Patients' and caregivers' experiences of virtual care in a primary care setting during the COVID-19 pandemic: A patient-oriented research study.

Objective: This study explored patient and caregiver expectations and experiences of virtual primary care in Manitoba, Canada. This study focused on accessibility of care, acceptability and perceptions of quality from 'users' of primary healthcare services. Due to the rapid implementation of virtual primary care during the COVID-19 pandemic in Canada, patient/public input was largely bypassed. Methods: A mixed method was conducted in collaboration with Patient and Caregiver Community Advisors. Data was obtained from 696 surveys and 9 focus groups (n = 41 patients and caregivers). Results: Data suggest good acceptance of virtual visits, although considered a new experience despite almost exclusive use of the telephone. Participants preferred more input for choosing the type of visit but experienced less stress, time and inconvenience by using virtual care. There were mixed opinions of quality. More complex visits were associated with incomplete consultations and serve as one exemplar of the limitations due to lack of physical presence or contact. Unique communication skills were required to convey health concerns adequately and accurately. A more transactional approach was perceived from the lack of visual cues and the awkwardness associated with pauses during the phone conversation. Virtual care may be better used for certain circumstances but should encompass patient-centred decision making for when and how. Many expressed interests in video options; technology access and user ability are additional considerations for advancing virtual care. Conclusions: The experiences and recommendations from patients and caregivers provide an important contribution to decision-making and integrating and sustaining quality virtual care for patient-centered healthcare service delivery. Keywords: Virtual care experiences, primary care, patient-oriented research, mixed methods, COVID-19.

Australian elapid snake envenomation in cats: Clinical priorities and approach.

Practical relevance: No fewer than 140 species of terrestrial snakes reside in Australia, 92 of which possess venom glands. With the exception of the brown tree snake, the venom-producing snakes belong to the family Elapidae. The venom of a number of elapid species is more toxic than that of the Indian cobra and eastern diamondback rattle snake, which has earned Australia its reputation for being home to the world's most venomous snakes. Clinical challenges: The diagnosis of elapid snake envenomation is not always easy. Identification of Australian snakes is not straightforward and there are no pathognomonic clinical signs. In cats, diagnosis of envenomation is confounded by the fact that, in most cases, there is a delay in seeking veterinary attention, probably because snake encounters are not usually witnessed by owners, and also because of the tendency of cats to hide and seek seclusion when unwell. Although the administration of antivenom is associated with improved outcomes, the snake venom detection kit and antivenom are expensive and so their use may be precluded if there are financial constraints. Evidence base: In providing comprehensive guidance on the diagnosis and treatment of Australian elapid snake envenomation in cats, the authors of this review draw on the published veterinary, medical and toxicology literature, as well as their professional experience as specialists in medicine, and emergency medicine and critical care.

Molecular diagnosis of sparganosis associated with pneumothorax in a dog.

Pneumothorax was diagnosed in a dog presenting with progressive exercise intolerance and tachypnoea. Needle thoracocentesis failed to resolve the pneumothorax, and an exploratomy thoracotomy was performed. Upon inspection of the thoracic cavity, numerous white nodules (2 to 4mm) were present throughout the mediastinum, parietal pleura and the lung lobes. The owners of the dog elected intra-operative euthanasia, and a post mortem examination was performed. At necropsy, structures consistent with the plerocercoid (larval) stage of a tapeworm were identified in association with inflammation of the pleural cavity. Molecular methods were used to identify the parasite as Spirometra erinacei. Molecular diagnosis, along with the clinical presentation and pathological findings, allowed the diagnosis of proliferative sparganosis.

A redox-active isopropylmalate dehydrogenase functions in the biosynthesis of glucosinolates and leucine in Arabidopsis.

We report a detailed functional characterization of an Arabidopsis isopropylmalate dehydrogenase (AtIPMDH1) that is involved in both glucosinolate biosynthesis and leucine biosynthesis. AtIPMDH1 shares high homology with enzymes from bacteria and yeast that are known to function in leucine biosynthesis. In plants, AtIPMDH1 is co-expressed with nearly all the genes known to be involved in aliphatic glucosinolate biosynthesis. Mutation of AtIPMDH1 leads to a significant reduction in the levels of free leucine and of glucosinolates with side chains of four or more carbons. Complementation of the mutant phenotype by ectopic expression of AtIPMDH1, together with the enzyme's substrate specificity, implicates AtIPMDH1 in both glucosinolate and leucine biosynthesis. This functional assignment is substantiated by subcellular localization of the protein in the chloroplast stroma, and the gene expression patterns in various tissues. Interestingly, AtIPMDH1 activity is regulated by a thiol-based redox modification. This work characterized an enzyme in plants that catalyzes the oxidative decarboxylation step in both leucine biosynthesis (primary metabolism) and methionine chain elongation of glucosinolates (specialized metabolism). It provides evidence for the hypothesis that the two pathways share a common origin, and suggests a role for redox regulation of glucosinolate and leucine synthesis in plants.

Inhibition of osteoblast apoptosis by thrombin.

The multifunctional serine protease thrombin has been shown to be a specific agonist for a variety of functional responses of cells including osteoblasts. The current study was conducted to determine if thrombin was capable of inhibiting apoptosis in osteoblasts, and if so, to examine the mechanism by which this occurred. Thrombin (20-100 nM) significantly inhibited apoptosis in serum-starved cultures of the human osteoblast-like Saos-2 cell line and cultures of primary osteoblasts isolated from mouse calvariae, as well as dexamethasone-treated primary mouse osteoblasts. Inhibition of serum deprivation-induced apoptosis was shown to require thrombin's specific proteolytic activity. Primary mouse osteoblasts were found to express two functional thrombin receptors, PAR-1 and PAR-4. Thrombin inhibited serum deprivation-induced apoptosis in osteoblasts isolated from PAR-1 null mice to the same degree as in osteoblasts isolated from wild-type mice. Treatment of serum-deprived osteoblasts, isolated from either PAR-1 null or wild-type mice, with a PAR-4-activating peptide failed to significantly inhibit apoptosis compared to the relevant control. Medium conditioned by thrombin-treated osteoblasts, in which thrombin had been inactivated, was able to inhibit serum deprivation-induced osteoblast apoptosis almost as well as thrombin itself. Blocking protein synthesis, by cycloheximide pretreatment of the conditioning cells, prevented this action. The ability of known osteoblast survival factors, such as transforming growth factor beta1, fibroblast growth factor-2, insulin-like growth factor-II, and interleukin-6, to inhibit serum deprivation-induced osteoblast apoptosis was also tested. None of these factors was able to inhibit serum deprivation-induced osteoblast apoptosis to the same extent as thrombin. The results presented here demonstrate that thrombin treatment of osteoblasts inhibits apoptosis induced either by dexamethasone or by serum deprivation. Furthermore, it does so independently of the known thrombin receptors by bringing about the synthesis and/or secretion of an unknown survival factor or factors, which then act in an autocrine fashion to inhibit apoptosis.