A comparison of soil liming requirement methodologies in temperate, Northern European pedo‐climates

ACKNOWLEDGEMENTS Funding for this research was provided through a PhD studentship by Scotland's Rural College (SRUC) and the University of Aberdeen.Peer reviewedPublisher PD

Brainstem Sources of Cardiac Vagal Tone and Respiratory Sinus Arrhythmia

KEY POINTS: Cardiac vagal tone is a strong predictor of health, although its central origins are unknown. Respiratory‐linked fluctuations in cardiac vagal tone give rise to respiratory sinus arryhthmia (RSA), with maximum tone in the post‐inspiratory phase of respiration. In the present study, we investigated whether respiratory modulation of cardiac vagal tone is intrinsically linked to post‐inspiratory respiratory control using the unanaesthetized working heart‐brainstem preparation of the rat. Abolition of post‐inspiration, achieved by inhibition of the pontine Kolliker‐Fuse nucleus, removed post‐inspiratory peaks in efferent cardiac vagal activity and suppressed RSA, whereas substantial cardiac vagal tone persisted. After transection of the caudal pons, part of the remaining tone was removed by inhibition of nucleus of the solitary tract. We conclude that cardiac vagal tone depends upon at least 3 sites of the pontomedullary brainstem and that a significant proportion arises independently of RSA. ABSTRACT: Cardiac vagal tone is a strong predictor of health, although its central origins are unknown. The rat working heart‐brainstem preparation shows strong cardiac vagal tone and pronounced respiratory sinus arrhythmia. In this preparation, recordings from the cut left cardiac vagal branch showed efferent activity that peaked in post‐inspiration, ∼0.5 s before the cyclic minimum in heart rate (HR). We hypothesized that respiratory modulation of cardiac vagal tone and HR is intrinsically linked to the generation of post‐inspiration. Neurons in the pontine Kölliker‐Fuse nucleus (KF) were inhibited with bilateral microinjections of isoguvacine (50–70 nl, 10 mm) to remove the post‐inspiratory phase of respiration. This also abolished the post‐inspiratory peak of cardiac vagal discharge (and cyclical HR modulation), although a substantial level of activity remained. In separate preparations with intact cardiac vagal branches but sympathetically denervated by thoracic spinal pithing, cardiac chronotropic vagal tone was quantified by HR compared to its final level after systemic atropine (0.5 μm). Bilateral KF inhibition removed 88% of the cyclical fluctuation in HR but, on average, only 52% of the chronotropic vagal tone. Substantial chronotropic vagal tone also remained after transection of the brainstem through the caudal pons. Subsequent bilateral isoguvacine injections into the nucleus of the solitary tract further reduced vagal tone: remaining sources were untraced. We conclude that cardiac vagal tone depends on neurons in at least three sites of the pontomedullary brainstem, and much of it arises independently of respiratory sinus arrhythmia

Selective sonographic screening for developmental dysplasia of the hip – increasing trends in late diagnosis

There are concerns that selective sonographic screening for developmental dysplasia of the hip (DDH) may be suboptimal. Our aim was to test this hypothesis by identifying trends in presentation and surgical treatment in patients with DDH. This is a retrospective review of children born between 1997-2018 who were treated surgically for DDH at our sub- regional paediatric orthopaedic unit. Demographic data, risk factors, age of diagnosis and surgical treatments were analysed. Late diagnosis was defined as greater than 4 months. 103 children (14 male, 89 female) underwent surgery. 93 hips were operated for dislocation and 21 for dysplasia. 13 patients presented with bilateral hip dislocations. The median age at diagnosis was 10 months (95% CI: 4-15). 62/103 (60.2%) were diagnosed late (after 4 months) and the median age for diagnosis in this group was 18.5 months (95% CI: 16-20.5). Significantly more patients were referred late (p=0.0077). The presence of risk factors (breech presentation or family history) was associated with early diagnosis. Over the duration of our study the operation rate per 1000 live births gradually increased, and on Poisson regression analysis there was a statistically significant increasing trend towards late diagnosis in recent years (p=0.0237), which necessitated more aggressive surgical management. In the UK, the current selective sonographic screening programme for DDH has shown a deterioration over the years of this study and this questions its current effectiveness. It appears that the majority of irreducible hip dislocations are diagnosed late, with an increased need for surgical management

Splinting for the non-operative management of developmental dysplasia of the hip (DDH) in children under six months of age

This is a protocol for a Cochrane Review (Intervention). The objectives are as follows: To determine the role of splinting and the optimal treatment strategy for the non-operative management of DDH in children under six months of age. To identify if there are particular subgroups of patients for whom the optimal management strategy may differ

On the presence and functional significance of sympathetic premotor neurons with collateralized spinal axons in the rat

KEY POINTS: Spinally-projecting neurons of the rostral ventrolateral medulla (RVLM) determine sympathetic outflow to different territories of the body. Previous studies suggest the existence of RVLM neurons with distinct functional classes, such as neurons that target sympathetic nerves bound for functionally-similar tissue types (e.g. muscle vasculature). The existence of RVLM neurons with more general actions had not been critically tested. Using viral tracing, we show that a significant minority of RVLM neurons send axon collaterals to disparate spinal segments (T2 and T10 ). Furthermore, optogenetic activation of sympathetic premotor neurons projecting to lumbar spinal segments also produced activation of sympathetic nerves from rostral spinal segments that innervate functionally diverse tissues (heart and forelimb muscle). These findings suggest the existence of individual RVLM neurons for which the axons branch to drive sympathetic preganglionic neurons of more than one functional class and may be able to produce global changes in sympathetic activity. ABSTRACT: We investigate the extent of spinal axon collateralization of rat rostral ventrolateral medulla (RVLM) sympathetic premotor neurons and its functional consequences. In anatomical tracing experiments, two recombinant herpes viral vectors with retrograde tropism and expressing different fluorophores were injected into the intermediolateral column at upper thoracic and lower thoracic levels. Histological analysis revealed that ∼21% of RVLM bulbospinal neurons were retrogradely labelled by both vectors, indicating substantial axonal collateralization to disparate spinal segments. In functional experiments, another virus with retrograde tropism, a canine adenovirus expressing Cre recombinase, was injected into the left intermediolateral horn around the thoracolumbar junction, whereas a Cre-dependent viral vector encoding Channelrhodopsin2 under LoxP control was injected into the ipsilateral RVLM. In subsequent terminal experiments, blue laser light (473 nm × 20 ms pulses at 10 mW) was used to activate RVLM neurons that had been transduced by both vectors. Stimulus-locked activation, at appropriate latencies, was recorded in the following pairs of sympathetic nerves: forelimb and hindlimb muscle sympathetic fibres, as well as cardiac and either hindlimb muscle or lumbar sympathetic nerves. The latter result demonstrates that axon collaterals of lumbar-projecting RVLM neurons project to, and excite, both functionally similar (forelimb and hindlimb muscle) and functionally dissimilar (lumbar and cardiac) preganglionic neurons. Taken together, these findings show that the axons of a significant proportion of RVLM neurons collateralise widely within the spinal cord, and that they may excite preganglionic neurons of more than one functional class

Early discharge in acute mental health: a rapid literature review

Long psychiatric hospital stays are unpopular with services users, harmful and costly. Economic pressures alongside a drive for recovery orientated care in the least restrictive contexts, have led to increasing pressure to discharge people from hospital early. Hospital discharge is however complex, stressful and risky for service users and families. This rapid literature review aimed to assess what is known about early discharge in acute mental health. Searches were conducted in nine bibliographic databases, reference lists and targeted grey literature sources. Fourteen included papers focused on early discharge in mental health, a population over 18 years with a mental health condition and reported outcomes on therapeutic care or service delivery. Quality appraisal was undertaken using The Mixed Method Appraisal Tool. The meta-summary of the literature found that early discharge was neither provided to all inpatients nor limited to the Crisis Resolution and Home Treatment (CRHT) service model internationally. Early discharge interventions required collaborative working and discharge planning. It was not associated with unplanned readmissions and had a small effect on length of stay. Most studies reported service outcomes whereas health outcomes were underreported. Professionals and service users were positive about early discharge and service users asked for peer support. Carers preferred hospital or day hospital care suggesting their need for respite. Limitations in the scope, detail and quality of the evidence about early discharge leaves an unclear picture of the components of early discharge as an intervention, its effectiveness, cost effectiveness or outcomes

African horse sickness: The potential for an outbreak in disease-free regions and current disease control and elimination techniques

African horse sickness (AHS) is an arboviral disease of equids transmitted by Culicoides biting midges. The virus is endemic in parts of sub-Saharan Africa and official AHS disease-free status can be obtained from the World Organization for Animal Health on fulfilment of a number of criteria. AHS is associated with case fatality rates of up to 95%, making an outbreak among naïve horses both a welfare and economic disaster. The worldwide distributions of similar vector-borne diseases (particularly bluetongue disease of ruminants) are changing rapidly, probably due to a combination of globalisation and climate change. There is extensive evidence that the requisite conditions for an AHS epizootic currently exist in disease-free countries. In particular, although the stringent regulations enforced upon competition horses make them extremely unlikely to redistribute the virus, there are great concerns over the effects of illegal equid movement. An outbreak of AHS in a disease free region would have catastrophic effects on equine welfare and industry, particularly for international events such as the Olympic Games. While many regions have contingency plans in place to manage an outbreak of AHS, further research is urgently required if the equine industry is to avoid or effectively contain an AHS epizootic in disease-free regions. This review describes the key aspects of AHS as a global issue and discusses the evidence supporting concerns that an epizootic may occur in AHS free countries, the planned government responses, and the roles and responsibilities of equine veterinarians.Matthew Robin's clinical training scholarship was funded by the Horserace Betting Levy Board.http://onlinelibrary.wiley.com/journal/10.1001/(ISSN)2042-33062017-09-30hb2017Companion Animal Clinical Studie

A case of autism with an interstitial deletion on 4q leading to hemizygosity for genes encoding for glutamine and glycine neurotransmitter receptor sub-units (AMPA 2, GLRA3, GLRB) and neuropeptide receptors NPY1R, NPY5R

BACKGROUND: Autism is a pervasive developmental disorder characterized by a triad of deficits: qualitative impairments in social interactions, communication deficits, and repetitive and stereotyped patterns of behavior. Although autism is etiologically heterogeneous, family and twin studies have established a definite genetic basis. The inheritance of idiopathic autism is presumed to be complex, with many genes involved; environmental factors are also possibly contributory. The analysis of chromosome abnormalities associated with autism contributes greatly to the identification of autism candidate genes. CASE PRESENTATION: We describe a child with autistic disorder and an interstitial deletion on chromosome 4q. This child first presented at 12 months of age with developmental delay and minor dysmorphic features. At 4 years of age a diagnosis of Pervasive Developmental Disorder was made. At 11 years of age he met diagnostic criteria for autism. Cytogenetic studies revealed a chromosome 4q deletion. The karyotype was 46, XY del 4 (q31.3-q33). Here we report the clinical phenotype of the child and the molecular characterization of the deletion using molecular cytogenetic techniques and analysis of polymorphic markers. These studies revealed a 19 megabase deletion spanning 4q32 to 4q34. Analysis of existing polymorphic markers and new markers developed in this study revealed that the deletion arose on a paternally derived chromosome. To date 33 genes of known or inferred function are deleted as a consequence of the deletion. Among these are the AMPA 2 gene that encodes the glutamate receptor GluR2 sub-unit, GLRA3 and GLRB genes that encode glycine receptor subunits and neuropeptide Y receptor genes NPY1R and NPY5R. CONCLUSIONS: The deletion in this autistic subject serves to highlight specific autism candidate genes. He is hemizygous for AMPA 2, GLRA3, GLRB, NPY1R and NPY5R. GluR2 is the major determinant of AMPA receptor structure. Glutamate receptors maintain structural and functional plasticity of synapses. Neuropeptide Y and its receptors NPY1R and NPY5R play a role in hippocampal learning and memory. Glycine receptors are expressed in very early cortical development. Molecular cytogenetic studies and DNA sequence analysis in other patients with autism will be necessary to confirm that these genes are involved in autism

Shiga Toxin-Mediated Hemolytic Uremic Syndrome: Time to Change the Diagnostic Paradigm?

Hemolytic uremic syndrome (HUS) is caused by enterohemorrhagic Escherichia coli (EHEC) which possess genes encoding Shiga toxin (stx), the major virulence factor, and adhesin intimin (eae). However, the frequency of stx-negative/eae-positive E. coli in stools of HUS patients and the clinical significance of such strains are unknown.Between 1996 and 2006, we sought stx-negative/eae-positive E. coli in stools of HUS patients using colony blot hybridization with the eae probe and compared the isolates to EHEC causing HUS. stx-negative/eae-positive E. coli were isolated as the only pathogens from stools of 43 (5.5%) of 787 HUS patients; additional 440 (55.9%) patients excreted EHEC. The majority (90.7%) of the stx-negative/eae-positive isolates belonged to serotypes O26:H11/NM (nonmotile), O103:H2/NM, O145:H28/NM, and O157:H7/NM, which were also the most frequent serotypes identified among EHEC. The stx-negative isolates shared non-stx virulence and fitness genes with EHEC of the corresponding serotypes and clustered with them into the same clonal complexes in multilocus sequence typing, demonstrating their close relatedness to EHEC.At the time of microbiological analysis, approximately 5% of HUS patients shed no longer the causative EHEC, but do excrete stx-negative derivatives of EHEC that lost stx during infection. In such patients, the EHEC etiology of HUS is missed using current methods detecting solely stx or Shiga toxin; this can hamper epidemiological investigations and lead to inappropriate clinical management. While maintaining the paradigm that HUS is triggered by Shiga toxin, our data demonstrate the necessity of considering genetic changes of the pathogen during infection to adapt appropriately diagnostic strategies