Bellingham Technical College

Increased tourism has augmented harassment to wildlife and posted signs are commonly used to manage such interactions. This study determined whether signs increased tourist compliance with regulations to remain >10 m from New Zealand fur seals (Arctocephalus forsteri) at Kaikoura Peninsula. We observed 362 tourist groups interacting with seals. The percentage of groups in which all members respected the posted distance was similar whether tourists saw the signs or not [60.6% vs. 65.9%; G(1) = 0.98, p = 0.32]. Results indicate that posted signs were ineffective in increasing compliance to regulations and suggest that alternative approaches must be considered to increase regulation compliance and better manage interactions between tourists and wildlife.

A unique citation identifier (CID) number is assigned to each article in the Proceedings of SPIE at the time of publication.Utilization of CIDs allows articles to be fully citable as soon as they are published online, and connects the same identifier to all online and print versions of the publication.SPIE uses a seven-digit CID article numbering system structured as follows: The first five digits correspond to the SPIE volume number. The last two digits indicate publication order within the volume using a Base 36 numbering system employing both numerals and letters.These two-number sets start with 00, 01, 02, 03, 04, 05, 06, 07, 08, 09, 0A, 0B … 0Z, followed by 10-1Z, 20-2Z, etc.The CID Number appears on each page of the manuscript.

Abstract BackgroundAdvances in ultrasensitive detection techniques for blood biomarkers allow the quantification of AD‐specific phosphorylated Tau proteins, including Tau phosphorylated at threonine 181 (pTau181) in patient plasma. pTau blood‐based biomarker have shown great promise as inclusion criteria and secondary endpoint evaluation in clinical trials.MethodThe University of British Columbia (UBC) CARD biobank plasma samples from clinically diagnosed AD and non‐AD patients were used to establish clinical and analytical validity of the pTau181 plasma assay per FDA fit‐for‐purpose guildelines (Neurcode USA, Inc.). We assessed the analytical measurement interval, clinical reportable range, linearity, intra‐laboratory precision, specimen stability, interference, and clinical performance.ResultThe pTau181 plasma assay provides a robust and accurate biomarker approach for independent determination of AD, with an AUC of 0.9 in our validation study cohort. The cut‐point (≥ 30 ng/L) had 100% sensitivity and 88% specificity for AD diagnosis in autopsy‐confirmed samples. The plasma pTau181 assay appears to be performing well as additional screening metric for inclusion of mild‐to‐moderate AD subjects in Phase 3 clinical trials (i.e. RETHINK‐ALZ and REFOCUS‐ALZ). 89% of the clinical sites participating in the REFOCUS‐ALZ study and 80% of sites participating in the RETHINK‐ALZ had at least 70% of screened subjects meeting this criterion.ConclusionAD plasma biomarker (pTau181) quantified using an RUO assay has great potential both as a diagnostic tool and to streamline clinical trials in AD.

Abstract Huntington’s Disease (HD) is a severe neurodegenerative disorder caused by expansion of the CAG trinucleotide repeat tract in the huntingtin gene. Inheritance of expanded CAG repeats is needed for HD manifestation, but further somatic expansion of the repeat tract in non-dividing cells, particularly striatal neurons, hastens disease onset. Called somatic repeat expansion, this process is mediated by the mismatch repair (MMR) pathway. Among MMR components identified as modifiers of HD onset, MutS Homolog 3 (MSH3) has emerged as a potentially safe and effective target for therapeutic intervention. Here, we identify fully chemically modified short interfering RNA (siRNA) that robustly silence MSH3in vitroandin vivo. When synthesized in a di-valent scaffold, siRNA-mediated silencing of MSH3 effectively blocked CAG repeat expansion in striatum of two HD mouse models without impacting tumor-associated microsatellite instability. Our findings establish a novel paradigm for treating patients with HD and other repeat expansion diseases.One Sentence SummarySilencing MSH3 in the CNS of two models of Huntington’s disease using di-valent siRNA blocks disease-accelerating somatic expansion of CAG repeats.

Autologous peripheral blood haematopoietic stem cell transplantation (HCT) cures 33%-40% of dogs with high-grade B-cell lymphoma. We hypothesized, based on human allogeneic bone marrow transplantation literature, that transplanting dogs using canine donor leukocyte-matched CD34+ cells would lead to fewer relapses and increased cure rates. We retrospectively reviewed medical records of dogs diagnosed with high-grade B-cell lymphoma who received an identical allogeneic HCT. A total of 15 dogs transplanted at four facilities were identified. Five of fifteen dogs relapsed before transplant. The mean number of donor CD34+ cells/kg harvested and infused into recipient dogs was 8.0 × 106 /kg (range: 2.08 × 106 /kg-2.9 × 107 /kg). The median disease-free interval and overall survival of all dogs was 1095 days (range: 9-2920 days) and 1115 days (range: 9-2920 days), respectively. Two of five dogs, not in remission at transplant, died in the hospital. The median disease-free interval and overall survival of the remaining three dogs was 25 days (range: 15-250 days) and 1100 days (range: 66-1902 days), respectively. The median disease-free interval and overall survival of the 10 dogs who had not relapsed was 1235 days (range: 19-2920 days) and 1235 days (range: 19-2920 days), respectively. One dog died soon after discharge of presumed gastric-dilatation-volvulus. Eight of nine remaining dogs lived >4yrs post-alloHCT, leading to a cure rate of 89%. Acute graft versus host disease was seen in three dogs. These results suggest that allogeneic HCT can cure ~50% more dogs than those treated with autologous HCT.

<p>Among the greatest constraints to accurately monitoring and understanding climate and climate change in many locations is limited in situ observing capacity and resolution in these places. Climate behaviours along with dependent environmental and societal processes are frequently highly localized, while observing systems in the region may be separated by hundreds of kilometers and may not adequately represent conditions between them. Similarly, generating climate equity in urban regions can be hindered by an inability to resolve urban heat islands at neighborhood scales. In both cases, higher density observations are necessary for accurate condition monitoring, research, and for the calibration and validation of remote sensing products and predictive models. Coincidentally, urban neighborhoods are heavily populated and thousands of individuals visit remote locations each day for recreational purposes. Many of these individuals are concerned about climate change and are keen to contribute to climate solutions. However, there are several challenges to creating a voluntary citizen science climate observing program that addresses these opportunities. The first is that such a program has the potential for limited uptake if participants are required to volunteer their time or incur a significant cost to participate. The second is that researchers and decision-makers may be reluctant to use the collected data owing to concern over observer bias. This paper describes the on-going development and implementation by 2DegreesC.org of a technology-driven citizen science approach in which participants are equipped with low-cost automated sensors that systematically sample and communicate scientifically valid climate observations while they focus on other activities (e.g., recreation, gardening, fitness). Observations are acquired by a cloud-based system that quality controls, anonymizes, and makes them openly available. Simultaneously, individuals of all backgrounds who share a love of the outdoors become engaged in the scientific process via data-driven communication, research, and educational interactions. Because costs and training are minimized as barriers to participation, data collection is opportunistic, and the technology can be used almost anywhere, this approach is dynamically scalable with the potential for millions of participants to collect billions of new, accurate observations that integrate with and enhance existing observational network capacity.</p>

A unique citation identifier (CID) number is assigned to each article in the Proceedings of SPIE at the time of publication. Utilization of CIDs allows articles to be fully citable as soon as they are published online, and connects the same identifier to all online and print versions of the publication. SPIE uses a seven-digit CID article numbering system structured as follows:

Patients with metaiodobenzylguanidine (MIBG)-avid relapsed or refractory neuroblastoma after initial therapy may exhibit transient responses to salvage treatment with iodine-131 metaiodobenzylguanidine (131 I-MIBG). It is unclear whether disease progression following 131 I-MIBG treatment occurs in previously involved versus new anatomic sites of disease. Understanding this pattern of relapse will inform the use of consolidation therapy following 131 I-MIBG administration. Patients with relapsed or refractory metastatic MIBG-avid neuroblastoma or ganglioneuroblastoma, who received single-agent 131 I-MIBG, had stable or responding disease 6-8weeks following 131 I-MIBG, but subsequently experienced disease progression were included. MIBG scans were reviewed to establish anatomic and temporal evolution of MIBG-avid disease. A total of 84 MIBG-avid metastatic sites were identified immediately prior to MIBG therapy in a cohort of 12 patients. At first progression, a total of 101 MIBG-avid sites were identified, of which 69 (68%) overlapped with pre-treatment disease sites, while 32 (32%) represented anatomically new disease areas. Eight of 12 patients had one or more new MIBG-avid sites at first progression. Of the 69 involved sites at progression that overlapped with pre-treatment disease, 11 represented relapsed sites that had cleared following MIBG therapy, two were persistent but increasingly MIBG-avid, and 56 were stably persistent. Previously involved anatomic disease sites predominate at disease progression following 131 I-MIBG treatment. Nevertheless, the majority of patients progressed in at least one new anatomic disease site. This suggests that consolidation focal therapies targeting residual disease sites may be of limited benefit in preventing systemic disease progression following 131 I-MIBG treatment of relapsed or refractory neuroblastoma.