Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8

Two voltage gated sodium channel α-subunits, Na(v)1.7 and Na(v)1.8, are expressed at high levels in nociceptor terminals and have been implicated in the development of inflammatory pain. Mis-expression of voltage-gated sodium channels by damaged sensory neurons has also been implicated in the development of neuropathic pain, but the role of Na(v)1.7 and Na(v)1.8 is uncertain. Here we show that deleting Na(v)1.7 has no effect on the development of neuropathic pain. Double knockouts of both Na(v)1.7 and Na(v)1.8 also develop normal levels of neuropathic pain, despite a lack of inflammatory pain symptoms and altered mechanical and thermal acute pain thresholds. These studies demonstrate that, in contrast to the highly significant role for Na(v)1.7 in determining inflammatory pain thresholds, the development of neuropathic pain does not require the presence of either Na(v)1.7 or Na(v)1.8 alone or in combination

The Rural Household Multiple Indicator Survey, data from 13,310 farm households in 21 countries

The Rural Household Multiple Indicator Survey (RHoMIS) is a standardized farm household survey approach which collects information on 758 variables covering household demographics, farm area, crops grown and their production, livestock holdings and their production, agricultural product use and variables underlying standard socio-economic and food security indicators such as the Probability of Poverty Index, the Household Food Insecurity Access Scale, and household dietary diversity. These variables are used to quantify more than 40 different indicators on farm and household characteristics, welfare, productivity, and economic performance. Between 2015 and the beginning of 2018, the survey instrument was applied in 21 countries in Central America, sub-Saharan Africa and Asia. The data presented here include the raw survey response data, the indicator calculation code, and the resulting indicator values. These data can be used to quantify on- and off-farm pathways to food security, diverse diets, and changes in poverty for rural smallholder farm households

Increasing frailty is associated with higher prevalence and reduced recognition of delirium in older hospitalised inpatients: results of a multi-centre study

Purpose: Delirium is a neuropsychiatric disorder delineated by an acute change in cognition, attention, and consciousness. It is common, particularly in older adults, but poorly recognised. Frailty is the accumulation of deficits conferring an increased risk of adverse outcomes. We set out to determine how severity of frailty, as measured using the CFS, affected delirium rates, and recognition in hospitalised older people in the United Kingdom. Methods: Adults over 65 years were included in an observational multi-centre audit across UK hospitals, two prospective rounds, and one retrospective note review. Clinical Frailty Scale (CFS), delirium status, and 30-day outcomes were recorded. Results: The overall prevalence of delirium was 16.3% (483). Patients with delirium were more frail than patients without delirium (median CFS 6 vs 4). The risk of delirium was greater with increasing frailty [OR 2.9 (1.8–4.6) in CFS 4 vs 1–3; OR 12.4 (6.2–24.5) in CFS 8 vs 1–3]. Higher CFS was associated with reduced recognition of delirium (OR of 0.7 (0.3–1.9) in CFS 4 compared to 0.2 (0.1–0.7) in CFS 8). These risks were both independent of age and dementia. Conclusion: We have demonstrated an incremental increase in risk of delirium with increasing frailty. This has important clinical implications, suggesting that frailty may provide a more nuanced measure of vulnerability to delirium and poor outcomes. However, the most frail patients are least likely to have their delirium diagnosed and there is a significant lack of research into the underlying pathophysiology of both of these common geriatric syndromes

Generation and characterisation of a nociceptor specific Cre expressing mouse

Examination of mouse null mutants provides useful insights into gene function, but perinatal lethality or developmental compensatory mechanisms may obscure behavioural phenotypes. The bacteriophage Cre-loxP system provides a method of producing deletion of genes in specific tissue. The tetrodotoxin-resistant voltage gated sodium channel, Nav1.8, is expressed exclusively in a subset of primary afferent neurons, more than 85% of which are nociceptors. The heterozygous Nav1.8 mouse has been shown to have a normal electrophysiological and behavioural phenotype. In this project gene targeting was used to insert the Cre-recombinase gene into the translational start of Nav1.8 in embryonic stem cells and transgenic mice expressing Cre under the control of the Nav1.8 promoter were generated. The expression pattern of functional Cre was examined using ROSA26 reporter mice and was found to be identical to Nav1.8. Expression started at E13 and was limited to small diameter neurons in dorsal root ganglia, trigeminal ganglia and nodose ganglia. There was no expression in non-neuronal cells or in the central nervous system. This pattern of expression did not alter in adult animals. Examination of the Nav1.8 mediated TTX-resistant current in small diameter dorsal root ganglion neurons from heterozygote Nav1.8Cre animals revealed that it was identical to that in wild type neurons. In addition, the nociceptive behavioural phenotype of adult heterozygote Nav1.8Cre mice both in tests of mechanical and thermal thresholds and in models of inflammatory and neuropathic pain, was identical to that of wild type mice. These findings demonstrate that the Nav1.8Cre mouse line is a suitable tool to examine the effects of nociceptor specific gene deletion on pain behaviour, and so provide insights into the role of widely expressed genes in nociception