3,895 research outputs found
Book Review: Grimwood, M and McHanwell, S. (2024) Evidencing Teaching Achievements in Higher Education. Critical Publishing.
No full textBook Review: Grimwood, M and McHanwell, S. (2024) Evidencing Teaching Achievements in Higher Education. Critical Publishing.
Christopher Little
Manchester Metropolitan University
Corresponding author: [email protected]
A Mixed-Method Approach for Quantifying Illegal Fishing and Its Impact on an Endangered Fish Species
No full textIllegal harvest is recognized as a widespread problem in natural resource management. The use of multiple methods for quantifying illegal harvest has been widely recommended yet infrequently applied. We used a mixed-method approach to evaluate the extent, charac- ter, and motivations of illegal gillnet fishing in Lake Hovsgol National Park, Mongolia and its impact on the lake’s fish populations, especially that of the endangered endemic Hovsgol grayling (Thymallus nigrescens). Surveys for derelict fishing gear indicate that gillnet fishing is widespread and increasing and that fishers generally use 3–4 cm mesh gillnet. Interviews with resident herders and park rangers suggest that many residents fish for subsistence during the spring grayling spawning migration and that some residents fish commercially year-round. Interviewed herders and rangers generally agree that fish population sizes are decreasing but are divided on the causes and solutions. Biological monitoring indicates that the gillnet mesh sizes used by fishers efficiently target Hovsgol grayling. Of the five species sampled in the monitoring program, only burbot (Lota lota) showed a significant decrease in population abundance from 2009–2013. However, grayling, burbot, and roach (Rutilus ruti- lus) all showed significant declines in average body size, suggesting a negative fishing impact. Data-poor stock assessment methods suggest that the fishing effort equivalent to each resident family fishing 50-m of gillnet 11–15 nights per year would be sufficient to over- exploit the grayling population. Results from the derelict fishing gear survey and interviews suggest that this level of effort is not implausible. Overall, we demonstrate the ability for a mixed-method approach to effectively describe an illegal fishery and suggest that these methods be used to assess illegal fishing and its impacts in other protected areas.Peer reviewe
Teacher formative assessment: the missing link in response to intervention
No full textResponse to Intervention (RtI) focuses on the assessment, intervention, and progress monitoring of student academic performance and social behavior. Despite requiring highly-qualified personnel for successful implementation, the implementation of Rtl has not focused on applying its foundational principles towards promoting teacher effectiveness through assessment, intervention, and progress monitoring of teacher classroom practice. Compounding this problem is the lack of availability of reliable and valid teacher assessments to apply in an Rtl model for teacher professional development. This chapter provides a rationale for applying RtI principles to teacher professional development and how teacher formative assessment can improve educator effectiveness, student learning, and social behaviors. The Classroom Strategies Scale (CSS, Reddy & Dudek, 2014), a new multidimensional assessment of instructional and behavioral management practices is discussed as an example of one promising tool for promoting teachers professional development within an Rtl model. We offer a synthesis of the theory, research, and evidence of reliability and validity of the CSS. The application of teacher formative assessment in job-embedded professional development/coaching models for schools is discussed. Finally, implications for practice and research are outlined.Peer reviewe
Heterozygous deletion of FOXA2 segregates with disease in a family with heterotaxy, panhypopituitarism, and biliary atresia
No full textBiliary atresia (BA) is a pediatric cholangiopathy with unknown etiology occurring in isolated and syndromic forms. Laterality defects affecting the cardiovascular and gastrointestinal systems are the most common features present in syndromic BA. Most cases are sporadic, although reports of familial cases have led to the hypothesis of genetic susceptibility in some patients. We identified a child with BA, malrotation, and interrupted inferior vena cava whose father presented with situs inversus, polysplenia, panhypopituitarism, and mildly dysmorphic facial features. Chromosomal microarray analysis demonstrated a 277 kb heterozygous deletion on chromosome 20, which included a single gene, FOXA2, in the proband and her father. This deletion was confirmed to be de novo in the father. The proband and her father share a common diagnosis of heterotaxy, but they also each presented with a variety of other issues. Further genetic screening revealed that the proband carried an additional protein-altering polymorphism (rs1904589; p.His165Arg) in the NODAL gene that is not present in the father, and this variant has been shown to decrease expression of the gene. As FOXA2 can be a regulator of NODAL expression, we propose that haploinsufficiency for FOXA2 combined with a decreased expression of NODAL is the likely cause for syndromic BA in this proband
Compound heterozygous mutations in NEK8 in siblings with end-stage renal disease with hepatic and cardiac anomalies
No full textWe studied two brothers who presented in the newborn period with cardiac, renal, and hepatic anomalies that were initially suggestive of ALGS, although no mutations in JAG1 or NOTCH2 were identified. Exome sequencing demonstrated compound heterozygous mutations intheNEK8gene (Never in mitosis A-related Kinase 8), a ciliary kinase indispensable for cardiac and renal development based on murine studies. The mutations included a c.2069_2070insC variant (p.Ter693LeufsTer86), and a c.1043C>T variant (p.Thr348Met) in the highly conserved RCC1 (Regulation of Chromosome Condensation 1) domain. The RCC1 domain is crucial for localization of the NEK8 protein to the centrosomes and cilia. Mutations in NEK8 have been previously reported in three fetuses (from a single family) with renal-hepatic-pancreatic dysplasia 2 (RHPD2), similar to Ivemark syndrome, and in three individuals with nephronophthisis (NPHP9). This is the third report of disease-causing mutations in the NEK8 gene in humans and only the second describing multi-organ involvement. The clinical features we describe differ from those in the previously published report in that (1) a pancreatic phenotype was not observed in the individuals reported here, (2) there were more prominent cardiac findings, (consistent with observations in murine models), and (3) we observed bile duct hypoplasia rather than ductal plate malformation.The patients reported here expand our understanding of the NEK8-associated phenotype. Our findings highlight the variable phenotypic expressivity and the spectrum of clinical manifestations due to mutations in the NEK8 gen
Replication of a GWAS signal in a Caucasian population implicates ADD3 in susceptibility to biliary atresia
No full textIn the United States, biliary atresia (BA) is the most frequent indication for liver transplantation in pediatric patients. BA is a complex disease, with suspected environmental and genetic risk factors. A genome-wide association study in Chinese patients identified association to the 10q24.2 (hg18) genomic region. This signal was upstream of two genes, XPNPEP1 and ADD3, both expressed in intrahepatic bile ducts. We tested association to this region in 171 BA patients and 1,630 controls of European descent and found the strongest signal to be at rs7099604 (p = 2.5 x 10(-3)) in intron 1 of the ADD3 gene. Moreover, expression data suggest that ADD3, but not XPNPEP1, is differentially expressed in BA patients. The role of ADD3 in biliary development is unclear, but our findings suggest that this gene may be functionally relevant for the development of BA
Oregon Justice Reinvestment Initiative: return on investment
No full textsubmitted to: Oregon Criminal Justice Commission ; principal investigator: Mauri Matsuda, Ph.D. ; co-investigators: Christopher Campbell, Ph.D., Christopher Dollar, M.S., Mark Leymon, Ph.D., Brian Renauer, Ph.D.This archived document is maintained by the State Library of Oregon as part of the Oregon Documents Depository Program. It is for informational purposes and may not be suitable for legal purposes.Includes bibliographical references (pages 38-39).Funded by: Oregon Criminal Justice Commission.Mode of access: Internet from the Oregon Government Publications Collection.Text in English
Pannexin-1 and P2X7-Receptor Are Required for Apoptotic Osteocytes in Fatigued Bone to Trigger RANKL Production in Neighboring Bystander Osteocytes
No full textOsteocyte apoptosis is required to induce intracortical bone remodeling after microdamage in animal models, but how apoptotic osteocytes signal neighboring “bystander” cells to initiate the remodeling process is unknown. Apoptosis has been shown to open pannexin-1 (Panx1) channels to release adenosine diphosphate (ATP) as a “find me” signal for phagocytic cells. To address whether apoptotic osteocytes use this signaling mechanism, we adapted the rat ulnar fatigue-loading model to reproducibly introduce microdamage into mouse cortical bone and measured subsequent changes in osteocyte apoptosis, receptor activator of NF-kB ligand (RANKL) expression and osteoclastic bone resorption in wild-type (WT; C57Bl/6) mice and in mice genetically deficient in Panx1 (Panx1KO). Mouse ulnar loading produced linear microcracks comparable in number and location to the rat model. WT mice showed increased osteocyte apoptosis and RANKL expression at microdamage sites at 3 days after loading and increased intracortical remodeling and endocortical tunneling at day 14. With fatigue, Panx1KO mice exhibited levels of microdamage and osteocyte apoptosis identical to WT mice. However, they did not upregulate RANKL in bystander osteocytes or initiate resorption. Panx1 interacts with P2X7R in ATP release; thus, we examined P2X7R-deficient mice and WT mice treated with P2X7R antagonist Brilliant Blue G (BBG) to test the possible role of ATP as a find-me signal. P2X7RKO mice failed to upregulate RANKL in osteocytes or induce resorption despite normally elevated osteocyte apoptosis after fatigue loading. Similarly, treatment of fatigued C57Bl/6 mice with BBG mimicked behavior of both Panx1 KO and P2X7RKO mice; BBG had no effect on osteocyte apoptosis in fatigued bone but completely prevented increases in bystander osteocyte RANKL expression and attenuated activation of resorption by more than 50%. These results indicate that activation of Panx1 and P2X7R are required for apoptotic osteocytes in fatigued bone to trigger RANKL production in neighboring bystander osteocytes and implicate ATP as an essential signal mediating this process.Peer reviewe
The protective effect of a diet rich in fish oil in an amphetamine toxicity model of Parkinson’s disease
No full textParkinson’s disease is a neurodegenerative disorder that damages the dopaminergic neurons of the substantia nigra and their axonal projections to the striatum. This cell death results in significant motor deficits that include muscular rigidity, resting tremor, and akinesia. Although there is no known cure for Parkinson’s disease, evidence from epidemiological studies suggests that consumption of fish oil, which is rich in omega-3 polyunsaturated fatty acids (PUFAs), may help to reduce the risk of this debilitating disorder. Furthermore, research using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) models of Parkinson’s disease supports this conclusion. Consequently, this dissertation examined the potential protective effect of fish oil in an amphetamine-toxicity model of Parkinson’s disease. In Experiment 1, mice were administered a diet rich in either corn oil or fish oil for one week and then were treated with either amphetamine or saline. After sacrifice 72 hours later, striatal tissue was assayed for neurochemical content using HPLC. It was determined that fish oil protects against amphetamine-induced depletions of dopamine and its metabolites. Given the role of oxidative stress in amphetamine toxicity, this protection may be a result of the antioxidant properties of fish oil. Experiment 2, in addition to successfully replicating this effect, extended the protective effect of fish oil to behavioral and physiological measures. More specifically, a diet rich in fish oil significantly altered amphetamine’s impact on behaviors including oral dyskinesia, self biting, stereotypy, and backwards walking; it also mitigated amphetamine-induced changes in dermal temperature. These results suggest that fish oil can moderate the elevated dopaminergic activity caused by amphetamine administration. Experiment 3 was designed to examine the time course of protection afforded by the fish oil-rich diet, and it was discovered that the protective effect of fish oil develops between 1 and 3 days of consumption. Experiment 4 was performed to determine if fish oil alters amphetamine-induced increases in oxidative stress and dopamine release. Fish oil did not impact these measures, indicating that other mechanisms may be responsible for the observed protection. Collectively, these findings indicate that the consumption of fish oil offers protection against amphetamine toxicity in a model of Parkinson’s disease.Ph. D.Includes bibliographical referencesIncludes vitaby Christopher M. Medveck
Heritability and Linkage Analysis of Appendicitis Utilizing Age at Onset
No full textAppendicitis usually afflicts the young, but there is a large tail in the distribution of onset age. The genetics of this disease are still not well understood. A heritability analysis and genome wide linkage analysis of a large twin dataset was undertaken. Treating age of onset of appendicitis as a censored survival trait revealed a heritability of 0.21, and found evidence of linkage to Chromosome 1p37.3. Author(s): Christopher Oldmeadow 1 * | Kerrie Mengersen 2 | Nicholas Martin 3 | David L. Duffy
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