Benefits of Veterinary Herd Health Management on German Dairy Farms: Status Quo and Farmers' Perspective.

Veterinary Herd Health Management plays an important role in veterinary medicine on dairy farms and has also been mandatory at the European Union level since April 21, 2021. Despite the increasing importance of VHHM, little is known about the extent of utilization of VHHM by dairy farmers and their view on this type of collaboration. Therefore, this cross-sectional study aimed to determine the status quo of the currently practiced VHHM in Germany. For this purpose, an online survey was conducted among dairy farmers in November and December 2020. From 216 analyzed questionnaires, about half (n = 106) of the surveyed dairy farmers used VHHM at different scopes. However, regardless of the group, the term "veterinary herd health management" generally was given most relative importance by the participants as a veterinary service for herd fertility improvement, rather than the actual definition of a holistic approach. In contrast to this, the actual motivation of the VHHM participants, to take part in such a program was primarily based on the desire to safeguard animal health by employing preventive measures, that is, to avoid the occurrence of diseases via improved management and to improve farm performance (and profitability). Dairy farmers who opted for VHHM tended to manage larger higher yielding herds than those who did not. Additionally, the farmers in latter farms were more likely to make joint animal health decisions with their veterinarians. Using a latent class analysis, two groups of farmers among farms that were not currently using VHHM were identified, one of which expressed great interest in using VHHM while the other did not. Since the new legal basis makes the topic even more relevant than before, dairy farmers, animals, and veterinarians might benefit from the study to exploit hidden opportunities for VHHM collaboration.

Angiotensin AT2-receptor stimulation improves survival and neurological outcome after experimental stroke in mice.

This study investigated the effect of post-stroke, direct AT2-receptor (AT2R) stimulation with the non-peptide AT2R-agonist compound 21 (C21) on infarct size, survival and neurological outcome after middle cerebral artery occlusion (MCAO) in mice and looked for potential underlying mechanisms. C57/BL6J or AT2R-knockout mice (AT2-KO) underwent MCAO for 30 min followed by reperfusion. Starting 45 min after MCAO, mice were treated once daily for 4 days with either vehicle or C21 (0.03 mg/kg ip). Neurological deficits were scored daily. Infarct volumes were measured 96 h post-stroke by MRI. C21 significantly improved survival after MCAO when compared to vehicle-treated mice. C21 treatment had no impact on infarct size, but significantly attenuated neurological deficits. Expression of brain-derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB) (receptor for BDNF) and growth-associated protein 43 (GAP-43) were significantly increased in the peri-infarct cortex of C21-treated mice when compared to vehicle-treated mice. Furthermore, the number of apoptotic neurons was significantly decreased in the peri-infarct cortex in mice treated with C21 compared to controls. There were no effects of C21 on neurological outcome, infarct size and expression of BDNF or GAP-43 in AT2-KO mice. From these data, it can be concluded that AT2R stimulation attenuates early mortality and neurological deficits after experimental stroke through neuroprotective mechanisms in an AT2R-specific way. Key message • AT2R stimulation after MCAO in mice reduces mortality and neurological deficits.• AT2R stimulation increases BDNF synthesis and protects neurons from apoptosis.• The AT2R-agonist C21 acts protectively when applied post-stroke and peripherally.

The endogenous cannabinoid system affects energy balance via central orexigenic drive and peripheral lipogenesis.

The cannabinoid receptor type 1 (CB1) and its endogenous ligands, the endocannabinoids, are involved in the regulation of food intake. Here we show that the lack of CB1 in mice with a disrupted CB1 gene causes hypophagia and leanness. As compared with WT (CB1+/+) littermates, mice lacking CB1 (CB1-/-) exhibited reduced spontaneous caloric intake and, as a consequence of reduced total fat mass, decreased body weight. In young CB1-/- mice, the lean phenotype is predominantly caused by decreased caloric intake, whereas in adult CB1-/- mice, metabolic factors appear to contribute to the lean phenotype. No significant differences between genotypes were detected regarding locomotor activity, body temperature, or energy expenditure. Hypothalamic CB1 mRNA was found to be coexpressed with neuropeptides known to modulate food intake, such as corticotropin-releasing hormone (CRH), cocaine-amphetamine-regulated transcript (CART), melanin-concentrating hormone (MCH), and preproorexin, indicating a possible role for endocannabinoid receptors within central networks governing appetite. CB1-/- mice showed significantly increased CRH mRNA levels in the paraventricular nucleus and reduced CART mRNA levels in the dorsomedial and lateral hypothalamic areas. CB1 was also detected in epidydimal mouse adipocytes, and CB1-specific activation enhanced lipogenesis in primary adipocyte cultures. Our results indicate that the cannabinoid system is an essential endogenous regulator of energy homeostasis via central orexigenic as well as peripheral lipogenic mechanisms and might therefore represent a promising target to treat diseases characterized by impaired energy balance.