding to the cell surface. Analysis of ECP mt1 (R34A/W35A/R36A/K38A) showed that these charged and aromatic residues were involved in ECP binding to heparin and the cell surface. A potential binding motif is located in the loop L3 region between helix ␣2 and strand ␤1, outside the RNA binding domain. The synthetic peptide derived from the loop L3 region displayed strong pentasaccharide binding affinity and blocked ECP binding to cells. In addition, ECP mt1 showed reduced cytotoxicity. Thus, the tight interaction between ECP and heparin acts as the primary step for ECP endocytosis. These results provide new insights into the structure and function of ECP for anti-asthma therapy.Eosinophil cationic protein (ECP), 2 a member of the ribonuclease A (RNase A) superfamily, is found in the specific granules of eosinophilic leukocytes. It is a single polypeptide with a molecular mass ranging from 16 to 21.4 kDa due to varying degrees of glycosylation. It shows a 67% amino acid sequence identity with eosinophil-derived neurotoxin (EDN), another eosinophil-secreted RNase. Although ECP shares the overall three-dimensional structure of RNase A, it has relatively lower RNase activity (1). ECP released by activated eosinophils contributes to the toxicity against helminth parasites, bacteria, and single strand RNA viruses (2-4). Together with other proteins secreted from eosinophils, ECP is thought to cause damage to epithelial cells, a common feature of airway inflammation in asthma (5).The mechanism underlying the cytotoxic property of ECP is unclear. It has been hypothesized that ECP cytotoxicity is due to destabilization of lipid membranes of target cells (6), and the degree of cytotoxicity is dependent on the cellular concentration (7). The binding of ECP to target cells has been attributed to its high arginine content (estimated pI ϭ 10.8), which facilitates the interaction between ECP and negatively charged molecules on the cell surface (7,8). Recently, we found that binding and endocytosis of ECP into bronchial epithelial cells were greatly dependent on the cell surface glycosaminoglycan, specifically heparan sulfate proteoglycans (HSPG) (9). The cytotoxicity of ECP was severely reduced toward cell lines with heparan sulfate (HS) deficiency.Heparin and HS are complex polysaccharides composed of alternating units of hexuronic acid and glucosamine. The uronic acid residues of heparin typically consist of 90% L-idopyranosyluronic acid and 10% D-glucopyranosyluronic acid (10). The N position of glucosamine may be substituted with an acetyl or sulfate grou...

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