Do aversive-based training methods actually compromise dog welfare?: A literature review

The methods by which dogs are trained vary between methods involving mainly negative reinforcement and positive punishment (aversive-based methods) and methods based essentially in positive reinforcement and negative punishment (reward-based methods). However, the use of aversive-based methods is highly controversial. While some people defend their merits, others are concerned with their potential negative effect on dog welfare. To date, some studies have been performed aiming to assess the effects of aversive- and rewardbased methods on the welfare and behaviour of dogs. In the present paper we perform a comprehensive review of those studies with the aim of characterizing the state of the art of scientific knowledge of the topic. Generally, the published studies suggest that the use of aversive-based methods is correlated with indicators of compromised welfare in dogs, namely stress‐related behaviours during training, elevated cortisol levels and problematic behaviours such as fear and aggression. However, there are a number of limitations that prevent any strong conclusion from being drawn. First, a considerable proportion of the studies relied upon surveys rather than on objective measures. Second, they focused on sub-populations of police and laboratory dogs and, thus, only represent a small portion of dogs undergoing training. Finally, the empirical studies have concentrated mainly on the effects of shock-collar training, which is only one of several tools used in aversive-based training, and, in some studies, the description of the training methodologies lacks details. Here we present a description of the published studies, discuss their limitations, debate other aspects that, in parallel with the nature of the training methods, may affect dog welfare, and point to future directions for research on the topic.Ana Catarina Vieira de Castro was funded by Fundação para a Ciência e a Tecnologia with an individual post-doc grant (SFRH/BPD/111509/2015). The work undergoing the present review paper did not receive any specific grant from funding agencies in the public, commercial, or notfor-profit sectors

Antibodies to the Mr 64,000 (64K) protein in islet cell antibody positive non-diabetic individuals indicate high risk for impaired Beta-cell function

A prospective study of a normal childhood population identified 44 islet cell antibody positive individuals. These subjects were typed for HLA DR and DQ alleles and investigated for the presence of antibodies to the Mr 64,000 (64K) islet cell antigen, complement-fixing islet cell antibodies and radiobinding insulin autoantibodies to determine their potency in detecting subjects with impaired Beta-cell function. At initial testing 64K antibodies were found in six of 44 islet cell antibody positive subjects (13.6%). The same sera were also positive for complement-fixing islet cell antibodies and five of them had insulin autoantibodies. During the follow-up at 18 months, islet cell antibodies remained detectable in 50% of the subjects studied. In all six cases who were originally positive, 64K antibodies were persistently detectable, whereas complement-fixing islet cell antibodies became negative in two of six and insulin autoantibodies in one of five individuals. HLA DR4 (p < 0.005) and absence of asparic acid (Asp) at position 57 of the HLA DQ chain (p < 0.05) were significantly increased in subjects with 64K antibodies compared with control subjects. Of 40 individuals tested in the intravenous glucose tolerance test, three had a first phase insulin response below the first percentile of normal control subjects. Two children developed Type 1 (insulin-dependent) diabetes mellitus after 18 and 26 months, respectively. Each of these subjects was non-Asp homozygous and had persistent islet cell and 64K antibodies. We conclude that 64K antibodies, complement-fixing islet cell antibodies and insulin autoantibodies represent sensitive serological markers in assessing high risk for a progression to Type 1 diabetes in islet cell antibody positive non-diabetic individuals

Circulating brain injury biomarkers increase after endoscopic surgery for pituitary tumors

Pituitary tumors and subsequent treatment with endoscopic transsphenoidal surgery (ETSS) may cause injury to suprasellar structures, causing long-term fatigue and neurocognitive impairment. A method to quantify brain injury after ETSS is not available. In this prospective, exploratory study of patients undergoing ETSS for pituitary tumors, a novel approach to detect possible neuronal damage is presented. Plasma concentrations of brain injury biomarkers (glial fibrillary acidic protein [GFAP], tau, and neurofilament light [NFL]) were measured the day before surgery, immediately after surgery, at day 1 and 5, and at 6 and 12 months after surgery, using enzyme-linked immunosorbent assays. The association between the increase of biomarkers with preoperative tumor extension and postoperative patient-perceived fatigue was evaluated. Suprasellar tumor extension was assessed from MRI scans, and self-perceived fatigue was assessed using the Multidimensional Fatigue Inventory before and 6 months after surgery. Thirty-five patients were included in the analysis. Compared to baseline, GFAP showed a maximal increase at day 1 after surgery (p = 0.0005), tau peaked postoperatively on the day of surgery (p = 0.019), and NFL reached its maximum at day 5 after surgery (p < 0.0001). The increase in GFAP correlated with preoperative chiasmal compression (p = 0.020). The increase in tau was correlated with preoperative chiasmal (p = 0.011) and hypothalamus compression (p = 0.016), and fatigue score 6 months after surgery (p = 0.016). In conclusion, the concentrations of brain injury biomarkers in blood increased after ETSS for pituitary tumors. The results indicate that postoperative plasma GFAP and tau might reflect astroglial and neuronal damage after ETSS

Predicting the risk of falling – efficacy of a risk assessment tool compared to nurses' judgement: a cluster-randomised controlled trial [ISRCTN37794278]

BACKGROUND: Older people living in nursing homes are at high risk of falling because of their general frailty and multiple pathologies. Prediction of falls might lead to an efficient allocation of preventive measures. Although several tools to assess the risk of falling have been developed, their impact on clinically relevant endpoints has never been investigated. The present study will evaluate the clinical efficacy and consequences of different fall risk assessment strategies. STUDY DESIGN: Cluster-randomised controlled trial with nursing home clusters randomised either to the use of a standard fall risk assessment tool alongside nurses' clinical judgement or to nurses' clinical judgement alone. Standard care of all clusters will be optimised by structured education on best evidence strategies to prevent falls and fall related injuries. 54 nursing home clusters including 1,080 residents will be recruited. Residents must be ≥ 70 years, not bedridden, and living in the nursing home for more than three months. The primary endpoint is the number of participants with at least one fall at 12 months. Secondary outcome measures are the number of falls, clinical consequences including side effects of the two risk assessment strategies. Other measures are fall related injuries, hospital admissions and consultations with a physician, and costs

Association of tamoxifen use and reduced risk of contralateral breast cancer for BRCA1 and BRCA2 mutation carriers

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Epidemiology of methicillin-resistant Staphylococcus aureus (MRSA) in Sweden 2000–2003, increasing incidence and regional differences

BACKGROUND: The occurrence of methicillin-resistant Staphylococcus aureus (MRSA) has gradually become more frequent in most countries of the world. Sweden has remained one of few exceptions to the high occurrence of MRSA in many other countries. During the late 1990s, Sweden experienced a large health-care associated outbreak which with resolute efforts was overcome. Subsequently, MRSA was made a notifiable diagnosis in Sweden in 2000. METHODS: From the start of being a notifiable disease in January 2000, the Swedish Institute for Infectious Disease Control (SMI) initiated an active surveillance of MRSA. RESULTS: The number of reported MRSA-cases in Sweden increased from 325 cases in 2000 to 544 in 2003, corresponding to an overall increase in incidence from 3.7 to 6.1 per 100000 inhabitants. Twenty five per cent of the cases were infected abroad. The domestic cases were predominantly found through cultures taken on clinical indication and the cases infected abroad through screening. There were considerable regional differences in MRSA-incidence and age-distribution of cases. CONCLUSION: The MRSA incidence in Sweden increased over the years 2000–2003. Sweden now poises on the rim of the same development that was seen in the United Kingdom some ten years ago. A quarter of the cases were infected abroad, reflecting that international transmission is now increasingly important in a low-endemic setting. To remain in this favourable situation, stepped up measures will be needed, to identify imported cases, to control domestic outbreaks and to prevent transmission within the health-care sector

Genetic Background Can Result in a Marked or Minimal Effect of Gene Knockout (GPR55 and CB2 Receptor) in Experimental Autoimmune Encephalomyelitis Models of Multiple Sclerosis

PMCID: PMC379391

Formyl Peptide Receptor as a Novel Therapeutic Target for Anxiety-Related Disorders

Formyl peptide receptors (FPR) belong to a family of sensors of the immune system that detect microbe-associated molecules and inform various cellular and sensorial mechanisms to the presence of pathogens in the host. Here we demonstrate that Fpr2/3-deficient mice show a distinct profile of behaviour characterised by reduced anxiety in the marble burying and light-dark box paradigms, increased exploratory behaviour in an open-field, together with superior performance on a novel object recognition test. Pharmacological blockade with a formyl peptide receptor antagonist, Boc2, in wild type mice reproduced most of the behavioural changes observed in the Fpr2/3(-/-) mice, including a significant improvement in novel object discrimination and reduced anxiety in a light/dark shuttle test. These effects were associated with reduced FPR signalling in the gut as shown by the significant reduction in the levels of p-p38. Collectively, these findings suggest that homeostatic FPR signalling exerts a modulatory effect on anxiety-like behaviours. These findings thus suggest that therapies targeting FPRs may be a novel approach to ameliorate behavioural abnormalities present in neuropsychiatric disorders at the cognitive-emotional interface