Nanobubble ozone treatment effects on cyanobacterial biomass and cyanotoxins in a small eutrophic lake

Cyanobacterial harmful algal blooms (CHABs) fueled by excessive nutrient runoff are becoming an increasing problem worldwide. Nanobubble ozone technology (NBOT) is an emerging treatment to remediate lakes from CHABs. NBOT was tested in Lake Sylvan, a 42-acre manmade eutrophic lake that experiences annual CHABs. NBOTs were deployed from 7 July to 17 September 2021, and dosage was tripled on 9 August. CHAB chlorophyll, microcystins, and saxitoxins (among other parameters) were measured June to October 2021, spanning pre-NBOT, NBOT deployment, and post NBOT treatment. CHAB chlorophyll increased throughout July (peaking at 100 μg/L) then sharply declined following the increased dose (25-35 μg/L) but increased again 3 weeks (51-78 μg/L) after increased dose. CHAB chlorophyll spiked (80-95 μg/L) in early October after NBOT treatment. Microcystins steadily increased from \u3c0.15 to 2.5 μg/L throughout June and July and remained between 0.4 to 1.0 μg/L August – October. No contact advisories were posted during 2021 unlike previous years. Total saxitoxins rapidly increased in mid-July peaking at 4 μg/L, and then declined. Several large rainstorms (10 cm/d) occurred during NBOT treatment which may contributed nutrients. These storms complicated the evaluation of NBOT efficacy. Lake Sylvan will be monitored in 2022 without NBOT treatment for baseline conditions

Field-scale evaluation of nanobubble ozone technology for cyanobacterial harmful algal bloom control

Effective Cyanobacterial Harmful Algal Bloom (CHAB) control strategies are needed to address recreational and drinking water impacts. Nanobubble ozone technology (NBOT) is an emerging treatment, but field-scale studies are limited. An 18-week NBOT treatment trial was conducted on a 42-acre CHAB impacted Ohio recreational lake in 2021. The trial was split into low ozone dose (60 g/h), higher dose (180 g/h), and pre- and post-treatment periods. Two multi-parameter sondes recorded continuous data and water samples and profiles were collected weekly at six sites and analyzed for nutrients, cyanotoxins, phytoplankton diversity and abundance, and additional parameters. Multi-spectral imagery was captured on seven drone flights and sediment cores were collected. Cyanobacteria chlorophyll concentrations sharply declined and remained low for four weeks after the ozone dose was increased, but concentrations increased in response to a 4.5” rain event. Microcystins and saxitoxins peaked at 2.5 and 4.0 µg/L during the low dose treatment period, then declined after increased ozone dose. Recreational CHAB advisories were not posted, in contrast to past summers. Residual ozone was only detected at NBOT unit locations, but ozone concentrations increased in held samples demonstrating potential for nanobubbles to release ozone over time. Additional NBOT trials are planned for 2022

Clinical findings, diagnostic test results, and treatment outcome in cats with hiatal hernia: 31 cases (1995-2018).

BackgroundInformation regarding clinical signs, assessment, treatment, and outcome in cats with hiatal hernia (HH) is limited.ObjectivesTo characterize the clinical presentation of HH and medical and surgical outcomes in a cohort of affected cats.AnimalsThirty-one client-owned cats with HH.MethodsMedical records of cats with HH were retrospectively reviewed for signalment, history, results of diagnostic tests, details of surgical and medical treatments, complications, and outcome. Long-term follow-up data were obtained by telephone communication. Relationships between clinical variables and outcome were evaluated by regression analysis.ResultsType I HH was present in 85.7% (24/28) of cats, and 64.5% (20/31) were >3 years of age at diagnosis. Twenty-one of 31 (67.7%) cats underwent surgical repair including phrenoplasty, esophagopexy, and left-sided gastropexy, and 10 of 31 cats were treated medically without surgery. Concurrent illness was common, and 77.4% cats had comorbidities. All cats survived to discharge, and median time to death or follow-up was 959 days (range, 3-4015 days). Cats treated medically survived longer than cats treated surgically, with median time to death or follow-up of 2559 and 771 days, respectively.Conclusions and clinical importanceType I HH is the most common type of HH in cats. A congenital etiology is possible, but many cats with HH were >3 years of age at diagnosis and suffered from comorbidities, including upper airway obstruction. Case selection and the presence of comorbidities likely influenced the outcome. Cats with HH may not be diagnosed until disease is advanced or concurrent illness draws attention to clinical signs

It's a tricky business! : the impact of identity work in negotiating research access

The process of gaining research access in the social sciences is becoming increasingly difficult. Changes in legislation and an increasingly managerialist and risk-averse approach to service provision have contributed to organizations adopting a protectionist stance when it comes to granting research access. The student researcher’s experience of negotiating this research access landscape has been neglected. This article explores the findings from three case studies of gaining research access to social service organizations for the purpose of undertaking PhD research. It outlines the reflexive approach which was adopted, through peer support and discussion groups, in order to develop the ideas presented. The article utilizes emerging evidence, policy and identity theory to contextualize and develop understanding around the difficulties experienced in these three case studies. In particular the article highlights how issues of identity impact on the research access process. The article suggests strategies for gaining research access which could be adopted by student researchers, supervisors and universities. The article also recommends that issues to do with research governance and research access be considered in plans aimed at developing social work research capacity

Knowledge and/as power : a feminist critique of trade related intellectual property rights

The article defines a research agenda that explores the relationship between gender, knowledge, innovation, and property rights against the backdrop of the recent processes of market liberalization and transformation of the relationship between states' and the global economy. It suggests that Trade Related Intellectual Property Rights are institutionalizing the historically exclusionary bounded definitions of what counts as knowledge, and thus denying the role of millions of women in the production of knowledge over time. It concludes that this property regime challenges women to engage in the struggle over meanings of knowledge, invention, and property

Hypomorphic Recessive Variants in SUFU Impair the Sonic Hedgehog Pathway and Cause Joubert Syndrome with Cranio-facial and Skeletal Defects

The Sonic Hedgehog (SHH) pathway is a key signaling pathway orchestrating embryonic development, mainly of the CNS and limbs. In vertebrates, SHH signaling is mediated by the primary cilium, and genetic defects affecting either SHH pathway members or ciliary proteins cause a spectrum of developmental disorders. SUFU is the main negative regulator of the SHH pathway and is essential during development. Indeed, Sufu knock-out is lethal in mice, and recessive pathogenic variants of this gene have never been reported in humans. Through whole-exome sequencing in subjects with Joubert syndrome, we identified four children from two unrelated families carrying homozygous missense variants in SUFU. The children presented congenital ataxia and cerebellar vermis hypoplasia with elongated superior cerebellar peduncles (mild "molar tooth sign"), typical cranio-facial dysmorphisms (hypertelorism, depressed nasal bridge, frontal bossing), and postaxial polydactyly. Two siblings also showed polymicrogyria. Molecular dynamics simulation predicted random movements of the mutated residues, with loss of the native enveloping movement of the binding site around its ligand GLI3. Functional studies on cellular models and fibroblasts showed that both variants significantly reduced SUFU stability and its capacity to bind GLI3 and promote its cleavage into the repressor form GLI3R. In turn, this impaired SUFU-mediated repression of the SHH pathway, as shown by altered expression levels of several target genes. We demonstrate that germline hypomorphic variants of SUFU cause deregulation of SHH signaling, resulting in recessive developmental defects of the CNS and limbs which share features with both SHH-related disorders and ciliopathies