Early Reading Abilities of Bilingual Children With Nonsyndromic Orofacial Clefts.

OBJECTIVE: To investigate the early reading abilities, and related cognitive-linguistic processes, in bilingual children with nonsyndromic cleft lip and/or palate (CL/P), and to identify deficits that might be amenable to intervention. DESIGN AND PARTICIPANTS: Bilingual participants with CL/P aged 5 to 6 years who were English-dominant ( n=17) or Mandarin-dominant ( n=18) were recruited using consecutive sampling from a national cleft treatment center and matched pairwise to a sample of typically developing (TD) children on language dominance, age, and socioeconomic status. All participants were assessed in English on single-word reading accuracy using the Wide Range Achievement Test (4th Ed), and key cognitive-linguistic factors associated with reading development: phonological awareness, rapid automatized naming (RAN), receptive and expressive vocabulary, and verbal short-term and working memory. RESULTS: CL/P and TD groups were compared within language dominance group (Mandarin or English) for all measures. The Mandarin-dominant CL/P group had significantly poorer reading accuracy and phonological awareness than their TD peers. Additionally, regardless of language dominance, faster RAN correlated significantly with better reading accuracy in both the CL/P groups but not the TD groups. CONCLUSIONS: Children with CL/P who are learning English as a second language are at greater risk of reading difficulties. Furthermore, the cognitive-linguistic processes underlying early reading in bilingual children with CL/P differ from those of their TD peers. Routine screening and tailored intervention is advisable.

Identity management, negotiation and resistance among women in the sex trade in London, Ontario.

Sex work, and ideas about women in the trade, have long been represented as tragic and/or threatening. However, such portrayals tell us very little about how women think about themselves and the kinds of work they do. The data for this paper come from an ethnographic, community-based study in London, Ontario, that involves women in street-based, indoor and transactional sex work. This discussion focuses on how women develop different individual identities, including the management of multiple selves, their sexual identities and what we have termed the 'good junkie' identity. We also examine how these women employ aspects of dominant representation of sex workers, namely the low status accorded to those in street-based work and the defamatory term 'whore' or 'ho', when negotiating the moral hierarchies that exist within various kinds of sex work (i.e., stripping, massage parlours) and making sense of their professional and personal lives. The work that goes into the creation and maintenance of the women's divergent identities sheds important light on this complicated and tremendously demanding, yet inadequately understood, aspect of life as women in the sex trade.

Lung endothelial cell platelet-activating factor production and inflammatory cell adherence are increased in response to cigarette smoke component exposure.

An early event in the pathogenesis of emphysema is the development of inflammation associated with accumulation of polymorphonuclear leukocytes (PMN) in small airways, and inflammatory cell recruitment from the circulation involves migration across endothelial and epithelial cell barriers. Platelet-activating factor (PAF) promotes transendothelial migration in several vascular beds, and we postulated that increased PAF production in the airways of smokers might enhance inflammatory cell recruitment and exacerbate inflammation. To examine this possibility, we incubated human lung microvascular endothelial cells (HMVEC-L) with cigarette smoke extract (CSE) and found that CSE inhibits PAF-acetylhydrolase (PAF-AH) activity. This enhances HMVEC-L PAF production and PMN adherence, and adherence is blocked by PAF receptor antagonists (CV3988 or ginkgolide B). CSE also inhibited PAF-AH activity of lung endothelial cells isolated from wild-type (WT) and iPLA(2)ß knockout mice, and with WT cells, CSE enhanced PAF production and RAW 264.7 cell adherence. In contrast, CSE did not affect PAF production or RAW 264.7 cell adherence to iPLA(2)ß-null cells, suggesting that iPLA(2)ß plays an important role in PAF production by lung endothelial cells. These findings suggest that inhibition of PAF-AH by components of cigarette smoke may initiate or exacerbate inflammatory lung disease by enhancing PAF production and promoting accumulation of inflammatory cells in small airways. In addition, iPLA(2)ß is identified as a potential target for therapeutic interventions to reduce airway inflammation and the progression of chronic lung disease.

Home Healthcare Nursing Visits for Nonhomebound Patients With Heart Failure After Hospital Discharge: A Quality-Improvement Pilot Project.

Frequent rehospitalizations among patients with heart failure (HF) result in patient burden and high cost. Homebound patients with HF qualify for home healthcare after hospital discharge. It is not known if nonhomebound patients with HF could also benefit from home healthcare nursing (HHN) visits to improve the transition from hospital to home. The purpose of this quality-improvement pilot study was to assess the impact of HHN visits provided to nonhomebound HF patients after hospital discharge on 30-day rehospitalization rates. We included patients with HF who were ineligible for home healthcare services due to their nonhomebound status. Home healthcare nurses followed a modified version of the discharge checklist from the American Heart Association's Rise Above Heart Failure materials, and provided education as appropriate based on patients' responses. We enrolled 68 patients in the study. The mean age was 60.2 years; 61.8% were male and 77.9% were White. Based on patient responses to the checklist, key areas addressed during HHN visits were medication management and HF self-care. In the HHN visit group, 15% of the patients experienced rehospitalization within 30 days, compared with 23% in the non-HHN visit group among 540 patients discharged in the same time frame who met the inclusion criteria but were not enrolled in the study (p = .12). Our pilot data show that HHN visits for nonhomebound patients are feasible and result in a numerically lower 30-day rehospitalization rate after discharge. Further study is needed to confirm the clinical efficacy of this approach.

Evaluation of child therapy and caregiver training in the treatment of school refusal.

OBJECTIVE: To evaluate the relative efficacy of (1) child therapy, (2) parent/teacher training, and (3) the combination of child therapy and parent/teacher training in the treatment of anxiety-based school refusal. METHOD: Sixty-one school-refusing children (aged 7-14 years) from throughout Melbourne, Australia, were randomized to a child therapy program, a parent and teacher training program, or a combination of the two. Children were assessed before and after treatment, and at 4.5-month follow-up, by means of attendance records, self-report of emotional distress and self-efficacy, parent and teacher reports of emotional distress, and clinician ratings of overall functioning. RESULTS: Statistically and clinically significant pretreatment-posttreatment change occurred for each group. Immediately posttreatment, child therapy appeared to be the least effective in increasing attendance. By follow-up, the attendance and adjustment of those in the child therapy group equalled that of children whose parents and teachers were involved in treatment, whether on their own (parent/teacher training) or together with their children (combined child therapy and parent/teacher training). CONCLUSION: Contrary to expectations, combined child therapy and parent/teacher training did not produce better outcomes at posttreatment or follow-up.

Tryptase activates calcium-independent phospholipase A2 and releases PGE2 in airway epithelial cells.

Human small airway epithelial cells (HSAEC) form the boundary between the external environmental allergens and the internal lung milieu. Mast cells are present in human lung tissue interspersed within the pulmonary epithelium and can secrete a host of pre- and newly formed mediators from their granules, which may propagate small airway inflammation. In this study, tryptase stimulation of HSAEC increased membrane-associated, calcium-independent phospholipase A(2)gamma (iPLA(2)gamma) activity, resulting in increased arachidonic acid and PGE(2) release. These responses were inhibited by pretreating HSAEC with the iPLA(2)-selective inhibitor bromoenol lactone. The tryptase-stimulated PGE(2) production was inhibited by treating HSAEC with the cyclooxygenase (COX)-1-selective inhibitor SC-560 and the nonselective COX inhibitor aspirin but not by the COX-2-selective inhibitor CAY10404, indicating that the early release of arachidonic acid is metabolized by constitutive COX-1 to form PGE(2) in tryptase-stimulated HSAEC. Additionally, platelet-activating factor production and neutrophil adherence to tryptase-stimulated HSAEC was also increased. This complex response can set up a cascade of inflammatory mediator production in small airways. We speculate that selective inhibition of iPLA(2)gamma-mediated phospholipid hydrolysis may prove beneficial in inflammatory airway diseases.

New leptin receptor mutations in mice: Lepr(db-rtnd), Lepr(db-dmpg) and Lepr(db-rlpy).

Three new spontaneous recessive mouse mutations in the leptin receptor gene (Lepr), Lepr(db-rtnd), Lepr(db-dmpg) and Lepr(db-rlpy), originated in the CBA/J (CBA), B10.D2-H8(b)(57N)/Sn (B10) and NU/J strains, respectively. Lepr(db-rtnd) and Lepr(db-dmpg) were maintained on C57BL/6J (B6), resulting in congenic lines of B6.CBA-Lepr(db-rtnd) and B6.B10-Lepr(db-dmpg). Lepr(db-rtnd) was also maintained on CBA post F1 generation of a cross between the B6 and the CBA, generating the congenic line CBA.B6CBA-Lepr(db-rtnd). Lepr(db-rlpy) was maintained as a coisogenic strain. The aims of this study were to determine the molecular bases for these new Lepr mutations and to characterize the new mutant stocks, with respect to obesity and diabetes. Mutations were analyzed by Southern blot analysis, reverse transcriptase-polymerase chain reaction and sequencing. Body weights and plasma glucose and insulin levels were measured, and the histology of the pancreas was carried out. Lepr(db-rtnd) contained one G deletion in exon 4 of Lepr, introducing a frameshift and premature termination. Lepr(db-dmpg) had a deletion in the extracellular domain of LEPR: Lepr(db-rlpy) exhibited a large DNA deletion, leading to a complete lack of LEPR: All three mutations led to morbid obesity and diabetes. It is noteworthy that Lepr(db-rtnd) caused milder hyperglycemia accompanied by higher plasma and pancreatic insulin contents on B6 compared to that on CBA backgrounds. In summary, we discovered three new mutations of Lepr, providing new mouse models for obesity and diabetes. Furthermore, our mutant stocks will be useful in elucidating the effects of the genetic background on the Lepr mutations and in testing the specificity of antibodies to LEPR.