A survey of acute pain services in the UK.

The organisational state of inpatient pain management in UK hospitals is difficult to determine. We sent an electronic questionnaire to 209 acute pain service leads throughout the UK. Questions were about staffing and service provision. We received 141 responses (67%); 47% of all UK hospitals. Each service was responsible for a median (IQR [range]) of 566 (400-839 [120-2800]) beds. Each acute pain specialist nurse was responsible for 299 (238-534 [70-1923]) beds. The mean (SD) number of consultant hours per week was 5.54 (4.62), delivered by a median of 1.0 (1.0-2.5 [0.2-7.0]) consultant. Overnight cover was provided by 20 (15%) acute pain services, and weekend cover by 39 (29%). Acute pain services commonly (in 50 (35%) hospitals) had roles in addition to acute pain management. Most teams (105, (77%)) reviewed medical patients and patients with chronic pain (in 131, (96%) teams). Half of the services (56, (49%)), reported that they were part of an integrated acute and chronic pain service, however, 83 (59%) did not have any members who work in chronic pain clinics. The majority (79, (70%)) were able to access a nominated chronic pain consultant for advice. Provision of acute pain services throughout the UK is highly variable. The majority do not meet core UK standards.

The receptor protein tyrosine phosphatase PTP69D antagonizes Abl tyrosine kinase to guide axons in Drosophila.

During Drosophila embryogenesis, both the cytoplasmic Abelson tyrosine kinase (Abl) and the membrane bound tyrosine phosphatase PTP69D are required for proper guidance of CNS and motor axons. We provide evidence that PTP69D modulates signaling by Abl and its antagonist, Ena. An Abl loss-of function mutation dominantly suppresses most Ptp69D mutant phenotypes including larval/pupal lethality and CNS and motor axon defects, while increased Abl and decreased Ena expression dramatically increase the expressivity of Ptp69D axonal defects. In contrast, Ptp69D mutations do not affect Abl mutant phenotypes. These results support the hypothesis that PTP69D antagonizes the Abl/Ena genetic pathway, perhaps as an upstream regulator. We also find that mutation of the gene encoding the cytoplasmic Src64B tyrosine kinase exacerbates Ptp69D phenotypes, suggesting that two different cytoplasmic tyrosine kinases, Abl and Src64B, modify PTP69D-mediated axon patterning in quite different ways.

Loss of phosphatase activity in Ptp69D alleles supporting axon guidance defects.

PTP69D is a receptor protein tyrosine phosphatase that was identified as a key regulator of neuromuscular axon guidance in Drosophila, and has subsequently been shown to play a similar role in the central nervous system and retina. Three Ptp69D alleles with mutations involving catalytically important residues exhibit a high degree of phenotypic variation with viability of mutant adult flies ranging from 0 to 96%, and ISNb motor nerve defects ranging from 11 to 57% [Desai and Purdy, 2003]. To determine whether mutations in Ptp69D affecting axon guidance and viability demonstrate losses of phosphatase activity and whether differences in catalytic potential underlie phenotypic variability, we expressed full-length wild-type and mutant PTP69D protein in Schneider 2 cells, and assessed phosphatase activity using the fluorogenic substrate 6,8-difluoro-4-methylumbelliferone phosphate (DiFMUP). Detailed biochemical characterization of wild-type PTP69D, including an examination of sensitivity to various inhibitors, in vitro catalytic efficiency, and the pH-k(cat) profile of the enzyme, suggests a common tyrosine phosphatase reaction mechanism despite lack of sequence conservation in the WPD loop. Analysis of mutant proteins revealed that every mutant had less than 1% activity relative to the wild-type enzyme, and these rates did not differ significantly from one another. These results indicate that mutations in Ptp69D resulting in axon guidance defects and lethality significantly compromise catalytic activity, yet the range of biological activity exhibited by Ptp69D mutants cannot be explained by differences in catalytic activity, as gauged by their ability to hydrolyze the substrate DiFMUP.

Identifying children with high mortality risk.

PIP: This issue reports selected results from a comprehensive study of infant and child mortality based on the National Family Health Survey data. The analysis distinguishes between neonatal, postneonatal, infant and child mortality since mortality and its causes vary considerably among children of different ages. Hazard regression analysis was used to estimate the effects of each individual variable as the factors that affect infant and child mortality tend to be correlated with each other. The study involves adjusted effects of selected socioeconomic and demographic characteristics on neonatal, postneonatal, infant, and child mortality for children born during the survey. Short birth intervals have a great effect on infant and child mortality. A previous birth interval of less than 24 months increases child mortality by about 67%. Neonatal mortality is highest among children of very young mothers. Child mortality is higher for girls in all states except Tamil Nadu, Kerala, and Goa. Seven groups of children who are especially vulnerable to infant and child mortality were identified. Thus, intervention programs, such as efforts to provide supplemental nutrition and basic immunization to pregnant mothers, infants and young children need to focus on these high-risk groups. Results for many states show elevated mortality rates for girls after the neonatal period. Family health programs aimed at overall improvement in mortality levels should pay attention to providing basic health care and supplemental nutrition to girls.^ieng

[Changes of the P wave in ischemic cardiopathy. Electrocardiographic correlation]. / Alteraciones de la onda P en la cardiopatía isquémica Correlación electroangiográfica.

1. In the presence of normal coronaries, it is possible to find--or not CAI, in patients with arteriosclerose cardiopathy. 2. When coronary obstructions are present, we also could find a clear dominance of CAI. It is necessary to emphasize the fact that every patient of these series who suffered of trivascular coronary illness presented CAI. 3. When CAI shows in at rest ECG of a patient clearly showing ischemic cardiopathy, more often than not we also find important coronary obstructions, but when this sign is not present it doesn't necessarily mean that we should discard the possibility of a vascular disease, it only points to us the presence of a trivascular coronary pathology. 4. Frequently we find a CVP between normal levels when CAI is not present. 5. We found CAI in every patient showing dysinesia and also in most of the patients with dysinergia.