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UNICEF and the International Children's Palliative Care Network undertook a joint analysis in three sub-Saharan countries—Zimbabwe, South Africa, and Kenya—to estimate the palliative care need among their children and to explore these countries' capacities to deliver children's palliative care (CPC). This report concerns the findings from South Africa. The study adopted a cross-sectional mixed-methods approach using both quantitative and qualitative data obtained from primary and secondary sources. CPC need was estimated using prevalence and mortality statistics. The response to the need and existing gaps were analysed using data obtained from a literature review, interviews with key persons, and survey data from service providers.The findings show very limited CPC service coverage for children in the public sector. In addition, services are mainly localised, with minimal reach. Less than 5% of the children needing care in South Africa are receiving it, with those receiving it being closer to the end of life. Barriers to the delivery of CPC include fear of opioid use, lack of education on CPC, lack of integration into the primary care system, lack of policies on CPC, and lack of community and health professional awareness of CPC needs and services. Estimating the need for CPC is a critical step in meeting the needs of children with life-threatening conditions and provides a sound platform to advocate for closure of the unacceptably wide gaps in coverage.

To determine the feasibility and performance of a routine screen for childhood asthma in new entrants to primary school relative to diagnosis by a paediatrician. Cross‐sectional study with a validation substudy. All 4539 new primary school entrants (mean age, 5.72 years; 95% CI, 5.71–5.74) in the Australian Capital Territory (ACT) in 1999; 180 of these children (73% of the 248 contacted) participated in the validation substudy. Performance of the screening test relative to a paediatrician's diagnosis of current asthma (defined as a history of wheeze suggestive of a clinical diagnosis of asthma within the past 12 months) based on history and examination. 3748 of the 4539 new primary school entrants (83%) returned completed asthma and respiratory questions. The screening test was positive in 38% of children. Estimated sensitivity was 92% (95% CI, 75%–99%); specificity, 76% (95% CI, 72%–80%); positive predictive value, 51% (95% CI, 41%–63%); negative predictive value, 98% (95% CI, 90%–100%); positive likelihood ratio, 3.8 (95% CI, 2.8–4.8); and negative likelihood ratio, 0.14 (95% CI, 0.02–0.33). It is feasible to conduct population screens for asthma that have good diagnostic test performance against a specialist paediatrician's diagnosis through school health programs. This approach could facilitate monitoring changes in asthma prevalence over time.

The yeast Saccharomyces cerevisiaeexpresses two phosphatidylserine decarboxylase (PSD) activities which are responsible for conversion of phosphatidylserine to phosphatidylethanolamine, and either enzyme alone is sufficient for normal cellular growth. However, strains containing a PSD1null allele and a mutation leading to loss of PSD2 activity (psd1-Δ1::TRP1 psd2) are auxotrophic for ethanolamine. This nutritional requirement was utilized to isolate the gene encoding the PSD2 enzyme by complementation. The PSD2gene encodes a protein of 1138 amino acids with a predicted molecular mass of 130 kDa. The deduced amino acid sequence shows significant identity (34%) to a PSD-like sequence from Clostridium pasteurianumand the yeast PSD1(19%) at the carboxyl end of the protein. Of particular interest is the presence of a sequence, GGST, which may be involved in post-translational processing and prosthetic group formation similar to other PSD enzymes. The PSD2 amino acid sequence also shows significant homology to the C2regions of protein kinase C and synaptotagmin. Physical mapping experiments demonstrate that the PSD2is located on chromosome 7. The PSD2gene was heterologously expressed by infection of Sf-9 insect cells with recombinant baculovirus, resulting in a 10-fold increase in PSD activity. The null allele of PSD2was introduced into yeast strains by one-step gene deletion/disruption with a HIS3marker gene. Strains expressing wild type PSD1and the psd2-Δ1::HIS3allele show a small decrease in overall PSD activity, but no noticeable effect upon [3H]serine incorporation into aminophospholipids. Strains containing both the psd1-Δ1::TRP1and psd2-Δ1::HIS3null alleles, however, express no detectable PSD activity, are ethanolamine auxotrophs and show a severe deficit in the conversion of [3H]serine-labeled phosphatidylserine to phosphatidylethanolamine. These data indicate that the gene isolated is the structural gene for PSD2 and that the PSD1 and PSD2 enzymes account for all yeast PSD activity.

Summaries

In an effort to understand molecular mechanisms of intracellular lipid transport, we have focused upon specific events required for de novoaminophospholipid synthesis in the yeast Saccharomyces cerevisiae. A genetic system for examining the steps between phosphatidylserine (PtdSer) synthesis in the endoplasmic reticulum and its transport to and decarboxylation by PtdSer decarboxylase 2 in the Golgi/vacuole has been developed. We have isolated a mutant, denoted pstB1, that accumulates PtdSer and has diminished phosphatidylethanolamine formation despite normal PtdSer decarboxylase 2 activity. The lesion in PtdSer metabolism is consistent with a defect in interorganelle lipid transport. A genomic DNA clone that complements the mutation was isolated, and sequencing revealed that the clone contains the STT4gene, encoding a phosphatidylinositol 4-kinase. The pstB1mutant exhibits a defect in Stt4p-type phosphatidylinositol 4-kinase activity, and direct gene replacement indicates that STT4is the defective gene in the mutant. Creation of an STT4null allele (stt4Δ::HIS3) demonstrates the gene is essential. These results provide evidence that implicates phosphoinositides in the regulation of intracellular aminophospholipid transport.

BackgroundComprehensive Behavioural Intervention for Tics (CBIT) is a behavioural therapy with strong empirical support for its effects on tic severity when offered as an individual therapy1and emerging evidence for its effectiveness in a group format.2This study compared the long-term effects of CBIT and psycho-educational groups on tic severity, neuropsychological functioning, quality of life (QOL) and school attendance.MethodThis is a follow-up study to a single-blinded, randomised controlled trial. Twenty-eight children that completed either psycho-educational or CBIT group treatment took part in this 12 month follow-up. Participants had a mean age of 12.1 years and a diagnosis of either Tourette Syndrome (TS) or Chronic Tic Disorder. Outcomes included the YGTSS, direct video observation, neuropsychological functioning measures (response inhibition, cognitive flexibility and motor dexterity), the GTS-QOL and school attendance data.ResultsBoth groups demonstrated long-term improvements in tic severity (p<0.001, ηp2= 0.32), with continued improvement across the follow-up period (F(1,26) = 7.52, p=0.011, ηp2=0.22). Self-reported QOL also improved during the follow-up period (F(1,19) = 5.73, p=0.027, ηp2= 0.23). The CBIT group demonstrated greater improvement in tic suppression ability (p=0.019, ηp2= 0.146) and a correlation was found between QOL and tic suppression ability at follow-up (r=−0.517, p=0.008). Both groups improved in school attendance (p=0.004, ηp2= 0.304).ConclusionGroups were associated with long-term improvements in tic severity, QOL and school attendance, offering support for the long-term acceptability of these group treatments for TS. The CBIT group showed a greater improvement in tic suppression ability over time and increased tic suppression ability was associated with improved quality of life, suggesting a relationship between self-reported QOL and a child’s sense of control over their tics through the use of behavioural strategies.References. J McGuire, J Piacentini, EA Brennan, AB Lewin, TK Murphy, BJ Small, EA Storch. A meta-analysis of behavior therapy for Tourette syndrome. Journal of psychiatric research2014;50:106–112.. R Yates, K Edwards, J King, O Luzon, M Evangeli, D Stark, F McFarlane, I Heyman, B Ince, J Kodric, T Murphy. Habit Reversal Training and Educational group treatments for children with Tourette syndrome: A preliminary randomised controlled trial. Behaviour Research and Therapy2016.