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Contemporary discourses regarding children’s spirituality in ECEC professional publication streams (academic and practitioner readership) were analysed, with consideration of impacts of these discourses on practice in the early years sector. Many established theoretical concepts regarding children’s spirituality were not evident in the early years texts analysed, suggesting that those theories are either not relevant, not accepted or simply not on the radar of early years specialists. Tacit acceptance of a young child’s spirituality was evident, alongside a focus on ensuring spiritual rights and wellbeing, rather than efforts to nurture or enhance a child’s spirituality. Whilst discourse analysis revealed that spirituality is viewed positively and as a valued component of a young child’s development and wellbeing, inclusion of spirituality in ECEC internet sources and academic literature is minimal, suggesting that in practice, spirituality is pushed aside in contemporary early years practice. More research is needed to understand how these discourses may impact upon early years practice, and to investigate the perspectives of practitioners and parents about spirituality in contemporary early childhood education and care. [ABSTRACT FROM AUTHOR]

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The possible presence of anticipation in bipolar affective disorder and schizophrenia has led to the hypothesis that repeat expansion mutations could contribute to the genetic etiology of these diseases. Using the repeat expansion detection (RED) assay, we have systematically examined genomic DNA from 100 unrelated probands with schizophrenia and 68 unrelated probands with bipolar affective disorder for the presence of CAG/CTG repeat expansions. Our results show that 28% of the probands with schizophrenia and 30% of probands with bipolar disorder have a CAG/CTG repeat in the expanded range, but that each expansion could be explained by one of three nonpathogenic repeat expansions known to exist in the general population. We conclude that novel CAG/CTG repeat expansions are not a common genetic risk factor for bipolar disorder or schizophrenia., (Copyright 2003 Wiley-Liss, Inc.)

Spinocerebellar ataxia type 12 (SCA12), now described in European-American and Asian (Indian) pedigrees, is unique among the SCAs from clinical, pathological, and molecular perspectives. Clinically, the distinguishing feature is early and prominent action tremor with variability in other signs. Pathologically, brain MRIs also suggest variability, with prominent cortical as well as cerebellar atrophy. Genetically, SCA12 is caused by a CAG repeat expansion that does not encode polyglutamine; we speculate that the mutation may affect expression of the gene PPP2R2B, which encodes a brain-specific regulatory subunit of the protein phosphatase PP2A., (Copyright 2003 S. Karger AG, Basel)

We recently described a disorder termed Huntington disease-like 2 (HDL2) that completely segregates with an unidentified CAG/CTG expansion in a large pedigree (W). We now report the cloning of this expansion and its localization to a variably spliced exon of JPH3 (encoding junctophilin-3), a gene involved in the formation of junctional membrane structures.

Spinocerebellar ataxia type 12 (SCA12) is an autosomal dominant neurodegenerative disorder which has been described in pedigrees of German American and Indian descent. The phenotype typically begins with tremor in the fourth decade, progressing to include ataxia and other cerebellar and cortical signs. SCA12 is associated with an expansion of a CAG repeat in the 5' region of the gene PPP2R2B which encodes a brain-specific regulatory subunit of the protein phosphatase PP2A. The repeat size ranges from 55 to 78 triplets in the mutant allele of affected individuals, and from 9 to 28 triplets in normal alleles. It is possible that an expansion mutation in PPP2R2B may influence PPP2R2B expression, perhaps altering the activity of PP2A, an enzyme implicated in multiple cellular functions, including cell cycle regulation, tau phosphorylation, and apoptosis.

With juvenile crime on the rise, understanding and preventing juvenile delinquency is one of the greatest challenges facing mental health professionals today. Recognizing early signs of conduct disorder (CD) can be difficult, but identifying risk factors is an important step in preventing a child's progression to CD or Antisocial Personality Disorder (APD). This paper focuses on various risk factors for CD and APD, such as intrinsic individual differences, psychosocial/environmental factors, genetic and neurochemical factors. Early recognition and intervention may prevent the progression from aggressive and maladaptive behaviors to CD and later APD.

To determine the extent to which depression complicates Parkinson's disease (PD), the authors analyzed the literature on depression in PD in order to report on its prevalence, clinical manifestations, and treatment. By means of MEDLINE literature searches, the analysis focused on 45 PD depression studies conducted from 1922 through 1998. The results indicate that the prevalence of depression is 31% for all PD patients. The clinical manifestations of PD depression include apathy, psychomotor retardation, memory impairment, pessimism, irrationality, and suicidal ideation without suicidal behavior. PD depression is effectively treated with a variety of antidepressants, most commonly at present the selective serotonin reuptake inhibitors. Anecdotal evidence supports the use of sertraline to treat PD depression.

Spinocerebellar ataxia 12 (SCA12) is an autosomal dominant cerebellar ataxia (ADCA) described in a single family with a CAG repeat expansion in the PPP2R2B gene. We screened 247 index cases, including 145 families with ADCA, for this expansion. An expanded repeat ranging from 55 to 61 triplets was detected in 6 affected and 3 unaffected individuals at risk in a single family from India. The association of the PPP2R2B CAG repeat expansion with disease in this new family provides additional evidence that the mutation is causative.

The purpose of this study was to identify and characterize caretakers who fail to utilize the poison center for unintentional poisonings involving children. We interviewed 210 caretakers of children evaluated for unintentional poisoning in the emergency center of an urban, university-based teaching hospital to determine (1) whether demographic differences exist between those caretakers who contacted a poison center prior to the emergency center visit and those who did not and (2) whether differences exist in prevalence of poison prevention knowledge and behaviors between the two groups. Ninety-six (46%) of caretakers did not contact the poison center prior to the emergency center visit. Significant differences were found between the two groups for the following caretaker variables: race/ethnicity, language preference, age, level of education, country in which schooling occurred, and type of insurance coverage for the child. When logistic regression was used to control for confounding, the two variables associated with failure to use the poison center were black race and schooled outside the United States (primarily in Mexico). Poison center callers reported a higher prevalence of poison prevention knowledge and behaviors than noncallers. Educational interventions should be targeted to the groups of caretakers identified who do not use the poison center.

To estimate the effectiveness of a poison center by determining the number of potential medical facility visits for childhood poisonings which are prevented, and to determine how callers learned about the poison center in order to help guide future public educational efforts, a cross-sectional telephone survey was done. A systematic sample of caretakers of children < 6-y-of-age living in Harris County, TX, and who called the poison center about a poisoning incident between February 1993 and January 1994, was taken. One hundred sixty-six/197 eligible caretakers (84%) completed the survey. Of the 166 caretakers, only 5 (3%) were referred by the poison center to a medical facility for treatment, although 6 (3.6%) actually sought medical attention. The remaining 160 (96.4%) were successfully managed at home. The majority of these (74%) required no intervention and the remaining 26% required only minimal treatment, including ipecac, dilution, irrigation or observation. Of the 160 caretakers managed at home, 69 (43%) would have sought medical attention for the child at a health care facility if the poison center did not exist, and of those 81% would have gone to an emergency center or hospital for evaluation. Callers learned about the poison center most often from family/ friends, doctors, Mr Yuk stickers, television, previous use, or pharmacists. Poison centers decrease health care costs by preventing unnecessary medical facility visits for minor childhood poisonings which can be successfully managed at home. Methods effective in educating the public about poison centers should be continued and other methods explored to increase poison centers' use.

Introduction: Lead toxicity is well recognized as a significant cause of morbidity in children, especially those under the age of six years. While lead toxicity has not been recognized as a public health problem in Houston, it is possible that children in the area suffer from low-level lead effects on the central nervous system., Objectives: To detect asymptomatic cases of lead toxicity in one population of Houston children and to assess the effectiveness of the lead risk questionnaire., Design: Venous blood samples for quantitative lead were analyzed utilizing the Anodic Stripping Voltameter. The Centers for Disease Control's lead risk assessment questionnaire was administered to each patient., Setting: Baylor College of Medicine Continuity Clinic at Texas Children's Hospital., Subjects: All patients, ages 9-72 months, seen for routine care between December 1992 and June 1994 were screened once., Results: Blood lead levels were obtained on 801 children; all but 47 completed lead risk questionnaires. The mean age of the study group was 2.37 years (SD 1.84) and they were 54% male. They were 39% Hispanic, 39% Black, and 18% White. Eighty-eight percent reported an annual income of < $20,000. They lived in 127 separate zip codes. Twenty-five (3.1%) patients had elevated blood lead, 21 between 10-14 micrograms/dL and 4 between 15-19 micrograms/dL. No patients had blood lead levels of > or = 20 micrograms/dL. No statistically significant differences were found between patients with blood lead < 10 micrograms/dL and those with > or = 10 micrograms/dL when comparing for age, sex, ethnicity, income, and zip code. Only those children living in or regularly visiting a pre-1960 home with peeling or chipping paint were significantly more likely to have elevated blood lead (p = .045)., Conclusion: Although the majority of children in our setting were poor and urban, the prevalence of blood lead > or = 10 micrograms/dL was 3.1%, well below the estimated 17% quoted by the Centers for Disease Control in recommending stringent screening guidelines. The lead risk assessment questionnaire failed to identify 32% of children with elevated blood lead levels. Since this questionnaire is critical to screening populations at low risk for lead toxicity, it is important to determine whether a revised questionnaire or a more careful elicitation of parental responses will improve identification of those children at risk.

Objective: To compare continuity clinic experiences by practice setting and postgraduate level., Design: Mailed questionnaire., Setting: Baylor College of Medicine pediatric residents selected 1 of 3 continuity practice settings, including community-based private offices (n = 35) and university-based clinics in a private (n = 71) and a public (n = 12) hospital., Subjects: One hundred eighteen pediatric residents, May 1993., Outcome Measures: Patient volume, continuity of care, type of patient visit, and faculty supervision., Results: The response rate was 77% (91/118). Pediatric residents in community-based private offices reported seeing more patients per session than those in the university-based private and public clinics (88%, 10%, and 0% residents in the respective practice settings reported > or = 4 patients per session), but were less likely to see patients repeatedly (6%, 68%, and 40% residents in the respective practice settings had seen more than half their patients > 2 times). Residents in private offices provided a smaller percentage of well child care (16%, 61%, and 90% residents in the respective practice settings reported > 50% patients were well) and more acute care (68%, 15% and 0% residents in the respective practice settings reported > 25% patients were acutely ill). Residents in private offices reported a higher percentage of time spent observing only (33%, 0%, and 0% residents in the respective practice settings observed > 25% of the time) and less time managing patients independently (93%, 59%, and 40% residents, respectively, managed < or = 25% of the time). No significant differences among postgraduate levels were found for these variables., Conclusions: Patient volume, continuity of care, type of patient visit, and faculty supervision were significantly different among continuity practice settings. Postgraduate level of training did not affect significantly these measures of continuity clinic experience. These differences need to be considered in curriculum development.

We previously isolated two human L1 elements (L1.2 and LRE2) as the progenitors of disease-producing insertions. Here, we show these elements can actively retrotranspose in cultured mammalian cells. When stably expressed from an episome in HeLa cells, both elements retrotransposed into a variety of chromosomal locations at a high frequency. The retrotransposed products resembled endogenous L1 insertions, since they were variably 5' truncated, ended in poly(A) tracts, and were flanked by target-site duplications or short deletions. Point mutations in conserved domains of the L1.2-encoded proteins reduced retrotransposition by 100- to 1000-fold. Remarkably, L1.2 also retrotransposed in a mouse cell line, suggesting a potential role for L1-based vectors in random insertional mutagenesis.

We have found a 2 kilobase insertion containing a rearranged L1 element in the dystrophin gene of a muscular dystrophy patient. We cloned the precursor of this insertion, the second known active human L1 element. The locus, LRE2, has one allele derived from the patient which matches the insertion sequence exactly. LRE2 has a perfect 13-15 bp target site duplication, two open reading frames, and an unusual 21 bp truncation of the 5' end, suggesting that a slightly truncated element can still retrotranspose. It differs from LRE1 by approximately 0.7%. There is an L1 element at LRE2 on approximately 66% of human chromosomes 1q, and the element is absent from chimpanzee and gorilla genomes. These data demonstrate that multiple active L1 elements exist in the human genome, and that a readthrough transcript of an active element is capable of retrotransposition.

Full-length human LINE-1 retrotransposons encode p40 proteins with varying electrophoretic mobilities under denaturing conditions. The p40 expressed from the first open reading frame in the LINE-1 copy designated L1.2A co-electrophoreses with the endogenous p40 in human teratocarcinoma cells. This finding is consistent with previous data indicating that L1.2A is an active element. The amino acid sequence in the central region of the L1.2A p40 accounts, at least in part, for its characteristic mobility. This region includes sequences which can, in principle, form a leucine zipper.

The stability of miconazole when mixed with peritoneal dialysis (PD) fluid and stored in plastic bags or glass ampuls was determined. Admixtures of miconazole and PD fluid were prepared in 2-L polyvinyl chloride (PVC) bags and in 1-mL glass ampuls to give a nominal initial concentration of 20 mg/mL. Duplicate samples of each solution were assayed in duplicate by high-performance liquid chromatography immediately after preparation and at various intervals up to nine days. All admixtures were stored in ambient light at 20 +/- 2 degrees C. A substantial loss of miconazole (greater than 10% of the initial concentration) occurred within four hours for admixtures stored in PVC bags, whereas similar solutions retained more than 90% of their initial miconazole concentration for at least three days when stored in glass ampuls under the same conditions. This suggests that the observed loss of miconazole from the PVC bags was largely due to an interaction with the container, rather than to chemical degradation in solution. About 28% of the miconazole lost from the solution during storage in PVC bags was recovered from the plastic by methanolic extraction. The rapid loss of miconazole when the drug was mixed with PD fluid and stored in PVC bags indicates that such admixtures should be prepared immediately before administration.

This study examines the stability of both components of the antibacterial combination, cotrimoxazole (trimethoprim and sulphamethoxazole) in peritoneal dialysis fluid stored in polyvinyl chloride bags and glass ampoules at room temperature for up to nine days. Greater than 10% loss of trimethoprim occurred within three days for admixtures stored in plastic bags, whereas the original concentration remained virtually unchanged after nine days for similar solutions stored in glass ampoules. This indicated that the loss of trimethoprim observed in solutions stored in plastic bags was associated primarily with the nature of the container, presumably due to some form of uptake by or loss through the plastic. Greater than 10% loss of sulphamethoxazole occurred within two days for all admixtures examined, stored in either glass or plastic containers. This degree of loss was achieved within 12 h for one admixture stored in plastic. There was also the time-dependent appearance of an additional peak in HPLC analyses of these solutions, indicating that loss of sulphamethoxazole was due to chemical decomposition of the drug in the peritoneal dialysis fluid. The shelf-life of such admixtures would be limited by the stability of the sulphamethoxazole component, with the available data suggesting a shelf-life of 12 h for solutions stored at room temperature.