Report and Recommendations for a Traveller Education Strategy

Irish Travellers are an indigenous minority who, according to historical evidence, have been part of Irish society for centuries. They have a long shared history, value system, language, customs and traditions that make them a group recognised by themselves and others as distinct. This distinctive life-style and culture, based on a nomadic tradition, sets them apart from the settled population. The history of the Traveller community includes a struggle to uphold their distinct cultural identity and to maintain a nomadic way of life. For the purposes of this report it is accepted that Travellers have shared a nomadic tradition and a means of communication, beliefs, values and practices distinct from the majority culture.

Report and Recommendations for a Traveller Education Strategy

Irish Travellers are an indigenous minority who, according to historical evidence, have been part of Irish society for centuries. They have a long shared history, value system, language, customs and traditions that make them a group recognised by themselves and others as distinct. This distinctive life-style and culture, based on a nomadic tradition, sets them apart from the settled population. The history of the Traveller community includes a struggle to uphold their distinct cultural identity and to maintain a nomadic way of life. For the purposes of this report it is accepted that Travellers have shared a nomadic tradition and a means of communication, beliefs, values and practices distinct from the majority culture.

p.L1612P, a novel voltage-gated sodium channel Nav1.7 mutation inducing a cold sensitive paroxysmal extreme pain disorder.

BACKGROUND: Mutations in the SCN9A gene cause chronic pain and pain insensitivity syndromes. We aimed to study clinical, genetic, and electrophysiological features of paroxysmal extreme pain disorder (PEPD) caused by a novel SCN9A mutation. METHODS: Description of a 4-generation family suffering from PEPD with clinical, genetic and electrophysiological studies including patch clamp experiments assessing response to drug and temperature. RESULTS: The family was clinically comparable to those reported previously with the exception of a favorable effect of cold exposure and a lack of drug efficacy including with carbamazepine, a proposed treatment for PEPD. A novel p.L1612P mutation in the Nav1.7 voltage-gated sodium channel was found in the four affected family members tested. Electrophysiologically the mutation substantially depolarized the steady-state inactivation curve (V1/2 from -61.8 ± 4.5 mV to -30.9 ± 2.2 mV, n = 4 and 7, P < 0.001), significantly increased ramp current (from 1.8% to 3.4%, n = 10 and 12) and shortened recovery from inactivation (from 7.2 ± 5.6 ms to 2.2 ± 1.5 ms, n = 11 and 10). However, there was no persistent current. Cold exposure reduced peak current and prolonged recovery from inactivation in wild-type and mutated channels. Amitriptyline only slightly corrected the steady-state inactivation shift of the mutated channel, which is consistent with the lack of clinical benefit. CONCLUSIONS: The novel p.L1612P Nav1.7 mutation expands the PEPD spectrum with a unique combination of clinical symptoms and electrophysiological properties. Symptoms are partially responsive to temperature but not to drug therapy. In vitro trials of sodium channel blockers or temperature dependence might help predict treatment efficacy in PEPD.

PHA Corporate Strategy 2011-2015

The PHA Corporate Strategy has been developed with input from staff across the PHA and taking account of feedback from external stakeholders.� It is a high level document, setting out the direction for the PHA over the next few years, and will be supported by the annual PHA Corporate Business Plan, Directorate Business Plans and the Joint Commissioning Plan.� The Strategy was approved by the PHA board at the November 2011 board meeting.�The PHA Corporate strategy sets out the role, direction and priorities of the PHA for the next four years, taking account of the requirements of the Comprehensive Spending Review.The goals set out in this strategy�are supported by annual plans detailing how the goals will be achieved.The strategy outlines the following:protecting health;improving health and wellbeing;improving quality and safety;improving early detection.

Consultation on Personal and Public Involvement strategy

Personal and Public Involvement (PPI) is an integral element of effective commissioning and is underpinned by a core set of values and principles - involving and listening to people in order to help us make services better.It brings about a number of recognised benefits if fully embraced into our culture and practice, these include:Use of service user knowledge and expertise;Better priority setting and decision making;More responsive, appropriate, efficient and tailored services;Transformation and reduction of complaints;Increased levels of service satisfaction;Increased dignity and self worth.The Public Health Agency (PHA) and Health and Social Care Board (HSCB) have now developed a joint Personal and Public Involvement (PPI) Strategy after extensive engagement and discussion. The Strategy has been approved by both organisations and is now being formally consulted on during the period 23rd June 2011 to 15th September 2011.The Strategy is now available for your consideration. We have developed the following documents (please see attachments below):Valuing People, Valuing Their Participation. Involving You and Listening to You Consultation Document.Valuing People, Valuing Their Participation, Involving You and Listening to You. [An Easy Read version of the Personal and Public Involvement Strategy].Valuing People, Valuing Their Participation. [An Equality and Human Rights Screening of the Strategy].Key Questions to guide consideration of the Personal and Public Involvement Strategy.People are encouraged to read the Strategy and to let us have your views.� There is a set of Key Questions, but any comments, ideas and or suggestions that you may have, that could support us in our efforts to embed Personal and Public Involvement into our culture and practice, would be most welcome.Responses should be returned by 4.00pm on Thursday 15th September 2011 to:By post:Martin QuinnRegional PPI LeadPublic Health AgencyGransha Park House15 Gransha ParkLondonderryBT47 6FNBy email: siobhan.carlin@hscni.net By telephone: (028) 7186 0086A more detailed version of the consultation document is avalable by clicking here or contacting Siobhan Carlin, email: siobhan.carlin@hscni.net, Tel: (028) 7186 0086.If you require any of these documents in an alternative format such as Braille, larger print or in another language if you are not fluent in English, please do not hesitate to contact us.A report of feedback received as part of this consultation can be made available upon request.Please be aware that the PHA and HSCB are also currently consulting on the Community Development Strategy.You are invited to consider responding to this consultation as well if appropriate.

Valuing People, Valuing Their Participation - A Strategy for Personal and Public Involvement for the Public Health Agency and Health and Social Care Board

Personal and Public Involvement (PPI) is about involving those who use Health and Social Care (HSC) services, or care for those who use services, with those who plan and deliver services. This involvement can sometimes relate to individuals (personal), or groups, or the wider community (public).This Strategy shows the direction that both the PHA and the HSCB are committed to, in their development of PPI.

Community Development Strategy May 2012

The Community Development Strategy for Health and Wellbeing has been developed jointly by the Health and Social Care Board and the Public Health Agency.�The main purpose of the strategy is to recognise and support the important and pivotal role that community development plays in improving health and wellbeing.�The HSCB and PHA want to see strong, resilient communities where everyone has good health and wellbeing - places where people look out for each other and have community pride in where they live.�We seek to narrow the gap in health inequalities and improve the health and wellbeing of the population.�This means working to address the determinants of ill health and reducing risk factors, including those associated with poverty and social exclusion, and this can only be achieved in partnership with the community.The strategy was influenced by a widespread consultation in 2011 - details available here - during which over 300 individuals and organisations attended workshops and 60 written responses were received.�The following documents are attached below:Community Development Strategy - Consultation ResponsesCommunity Development Strategy - Executive SummaryCommunity Development Action PlanCommunity Development Strategy Community Development Strategy - Performance Management Framework

mitoKATP channel activation in the postanoxic developing heart protects E-C coupling via NO-, ROS-, and PKC-dependent pathways.

Whereas previous studies have shown that opening of the mitochondrial ATP-sensitive K(+) (mitoK(ATP)) channel protects the adult heart against ischemia-reperfusion injury, it remains to be established whether this mechanism also operates in the developing heart. Isolated spontaneously beating hearts from 4-day-old chick embryos were subjected to 30 min of anoxia followed by 60 min of reoxygenation. The chrono-, dromo-, and inotropic disturbances, as well as alterations of the electromechanical delay (EMD), reflecting excitation-contraction (E-C) coupling, were investigated. Production of reactive oxygen species (ROS) in the ventricle was determined using the intracellular fluorescent probe 2',7'-dichlorofluorescin (DCFH). Effects of the specific mitoK(ATP) channel opener diazoxide (Diazo, 50 microM) or the blocker 5-hydroxydecanoate (5-HD, 500 microM), the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 50 microM), the antioxidant N-(2-mercaptopropionyl)glycine (MPG, 1 mM), and the PKC inhibitor chelerythrine (Chel, 5 microM) on oxidative stress and postanoxic functional recovery were determined. Under normoxia, the baseline parameters were not altered by any of these pharmacological agents, alone or in combination. During the first 20 min of postanoxic reoxygenation, Diazo doubled the peak of ROS production and, interestingly, accelerated recovery of ventricular EMD and the PR interval. Diazo-induced ROS production was suppressed by 5-HD, MPG, or L-NAME, but not by Chel. Protection of ventricular EMD by Diazo was abolished by 5-HD, MPG, L-NAME, or Chel, whereas protection of the PR interval was abolished by L-NAME exclusively. Thus pharmacological opening of the mitoK(ATP) channel selectively improves postanoxic recovery of cell-to-cell communication and ventricular E-C coupling. Although the NO-, ROS-, and PKC-dependent pathways also seem to be involved in this cardioprotection, their interrelation in the developing heart can differ markedly from that in the adult myocardium.

A review of the breastfeeding strategy for Northern Ireland

This review of the Breastfeeding strategy for Northern Ireland, was led by the Breastfeeding Strategy Review Group and carried out by the PHA. It aimed to examine progress on the recommendations of the document and potential barriers to implementation, by consulting widely with key stakeholders. A number of suggestions on the way forward towards formulating a new strategy also emerged.�

Strategy for personal and public involvement in Health and Social Care research

This report outlines the strategic need for, and benefits of,�personal and public involvement�to all levels of Health and Social Care Research�&�Development Division activity.

Strategy for personal and public involvement

Local and national policy increasingly emphasises the central role of service users and the public in shaping Health and Social Care (HSC). This is the second edition of the HSC R&D Division��'s Personal and Public Involvement (PPI) Strategy, which highlights the importance of involving patients and the public in research and outlines the progress already made in implementing PPI in research in Northern Ireland.

Correlated evolution of mating strategy and inbreeding depression within and among populations of the hermaphroditic snail Physa acuta

Inbreeding depression is one of the main forces opposing the evolution of self-fertilization. Of central importance is the hypothesis that inbreeding depression and selfing coevolve antagonistically, generating either low selfing rate and high inbreeding depression or vice versa. However, there is limited evidence for this coevolution within species. We investigated this topic in the hermaphroditic snail Physa acuta. In this species, isolated individuals delay the onset of egg laying compared to individuals having access to mates. Longer delays (''waiting times'') indicate more intense selfing avoidance. We measured inbreeding depression and waiting time in a large quantitative-genetic experiment (281 outbred families derived from 26 natural populations). We observed large genetic variance for both traits and a strong positive genetic covariance between them, most of which resided within rather than among populations. It means that, within populations, individuals with higher mutation load avoided selfing more strongly on average. This genetic covariance may result from pleiotropy and/or linkage disequilibrium. Whatever its genetic architecture, the fact it emerges specifically when individuals are deprived of mates suggests it is not fortuitous and rather reflects the action of natural selection. We conclude that a diversity of mating strategies can arise within populations subjected to variation in inbreeding depression.

The transmembrane serine protease (TMPRSS3) mutated in deafness DFNB8/10 activates the epithelial sodium channel (ENaC) in vitro.

TMPRSS3 encodes a transmembrane serine protease that contains both LDLRA and SRCR domains and is mutated in non-syndromic autosomal recessive deafness (DFNB8/10). To study its function, we cloned the mouse ortholog which maps to Mmu17, which is structurally similar to the human gene and encodes a polypeptide with 88% identity to the human protein. RT-PCR and RNA in situ hybridization on rat and mouse cochlea revealed that Tmprss3 is expressed in the spiral ganglion, the cells supporting the organ of Corti and the stria vascularis. RT-PCR on mouse tissues showed expression in the thymus, stomach, testis and E19 embryos. Transient expression of wild-type or tagged TMPRSS3 protein showed a primary localization in the endoplasmic reticulum. The epithelial amiloride-sensitive sodium channel (ENaC), which is expressed in many sodium-reabsorbing tissues including the inner ear and is regulated by membrane-bound channel activating serine proteases (CAPs), is a potential substrate of TMPRSS3. In the Xenopus oocyte expression system, proteolytic processing of TMPRSS3 was associated with increased ENaC mediated currents. In contrast, 6 TMPRSS3 mutants (D103G, R109W, C194F, W251C, P404L, C407R) causing deafness and a mutant in the catalytic triad of TMPRSS3 (S401A), failed to undergo proteolytic cleavage and activate ENaC. These data indicate that important signaling pathways in the inner ear are controlled by proteolytic cleavage and suggest: (i) the existence of an auto-catalytic processing by which TMPRSS3 would become active, and (ii) that ENaC could be a substrate of TMPRSS3 in the inner ear.

A novel neutrophil elastase inhibitor prevents elastase activation and surface cleavage of the epithelial sodium channel expressed in Xenopus laevis oocytes.

The amiloride-sensitive epithelial sodium channel (ENaC) constitutes a limiting step in sodium reabsorption across distal airway epithelium and controlling mucociliary clearance. ENaC is activated by serine proteases secreted in the extracellular milieu. In cystic fibrosis lungs, high concentrations of secreted neutrophil elastase (NE) are observed. hNE could activate ENaC and contribute to further decreased mucociliary clearance. The aims of this study were (i) to test the ability of an engineered human neutrophil elastase inhibitor (EPI-hNE4) to specifically inhibit the elastase activation of ENaC-mediated amiloride-sensitive currents (I(Na)) and (ii) to examine the effect of elastase on cell surface expression of ENaC and its cleavage pattern (exogenous proteolysis). Oocytes were exposed to hNE (10-100 microg/ml) and/or trypsin (10 microg/ml) for 2-5 min in the presence or absence of EPI-hNE4 (0.7 microm). hNE activated I(Na) 3.6-fold (p < 0.001) relative to non-treated hENaC-injected oocytes. EPI-hNE4 fully inhibited hNE-activated I(Na) but had no effect on trypsin- or prostasin-activated I(Na). The co-activation of I(Na) by hNE and trypsin was not additive. Biotinylation experiments revealed that cell surface gamma ENaC (but not alpha or beta ENaC) exposed to hNE for 2 min was cleaved (as a 67-kDa fragment) and correlated with increased I(Na). The elastase-induced exogenous proteolysis pattern is distinct from the endogenous proteolysis pattern induced upon preferential assembly, suggesting a causal relationship between gamma ENaC cleavage and ENaC activation, taking place at the plasma membrane.