Impact of asynchronous virtual learning on student well-being and success.

INTRODUCTION: As the world has rapidly changed during the COVID-19 pandemic, doctor of pharmacy (PharmD) students' overall well-being has been prioritized. This study aimed to evaluate PharmD students' well-being and perceived academic engagement when moved involuntarily to a majority asynchronous and virtual curriculum during the 2020-2021 academic year in response to the COVID-19 pandemic. Additionally, this study aimed to assess demographic predictors relating student well-being and academic engagement. METHODS: A survey administered via Qualtrics (SAP) was sent to three cohorts of professional students (Classes of 2022 to 2024) enrolled in the PharmD program at The Ohio State University College of Pharmacy. These cohorts were engaged in a primarily asynchronous and virtual curriculum due to COVID-19. RESULTS: Although students displayed mixed results on how asynchronous learning affected their well-being, students replied that they would want to continue learning via a hybrid model (53.3%) or completely asynchronous (24%), while 17.3% wanted primarily synchronous and 5.3% did not reply. CONCLUSIONS: Our results indicated that aspects of the majority asynchronous and virtual learning environment were favored by students. Through student responses, our faculty and staff can take into consideration students' opinions when making future changes to the curriculum. We provided this data for others to consider when evaluating well-being and engagement with a virtual and asynchronous curriculum.

Diabetes: how to manage diabetic peripheral neuropathy.

Diabetic peripheral neuropathy (DPN) is a major complication of diabetes mellitus. Tight glycaemic management focused on lowering haemoglobin A1C and increasing time in the target glucose range along with metabolic risk factor management form the cornerstone of DPN prevention. However, there is limited evidence supporting the efficacy of glycaemic and metabolic control in reducing the symptoms and complications of DPN, including pain once painful DPN develops. DPN treatments include pharmacological agents and non-pharmacological interventions such as foot care and lifestyle modifications. Pharmacological agents primarily address pain symptoms, which affect 25-35% of people with DPN. First-line agents include the anticonvulsants pregabalin and gabapentin, the serotonin-norepinephrine reuptake inhibitors duloxetine and venlafaxine, and secondary amine tricyclic antidepressants, including nortriptyline and desipramine. All agents have unique pharmacological, safety and clinical profiles, and agent selection should be guided by the presence of comorbidities, potential for adverse effects, drug interactions and costs. Even with the current treatment options, people are commonly prescribed less than the recommended dose of medications, leading to poor management of DPN symptoms and treatment discontinuation. By keeping up with the latest therapy algorithms and treatment options, healthcare professionals can improve the care for people with DPN.

Kidney toxicity of the BRAF-kinase inhibitor vemurafenib is driven by off-target ferrochelatase inhibition.

A multitude of disease and therapy related factors drive the frequent development of kidney disorders in cancer patients. Along with chemotherapy, the newer targeted therapeutics can also cause kidney dysfunction through on and off-target mechanisms. Interestingly, among the small molecule inhibitors approved for the treatment of cancers that harbor BRAF-kinase activating mutations, vemurafenib can trigger tubular damage and acute kidney injury. BRAF is a proto-oncogene involved in cell growth. To investigate the underlying mechanisms, we developed cell culture and mouse models of vemurafenib kidney toxicity. At clinically relevant concentrations vemurafenib induces cell-death in transformed and primary mouse and human kidney tubular epithelial cells. In mice, two weeks of daily vemurafenib treatment causes moderate acute kidney injury with histopathological characteristics of kidney tubular epithelial cells injury. Importantly, kidney tubular epithelial cell-specific BRAF gene deletion did not influence kidney function under normal conditions or alter the severity of vemurafenib-associated kidney impairment. Instead, we found that inhibition of ferrochelatase, an enzyme involved in heme biosynthesis contributes to vemurafenib kidney toxicity. Ferrochelatase overexpression protected kidney tubular epithelial cells and conversely ferrochelatase knockdown increased the sensitivity to vemurafenib-induced kidney toxicity. Thus, our studies suggest that vemurafenib-associated kidney tubular epithelial cell dysfunction and kidney toxicity is BRAF-independent and caused, in part, by off-target ferrochelatase inhibition.

SOX9 promotes stress-responsive transcription of VGF nerve growth factor inducible gene in renal tubular epithelial cells.

Acute kidney injury (AKI) is a common clinical condition associated with diverse etiologies and abrupt loss of renal function. In patients with sepsis, rhabdomyolysis, cancer, and cardiovascular disorders, the underlying disease or associated therapeutic interventions can cause hypoxia, cytotoxicity, and inflammatory insults to renal tubular epithelial cells (RTECs), resulting in the onset of AKI. To uncover stress-responsive disease-modifying genes, here we have carried out renal transcriptome profiling in three distinct murine models of AKI. We find that Vgf nerve growth factor inducible gene up-regulation is a common transcriptional stress response in RTECs to ischemia-, cisplatin-, and rhabdomyolysis-associated renal injury. The Vgf gene encodes a secretory peptide precursor protein that has critical neuroendocrine functions; however, its role in the kidneys remains unknown. Our functional studies show that RTEC-specific Vgf gene ablation exacerbates ischemia-, cisplatin-, and rhabdomyolysis-associated AKI in vivo and cisplatin-induced RTEC cell death in vitro Importantly, aggravation of cisplatin-induced renal injury caused by Vgf gene ablation is partly reversed by TLQP-21, a Vgf-derived peptide. Finally, in vitro and in vivo mechanistic studies showed that injury-induced Vgf up-regulation in RTECs is driven by the transcriptional regulator Sox9. These findings reveal a crucial downstream target of the Sox9-directed transcriptional program and identify Vgf as a stress-responsive protective gene in kidney tubular epithelial cells.

A comparative study of antiplaque and antigingivitis effects of herbal mouthrinse containing tea tree oil, clove, and basil with commercially available essential oil mouthrinse.

BACKGROUND: The relatively safe nature and cost-effectiveness of herbal extracts have led to a resurgent interest in their utility as therapeutic agents. Therefore, this prospective, double-blind, randomly controlled clinical trial was designed to compare the antiplaque and antigingivitis effects of newly formulated mouthrinse containing tea tree oil (TTO), clove, and basil with those of commercially available essential oil (EO) mouthrinse. MATERIALS AND METHODS: Forty patients were selected for a 21-day study period and randomly divided into two groups. The test group patients were given newly formulated herbal mouthrinse and the control group patients were given commercially available EO mouthrinse. The Plaque Index (PI), Gingival Index (GI), and Papillary Marginal Attachment (PMA) Index were recorded at baseline, 14 days, and 21 days. The microbial colony forming units (CFU) were assessed at baseline and 21 days. RESULTS: Test group patients using herbal mouthrinse showed significant improvement in GI (0.16), PI (0.57), and PMA (0.02) scores. These improvements were comparable to those achieved with commercially available EO mouthrinse. However, the aerobic and anaerobic CFU of microbiota were reduced with the herbal mouthrinse (P = 0.0000). CONCLUSION: The newly formulated herbal mouthrinse and commercially available mouthrinse were beneficial clinically as antiplaque and antigingivitis agents. Newly formulated mouthrinses showed significant reduction in microbial CFU at 21 days. So, our findings support the regular use of herbal mouthrinse as an antiplaque, antigingivitis, and antimicrobial rinse for better efficacy.

Listeria: A foodborne pathogen that knows how to survive.

The foodborne pathogen Listeria is the causative agent of listeriosis, a severe disease with high hospitalization and case fatality rates. Listeria monocytogenes can survive and grow over a wide range of environmental conditions such as refrigeration temperatures, low pH and high salt concentration. This allows the pathogen to overcome food preservation and safety barriers, and pose a potential risk to human health. This review focuses on the key issues such as survival of the pathogen in adverse environments, and the important adaptation and survival mechanisms such as biofilm formation, quorum sensing and antimicrobial resistance. Studies on the development of technologies to prevent and control L. monocytogenes contamination in foods and food processing facilities are also discussed.

Efficacy of chlorine and calcinated calcium treatment of alfalfa seeds and sprouts to eliminate Salmonella.

The efficacy of a 20,000 ppm calcium hypochlorite treatment of alfalfa seeds artificially contaminated with Salmonella was studied. Salmonella populations reached >7.0 log on sprouts grown from seeds artificially contaminated with Salmonella and then treated with 20,000 ppm Ca(OCl)(2). The efficacy of spray application of chlorine (100 ppm) to eliminate Salmonella during germination and growth of alfalfa was assessed. Alfalfa seed artificially contaminated with Salmonella was treated at germination, on day 2 or day 4, or for the duration of the growth period. Spray application of 100 ppm chlorine at germination, day 2, or day 4 of growth was minimally effective resulting in approximately a 0.5-log decrease in population of Salmonella. Treatment on each of the 4 days of growth reduced populations of Salmonella by only 1.5 log. Combined treatment of seeds with 20,000 ppm Ca(OCl)(2) and followed by 100 ppm chlorine or calcinated calcium during germination and sprout growth did not eliminate Salmonella.

Exposure of Salmonella Enteritidis to chlorine or food preservatives decreases [corrected] susceptibility to antibiotics.

Mutants of Salmonella Enteritidis selected following exposure to the sanitizer chlorine or to the preservatives sodium nitrite, sodium benzoate or acetic acid show resistance to multiple antibiotics (tetracycline, chloramphenicol, nalidixic acid, and ciprofloxacin). Complementation experiments with a functional marR restored antibiotic susceptibility of selected mutants to levels similar to wild-type strains, suggesting that mar mutation was responsible for resistance. The multiple antibiotic resistance (mar) operon is a global regulator controlling intrinsic resistance towards structurally and functionally unrelated antibiotics and other noxious agents. Mutants selected after exposure to an inducing agent maintained elevated antibiotic resistance after serial subculture in media void of the inducing agent. Results highlight the importance of monitoring the use of antimicrobial agents to ensure that concentrations capable of inactivating target pathogens are used.