Miracle-dz/UniFAR-FTUs huggingface dataset:
Sex recognition by odour and variation in the uropygial gland secretion in starlings.

1. Although a growing body of evidence supports that olfaction based on chemical compounds emitted by birds may play a role in individual recognition, the possible role of chemical cues in sexual selection of birds has been only preliminarily studied. 2. We investigated for the first time whether a passerine bird, the spotless starling Sturnus unicolor, was able to discriminate the sex of conspecifics by using olfactory cues and whether the size and secretion composition of the uropygial gland convey information on sex, age and reproductive status in this species. 3. We performed a blind choice experiment during mating, and we found that starlings were able to discriminate the sex of conspecifics by using chemical cues alone. Both male and female starlings preferred male scents. Furthermore, the analysis of the chemical composition of the uropygial gland secretion by using gas chromatography-mass spectrometry (GC-MS) revealed differences between sexes, ages and reproductive status. 4. In conclusion, our study reveals for first time that a passerine species can discriminate the sex of conspecifics by relying on chemical cues and suggests that the uropygial gland secretion may potentially function as a chemical signal used in mate choice and/or intrasexual competition in this species.
Endothelin Induces Rapid, Dynamin-mediated Budding of Endothelial Caveolae Rich in ET-B*

Background: Whether physiological ligands can regulate caveolae trafficking in endothelial cells is unknown. Results: ET-B is concentrated in endothelial caveolae. Endothelins are very potent stimulators of rapid dynamin-mediated internalization of caveolae and their cargo in endothelial cells in vitro and under native conditions in tissue. Conclusion: Caveolae can mediate rapid endocytosis when induced by select GPCR ligands. Significance: We reveal a new function for endothelin in regulated caveolae trafficking in endothelial cells. Clathrin-independent trafficking pathways for internalizing G protein-coupled receptors (GPCRs) remain undefined. Clathrin-mediated endocytosis of receptors including ligand-engaged GPCRs can be very rapid and comprehensive (<10 min). Caveolae-mediated endocytosis of ligands and antibodies has been reported to be much slower in cell culture (≫10 min). Little is known about the role of physiological ligands and specific GPCRs in regulating caveolae trafficking. Here, we find that one receptor for endothelin, ET-B but not ET-A, resides on endothelial cell surfaces in both tissue and cell culture primarily concentrated within caveolae. Reconstituted cell-free budding assays show that endothelins (ETs) induce the fission of caveolae from endothelial plasma membranes purified from rat lungs. Electron microcopy of lung tissue sections and tissue subcellular fractionation both show that endothelin administered intravascularly in rats also induces a significant loss of caveolae at the luminal surface of lung vascular endothelium. Endothelial cells in culture show that ET stimulates very rapid internalization of caveolae and cargo including caveolin, caveolae-targeting antibody, and itself. The ET-B inhibitor BQ788, but not the ET-A inhibitor BQ123, blocks the ET-induced budding of caveolae. Both the pharmacological inhibitor Dynasore and the genetic dominant negative K44A mutant of dynamin prevent this induced budding and internalization of caveolae. Also shRNA lentivirus knockdown of caveolin-1 expression prevents rapid internalization of ET and ET-B. It appears that endothelin can engage ET-B already highly concentrated in caveolae of endothelial cells to induce very rapid caveolae fission and endocytosis. This transport requires active dynamin function. Caveolae trafficking may occur more rapidly than previously documented when it is stimulated by a specific ligand to signaling receptors already located in caveolae before ligand engagement.
Extracellular Signal-regulated Kinase (ERK) Regulates Cortactin Ubiquitination and Degradation in Lung Epithelial Cells*

Background: Cortactin is essential for barrier integrity. Results: ERK inhibition attenuates cortactin phosphorylation, ubiquitination, and degradation via the β-Trcp-mediated ubiquitin-proteasome system. Conclusion: Cortactin stability is coordinately regulated by stress kinases and the ubiquitin-proteasomal network. Significance: Understanding cortactin stability provides new targets to regulate epithelial barrier integrity. Cortactin, an actin-binding protein, is essential for cell growth and motility. We have shown that cortactin is regulated by reversible phosphorylation, but little is known regarding cortactin protein stability. Here, we show that lipopolysaccharide (LPS)-induced cortactin degradation is mediated by extracellular regulated signal kinase (ERK). LPS induces cortactin serine phosphorylation, ubiquitination, and degradation in mouse lung epithelia, an effect abrogated by ERK inhibition. Serine phosphorylation sites mutant, cortactinS405A/S418A, enhances its protein stability. Cortactin is polyubiquitinated and degraded within the proteasome, whereas a cortactinK79R mutant exhibited proteolytic stability during cyclohexamide (CHX) or LPS treatment. The E3 ligase subunit β-Trcp interacts with cortactin, and its overexpression reduced cortactin protein levels, an effect attenuated by ERK inhibition. Overexpression of β-Trcp was sufficient to reduce the protective effects of exogenous cortactin on epithelial cell barrier integrity, an effect not observed after expression of a cortactinK79R mutant. These results provide evidence that LPS modulation of cortactin stability is coordinately regulated by stress kinases and the ubiquitin-proteasomal network.
A Systematic Review of Intervention Studies Using Health Action Process Approach (HAPA) Model Components to Prevent and Manage Chronic Diseases

BACKGROUND The HAPA model and HAPA-like approaches (incorporating self-efficacy plus multiple motivational and volitional components) are increasingly applied in intervention studies. This review: 1) describes how HAPA-based approaches have been used to design or evaluate interventions to change behaviours for preventing/managing chronic disease; 2) examines the effectiveness of HAPA-based interventions. METHODS Relevant studies were identified, selected and synthesised as per our protocol: www.crd. york.ac. uk/PROSPERO/display_record. asp? ID=CRD42013003596 FINDINGS 402 of 669 potentially relevant papers initially identified were selected for full text review, with 54 studies included. Over half were published in the last 2 years and half were European. Apart from self-efficacy, intention/goal-setting was the most used, and risk perception the least used component. Most studies were trials and targeted exercise, diet and/or weight loss. Detailed data extraction is ongoing. DISCUSSION This review assesses the use and effectiveness of HAPA-based approaches in interventions, suggesting there is scope for their application to a wide range of preventative and disease management behaviours.
Biofilms in drinking water systems: a possible reservoir for Helicobacter pylori

A laboratory model system was utilised to investigate the persistence of Helicobacter pylori in mixed‐species heterotrophic biofilms. A single‐stage continuous culture vessel was linked to a modified‐Robbins device (mRD) incorporating removable stainless steel coupons. The system was innoculated with H. pylori (NCTC 11637) and the fate of the organism monitored by polymerase chain reaction (PCR) analysis. Helicobacter pylari was detected in biofilm material for a period of up to 192 h. Theoretical washout would have occurred at around 48 h thus detection of H. pylori for a prolonged period after theoretical washout suggested that the organism possessed the ability to persist in the mixed‐species heterotrophic biofilm. Preliminary studies using heat‐inactivated H. pylori showed that the organism was not detected in biofilm material at any time post‐challenge suggesting that the persistence of H. pylori in such material was a phenomenon requiring the organism to be in a viable state. Further investigations to assess the biological basis for the association of H. pylori with drinking water biofilms and the risk that this may pose to public health are being undertaken.
Global microbial ecology: biogeography and diversity of Vibrios as a model

An environmental source of cholera was hypothesized as early as the late nineteenth century by Robert Koch, but not proven because of the ability of Vibrio cholera, the causative agent of cholera, to enter a dormant phase between epidemics. Standard bacteriological procedures for isolation of the vibrios from the environmental samples, including water, between epidemics generally were unsuccessful. Vibrio cholera, a marine vibrio requiring salt for growth, enters into a dormant ‘viable but non‐culturable’ stage when conditions are unfavourable for growth and reproduction. The association of V. cholera with plankton, notably copepods, provides evidence for the environmental origin of cholera, as well as an explanation for the sporadic and erratic nature of cholera epidemics. Thus, the association of V. cholera with plankton was established only recently, allowing analysis of epidemic patterns of cholera, especially in those countries where cholera is endemic. The sporadic and erratic nature of cholera epidemics can now be related to climate and climate events, such as El Niño. Since zooplankton have been shown to harbour the bacterium and zooplankton blooms follow phytoplankton blooms, remote sensing can be employed to determine the relationship of cases of cholera with chlorophyll, as well as sea surface temperature (SST), ocean height, and turbidity.
Chapter 3: Theoretical Basis for Transcultural Care

Margaret Andrews, PhD, RN, CTN, FAAN1 Jeffrey R. Backstrand, PhD2 Joyceen S. Boyle, PhD, RN, CTN, FAAN3 Josepha Campinha-Bacote, PhD, MAR, PMHCNS-BC, CTN-A, FAAN4 Ruth E. Davidhizar, DNSc, RN, APRN, BC, FAAN (deceased)5 Dawn Doutrich, PhD, RN, CNS6 Mercedes Echevarria, DNP, APN7 Joyce Newman Giger, EdD, APRN, BC, FAAN8 Jody Glittenberg, PhD, RN, FAAN, TNS9 Carol Holtz, PhD, RN10 Marianne R. Jeffreys, EdD, RN11 Janet R. Katz, PhD, RN12 Marilyn R. McFarland, PhD, RN, FNP-BC, CTN-A13 Gloria J. McNeal, PhD, MSN, ACNS-BC, FAAN14 Dula F. Pacquiao, EdD, RN, CTN15 Irena Papadopoulos, PhD, MA, RN, RM, FHEA16 Larry Purnell, PhD, RN, FAAN17 Marilyn A. Ray, PhD, MA, RN, CTN-A18 Mary C. Sobralske, PhD, RN, CTN19 Rachel Spector, PhD, RN, CTN-A, FAAN20 Marian K. Yoder, EdD, RN21 Rick Zoucha, PhD, PMHCNS-BC, CTN22
Student and Teacher Effects of Elementary School Tracking: An Examination of a Rural Georgia School District

This study examines the effects of homogeneous and heterogeneous ability grouping on teacher and student performance within three elementary schools in a rural Georgia school district. Research methodologies included an analyses of standardized achievement test scores, a teacher questionnaire, and individual interviews with teachers. The analyses of standardized test scores revealed that 2nd grade students who were heterogeneously grouped performed significantly better on math and verbal skills than 2nd grade students who were homogeneously grouped. Teacher questionnaire responses did not reveal significant differences between homogeneous and heterogeneous years in student self-esteem, discipline, or classroom management. However, teachers who had formerly taught lower ability homogeneous classes, stated in interviews that discipline and student self-esteem was much improved for low ability students under heterogeneous grouping. Teacher questionnaire responses revealed that planning lessons and teaching the range of students were perceived to be more difficult under heterogeneous grouping than under homogeneous grouping. Effects of the grouping change upon teacher morale was also examined. ACKNOWLEDGMENTS This study was funded by the Bulloch County Board of Education through the Center for Rural Health and Research. The Center for Rural Health and Research, directed by Dr. Charlene M. Hanson, is part of the College of Health and Professional Studies at Georgia Southern University. The Board of Education collected scores from the Iowa Test of Basic Skills (ITBS) and arranged for the administration of the teacher questionnaires and interviews. Thanks all of the Board of Education staff, principals, instructional coordinators, school counselors, and teachers who participated in this study for their cooperation. I greatly appreciate the contribution of my thesis committee. Dr. Howard Kaplan, chair of the committee, gave direction and guidance for the thesis. I am also indebted to him for the training in program evaluation I received in my graduate program. Dr. Marilyn Morgan conducted a conscientious review of the thesis and served as a member of my committee. Dr. Jay Strickland served as a member of the committee and contributed many hours of guidance and instruction far above the call of duty through each stage of
Inactivation of Pink1 Gene in Vivo Sensitizes Dopamine-producing Neurons to 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and Can Be Rescued by Autosomal Recessive Parkinson Disease Genes, Parkin or DJ-1

Background: Mutations in Pink1 are associated with Parkinson disease. Results: Mouse Pink1 deficiency results in hypersensitivity to MPTP-induced dopaminergic neuronal loss, which can be rescued with expression of human Parkin or DJ-1. Conclusion: Pink1 gene can regulate response to exogenous stress. Significance: These results indicate how endogenous Pink1 plays an important role in management of exogenous stress in mouse brain. Mutations in the mitochondrial PTEN-induced kinase 1 (Pink1) gene have been linked to Parkinson disease (PD). Recent reports including our own indicated that ectopic Pink1 expression is protective against toxic insult in vitro, suggesting a potential role for endogenous Pink1 in mediating survival. However, the role of endogenous Pink1 in survival, particularly in vivo, is unclear. To address this critical question, we examined whether down-regulation of Pink1 affects dopaminergic neuron loss following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the adult mouse. Two model systems were utilized: virally delivered shRNA-mediated knockdown of Pink1 and germ line-deficient mice. In both instances, loss of Pink1 generated significant sensitivity to damage induced by systemic MPTP treatment. This sensitivity was associated with greater loss of dopaminergic neurons in the Substantia Nigra pars compacta and terminal dopamine fiber density in the striatum region. Importantly, we also show that viral mediated expression of two other recessive PD-linked familial genes, DJ-1 and Parkin, can protect dopaminergic neurons even in the absence of Pink1. This evidence not only provides strong evidence for the role of endogenous Pink1 in neuronal survival, but also supports a role of DJ-1 and Parkin acting parallel or downstream of endogenous Pink1 to mediate survival in a mammalian in vivo context.
Native Presynaptic Metabotropic Glutamate Receptor 4 (mGluR4) Interacts with Exocytosis Proteins in Rat Cerebellum*

Background: mGluR4 negatively modulates neurotransmission at glutamatergic synapses. Results: Using proteomic approaches, we show that native mGluR4 interacts with exocytosis proteins. Conclusion: Native mGluR4 could inhibit glutamate release via interactions with exocytosis proteins. Significance: Because mGluR4 plays key roles in regulation of neurotransmission and is considered as a promising target for treatment of various brain diseases, the identification of its mechanisms of action is fundamental. The eight pre- or/and post-synaptic metabotropic glutamatergic receptors (mGluRs) modulate rapid excitatory transmission sustained by ionotropic receptors. They are classified in three families according to their percentage of sequence identity and their pharmacological properties. mGluR4 belongs to group III and is mainly localized presynaptically. Activation of group III mGluRs leads to depression of excitatory transmission, a process that is exclusively provided by mGluR4 at parallel fiber-Purkinje cell synapse in rodent cerebellum. This function relies at least partly on an inhibition of presynaptic calcium influx, which controls glutamate release. To improve the understanding of molecular mechanisms of the mGluR4 depressant effect, we decided to identify the proteins interacting with this receptor. Immunoprecipitations using anti-mGluR4 antibodies were performed with cerebellar extracts. 183 putative partners that co-immunoprecipitated with anti-mGluR4 antibodies were identified and classified according to their cellular functions. It appears that native mGluR4 interacts with several exocytosis proteins such as Munc18-1, synapsins, and syntaxin. In addition, native mGluR4 was retained on a Sepharose column covalently grafted with recombinant Munc18-1, and immunohistochemistry experiments showed that Munc18-1 and mGluR4 colocalized at plasma membrane in HEK293 cells, observations in favor of an interaction between the two proteins. Finally, affinity chromatography experiments using peptides corresponding to the cytoplasmic domains of mGluR4 confirmed the interaction observed between mGluR4 and a selection of exocytosis proteins, including Munc18-1. These results could give indications to explain how mGluR4 can modulate glutamate release at parallel fiber-Purkinje cell synapses in the cerebellum in addition to the inhibition of presynaptic calcium influx.
Developing community-based tourism in South Africa : Addressing the missing link

Tourism has been widely proposed as a tool contributing to development. Community-based tourism (CBT) has been specifically recognised as a tourism development approach aimed at facilitating the development of disadvantaged communities. However, realising this potential is often difficult and it may additionally be jeopardised by the lack of specific structures intended to facilitate the CBT development process. Moreover, government entities should be the protagonists in facilitating CBT development. The aim of this paper is to draw attention to a possible gap between policies and practice in order to more effectively facilitate CBT development for the benefit of disadvantaged communities in South Africa. While CBT organisations operate in various parts of the world, South Africa lacks this structure. This paper, therefore, proposes a specific structure, to fill the gap between policies and practices in the facilitation of CBT development.
Interactions of Nucleolin and Ribosomal Protein L26 (RPL26) in Translational Control of Human p53 mRNA*

Background: Increased translation of p53 mRNA is important for stress induction of p53 protein. Results: RPL26 and nucleolin proteins interact with each other and with a double-stranded RNA structure in p53 mRNA to regulate p53 translation after stress. Conclusion: Nucleolin represses basal p53 translation and recruits RPL26 after cellular stress to enhance p53 translation. Significance: This study has increased our knowledge of the molecular details of the process regulating p53 induction. Ribosomal protein RPL26 enhances p53 translation after DNA damage, and this regulation depends upon interactions between the 5′- and 3′-UTRs of human p53 mRNA (Takagi, M., Absalon, M. J., McLure, K. G., and Kastan, M. B. (2005) Cell 123, 49–63; Chen, J., and Kastan, M. B. (2010) Genes Dev. 24, 2146–2156). In contrast, nucleolin (NCL) suppresses the translation of p53 mRNA and its induction after DNA damage. We confirmed reports that RPL26 and NCL interact with each other and then explored the potential role of this interaction in the translational control of p53 after stress. NCL repression of p53 translation utilizes both the 5′- and 3′-UTRs of p53 mRNA, and NCL binds to the same 5′-3′-UTR interaction region that is critical for the recruitment of RPL26 to p53 mRNA after DNA damage. We also found that NCL is able to oligomerize, consistent with a model in which NCL stabilizes this double-stranded RNA structure. We found that the RNA-binding domain of NCL participates in binding to p53 mRNA, is required for both NCL dimerization and NCL-mediated translational repression, and is the domain of NCL that interacts with RPL26. Excessive RPL26 disrupts NCL dimerization, and point mutations in the NCL-interacting region of RPL26 reduce NCL-RPL26 interactions and attenuate both RPL26 binding to human p53 mRNA and p53 induction by RPL26. These observations suggest a model in which the base pairings in the p53 UTR interaction regions are critical for both translational repression and stress induction of p53 by NCL and RPL26, respectively, and that disruption of a NCL-NCL homodimer by RPL26 may be the switch between translational repression and activation after stress.
Activation of Natural Killer T Cells Promotes M2 Macrophage Polarization in Adipose Tissue and Improves Systemic Glucose Tolerance via Interleukin-4 (IL-4)/STAT6 Protein Signaling Axis in Obesity*

Background: Obesity is associated with a state of chronic low grade inflammation. Results: Activation of natural killer T (NKT) cells attenuates inflammation in adipose tissue and improves systemic glucose homeostasis in mice at different stages of obesity. Conclusion: Upon activation, NKT cells have significant impact on inflammatory responses and systemic glucose tolerance in obesity. Significance: NKT-activating glycolipids may be useful in treating obesity-associated complications. Natural killer T (NKT) cells are important therapeutic targets in various disease models and are under clinical trials for cancer patients. However, their function in obesity and type 2 diabetes remains unclear. Our data show that adipose tissues of both mice and humans contain a population of type 1 NKT cells, whose abundance decreases with increased adiposity and insulin resistance. Although loss-of-function of NKT cells had no effect on glucose tolerance in animals with prolonged high fat diet feeding, activation of NKT cells by lipid agonist α-galactosylceramide enhances alternative macrophage polarization in adipose tissue and improves glucose homeostasis in animals at different stages of obesity. Furthermore, the effect of NKT cells is largely mediated by the IL-4/STAT6 signaling axis in obese adipose tissue. Thus, our data identify a novel therapeutic target for the treatment of obesity-associated inflammation and type 2 diabetes.
Autistic and Rett‐like features associated with 2q33.3–q34 interstitial deletion

We describe the fourth reported case of a de novo 2q33.3–q34 interstitial deletion and review the literature in attempt to identify relevant candidate genes. A 15‐month‐old female patient presented for evaluation with poor eye contact and developmental delay. She had microcephaly and mild dysmorphic features, such as downslanting palpebral fissures, high forehead, small mouth, high palate, and general hypotonia. At 30 months of age, she was referred to the genetic clinic for an evaluation of persistent developmental delay, autistic traits, and Rett‐like features, including bruxism and repetitive movement of the left hand. Chromosome analysis revealed 46,XX at the 550 band level. No abnormalities were found on analysis of MECP2 gene for Rett syndrome and a DNA methylation test for Prader–Willi syndrome. An array comparative genomic hybridization analysis revealed a de novo 2q33.3–q34 heterozygous deletion (206,048,173–211,980,867). The deletion was estimated to be 5.9 Mb in size and contained 34 known genes. Candidate genes were identified as NRP2, ADAM23, KLF7, CREB1, MAP2, UNC80, and LANCL1 for the 2q33.3–q34 interstitial deletion. © 2015 Wiley Periodicals, Inc.