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Animal-borne video cameras equipped with depth and temperature sensors were deployed on 16 reef manta rays (Mobula alfredi) in Raa Atoll, Maldives and 12 oceanic manta rays (Mobula birostris) in the Revillagigedo Archipelago, Mexico. These deployments provided descriptive behavioural data that give vital context to existing biotelemetry data and enabled a comparison of the social dynamics between the two manta ray species. Overall, cruising was the most dominant daytime behaviour recorded for both species. For M. alfredi , cleaning was the second most common behaviour, followed by courtship and feeding. No courtship behaviour was recorded for M. birostris. Across M. alfredi and M. birostris deployments, individuals spent an average of 43 and 8% of recorded time interacting with conspecifics, respectively. Sociability was higher in M. alfredi than M. birostris , however the findings should be interpreted with caution beyond the two deployment populations and times. Crittercams captured multiple courtship events of M. alfredi at depths greater than recreational scuba diving limits and captured previously undocumented interspecific interactions with M. mobular. Crittercam deployments also recorded M. alfredi travelling in groups and hugging the contours of the ocean floor, possibly as a tactic to reduce predation risk and/or improve swimming efficiency, enforcing the importance of this novel technology as a valuable tool to gain new insight into the ecological drivers of habitat use by these species. Lastly, these quantitative and descriptive results provide context for future hypothesis-driven research questions using animal-borne video cameras for mobulid rays. [ABSTRACT FROM AUTHOR]

I. Introduction Social media (1) has taken the world by storm. (2) As of 2016, over three billion people in the world are active Internet users, (1) and over two [...]

Manta and devil rays (collectively mobulids) belong to the monogeneric Mobulidae, which currently comprises 10 species, including a putative third manta ray species (Mobula cf. birostris). These large planktivorous rays are distributed throughout the tropical and subtropical oceans of the world. To date, six mobulid species are reported for the western Atlantic Ocean and the Caribbean Sea, three of which had previously been reported in Venezuela (Mobula birostris, Mobula tarapacana and Mobula hypostoma). A preliminary assessment of fishery landings and citizen science data was conducted to further the scientific knowledge of mobulid species in Venezuela. Fisheries landing data were collected at Margarita Island between 2006 and 2007, and again in 2014. Data mining of internet search engines and social media platforms spanning the past two decades was also conducted. A total of 117 individuals of five mobulid species were recorded: Mobula sp. (n = 27), M. birostris (n = 36), M. tarapacana (n = 3), Mobula mobular (n = 26), Mobula thurstoni (n = 14) and M. cf. birostris (n = 11). The latter three species are the first confirmation of these species in Venezuela. The authors found no records of the previously reported M. hypostoma during this study. Although the occurrence of M. hypostoma in Venezuela remains possible because of the broad regional range of this species, its current presence in Venezuela is invalidated given the repeated misidentifications which have occurred in previous publications. The results of this study increase the number of reported mobulid ray species in Venezuela to five (excluding M. hypostoma). The overall data from juvenile manta rays and pregnant M. mobular and M. thurstoni recorded in this study, combined with the occurrence of all but one species of mobulid ray found in the western Atlantic Ocean, suggest Venezuela provides important habitat for this threatened family of rays. [ABSTRACT FROM AUTHOR]

The mutagenesis of various complexes, including lysine 62, asparagine 64 and conserved region 1 is found to highly reduce the activity of the human ecto-ATPase (NTPDase) that contains several conserved motifs and lysine and arginine residues. The results show that most of the residues in the complex are essential for protein expression and that the substitution of such acidic residues by alanine leads to a decreased divalent ion binding.

In this study we examined the effects of exposure to the antiandrogenic fungicide vindozolin (Vz) on the development of two sex-differentiated behaviors that are organized by the perinatal actions of [...]

Background: The changing diabetes in children (CDiC) project is a public‐private partnership implemented by Novo Nordisk, to improve access to diabetes care for children with type 1 diabetes. This paper outlines the findings from an evaluation of CDiC in Bangladesh and Kenya, assessing whether CDiC has achieved its objectives in each of six core program components. Research design and methods: The Rapid Assessment Protocol for Insulin Access (RAPIA) framework was used to analyze the path of insulin provision and the healthcare infrastructure in place for diagnosis and treatment of diabetes. The RAPIA facilitates a mixed‐methods approach to multiple levels of data collection and systems analysis. Information is collected through questionnaires, in‐depth interviews and focus group discussions, site visits, and document reviews, engaging a wide range of stakeholders (N = 127). All transcripts were analyzed thematically. Results: The CDiC scheme provides a stable supply of free insulin to children in implementing facilities in Kenya and Bangladesh, and offers a comprehensive package of pediatric diabetes care. However, some elements of the CDiC program were not functioning as originally intended. Transitions away from donor funding and toward government ownership are a particular concern, as patients may incur additional treatment costs, while services offered may be reduced. Additionally, despite subsidized treatment costs, indirect costs remain a substantial barrier to care. Conclusion: Public‐private partnerships such as the CDiC program can improve access to life‐saving medicines. However, our analysis found several limitations, including concerns over the sustainability of the project in both countries. Any program reliant on external funding and delivered in a high‐turnover staffing environment will be vulnerable to sustainability concerns. [ABSTRACT FROM AUTHOR]

Key points: Intracerebroventricular insulin increased sympathetic nerve activity (SNA) and baroreflex control of SNA and heart rate more dramatically in obese male rats; in obese females, the responses were abolished.In obese males, the enhanced lumbar SNA (LSNA) responses were associated with reduced tonic inhibition of LSNA by neuropeptide Y (NPY) in the PVN. However, PVN NPY injection decreased LSNA similarly in obesity prone/obesity resistant/control rats. Collectively, these results suggest that NPY inputs were decreased. In obese females, NPY inhibition in the PVN was maintained. Moreover, NPY neurons in the arcuate nucleus became resistant to the inhibitory effects of insulin.A high‐fat diet did not alter arcuate NPY neuronal InsR expression in males or females.Obesity‐induced 'selective sensitization' of the brain to the sympathoexcitatory effects of insulin and leptin may contribute to elevated basal SNA, and therefore hypertension development, in males with obesity.These data may explain in part why obesity increases SNA less in women compared to men. Obesity increases sympathetic nerve activity (SNA) in men but not women; however, the mechanisms are unknown. We investigated whether intracerebroventricular insulin infusion increases SNA more in obese male than female rats and if sex differences are mediated by changes in tonic inhibition of SNA by neuropeptide Y (NPY) in the paraventricular nucleus (PVN). When consuming a high‐fat diet, obesity prone (OP) rats accrued excess fat, whereas obesity resistant (OR) rats maintained adiposity as in rats eating a control (CON) diet. Insulin increased lumbar SNA (LSNA) similarly in CON/OR males and females under urethane anaesthesia. The LSNA response was magnified in OP males but abolished in OP females. In males, blockade of PVN NPY Y1 receptors with BIBO3304 increased LSNA in CON/OR rats but not OP rats. Yet, PVN nanoinjections of NPY decreased LSNA similarly between groups. Thus, tonic PVN NPY inhibition of LSNA may be lost in obese males as a result of a decrease in NPY inputs. By contrast, in females, PVN BIBO3304 increased LSNA similarly in OP, OR and CON rats. After insulin, PVN BIBO3304 failed to increase LSNA in CON/OR females but increased LSNA in OP females, suggesting that with obesity NPY neurons become resistant to the inhibitory effects of insulin. These sex differences were not associated with changes in arcuate NPY neuronal insulin receptor expression. Collectively, these data reveal a marked sex difference in the impact of obesity on the sympathoexcitatory actions of insulin and implicate sexually dimorphic changes in NPY inhibition of SNA in the PVN as one mechanism. Key points: Intracerebroventricular insulin increased sympathetic nerve activity (SNA) and baroreflex control of SNA and heart rate more dramatically in obese male rats; in obese females, the responses were abolished.In obese males, the enhanced lumbar SNA (LSNA) responses were associated with reduced tonic inhibition of LSNA by neuropeptide Y (NPY) in the PVN. However, PVN NPY injection decreased LSNA similarly in obesity prone/obesity resistant/control rats. Collectively, these results suggest that NPY inputs were decreased. In obese females, NPY inhibition in the PVN was maintained. Moreover, NPY neurons in the arcuate nucleus became resistant to the inhibitory effects of insulin.A high‐fat diet did not alter arcuate NPY neuronal InsR expression in males or females.Obesity‐induced 'selective sensitization' of the brain to the sympathoexcitatory effects of insulin and leptin may contribute to elevated basal SNA, and therefore hypertension development, in males with obesity.These data may explain in part why obesity increases SNA less in women compared to men. [ABSTRACT FROM AUTHOR]

Human exposure to polycyclic aromatic hydrocarbons (PAH) is a significant and growing public health problem. Frequent, high dose exposures are likely to increase due to a warming climate and increased frequency of large-scale wildfires. Here, we characterize an epigenetic memory at the cytochrome P450 1A ( CYP1A ) gene in a population of wild Fundulus heteroclitus that has adapted to chronic, extreme PAH pollution. In wild-type fish, CYP1A is highly induced by PAH. In PAH-tolerant fish, CYP1A induction is blunted. Since CYP1A metabolically activates PAH, this memory protects these fish from PAH-mediated cancer. However, PAH-tolerant fish reared in clean water recover CYP1A inducibility, indicating that blunted induction is a non-genetic memory of prior exposure. To explore this possibility, we bred depurated wild fish from PAH-sensitive and - tolerant populations, manually fertilized exposure-naïve embryos, and challenged them with PAH. We observed epigenetic control of the reversible memory of generational PAH stress in F 1 PAH-tolerant embryos. Specifically, we observed a bivalent domain in the CYP1A promoter enhancer comprising both activating and repressive histone post-translational modifications. Activating modifications, relative to repressive ones, showed greater increases in response to PAH in sensitive embryos, relative to tolerant, consistent with greater gene activation. Also, PAH-tolerant adult fish showed persistent induction of CYP1A long after exposure cessation, which is consistent with defective CYP1A shutoff and recovery to baseline. Since CYP1A expression is inversely correlated with cancer risk, these results indicate that PAH-tolerant fish have epigenetic protection against PAH-induced cancer in early life that degrades in response to continuous gene activation., Competing Interests: Competing Interests The authors declare no competing interests.

Whether leptin acts in the paraventricular nucleus (PVN) to increase sympathetic nerve activity (SNA) is unclear, since PVN leptin receptors (LepR) are sparse. We show in rats that PVN leptin slowly increases SNA to muscle and brown adipose tissue, because it induces the expression of its own receptor and synergizes with local glutamatergic neurons. PVN LepR are not expressed in astroglia and rarely in microglia; instead, glutamatergic neurons express LepR, some of which project to a key presympathetic hub, the rostral ventrolateral medulla (RVLM). In PVN slices from mice expressing GCaMP6, leptin excites glutamatergic neurons. LepR are expressed mainly in thyrotropin-releasing hormone (TRH) neurons, some of which project to the RVLM. Injections of TRH into the RVLM and dorsomedial hypothalamus increase SNA, highlighting these nuclei as likely targets. We suggest that this neuropathway becomes important in obesity, in which elevated leptin maintains the hypothalamic pituitary thyroid axis, despite leptin resistance., Competing Interests: ZS, NP, JW, BL, AS, CM, DM, VB No competing interests declared, (© 2020, Shi et al.)