Detection of the phototoxic dye phloxine B in \u3ci\u3eAnastrepha ludens\u3c/i\u3e (Loew) (Diptera: Tephritidae), \u3ci\u3eApis mellifera\u3c/i\u3e Linnaeus (Hymenoptera: Apidae) and honey

A spectrophotometric method for detection of phloxine B, a phototoxic dye proposed as a replacement for malathion bait sprays, in extracted tissues of Anastrepha ludens, Apis mellifera and in honey was developed. Dye detection was increased with a pH change from 6 to 13.7 in tissues or from 3.7 to 8 in honey with 2% sodium hydroxide. An LC 50 of 29.62 ppm phloxine B in 30% sucrose was obtained by feeding honey bees. A predictive model for dye in insect tissues and honey was developed and shown to be 89–92% effective. This study provides a forensic approach to determine if bees were killed or honey was contaminated by phloxine B sprays

Exploring Shared Trauma in the Time of COVID: A Simulation-Based Survey Study of Mental Health Clinicians

From fear of contracting the virus, isolation from physical distancing, to navigating lifework balance, the COVID-19 pandemic is expected to leave long-lasting psychosocial impacts on many. Shared trauma refers to similar psychological reactions to an extraordinary community event when experienced by both the clinicians and clients. We examined the experiences mong mental health clinicians in Canada and the United States (n = 196) in this online survey study during the second phase of the pandemic (Spring 2021). In addition to using traditional survey items (e.g., demographics, scales, and short answers), we also used video-recorded Simulated Clients (SC; i.e., professional actors) as a novel method to elicit the participants’ assessment of the SCs and the psychosocial impacts of the COVID-19 pandemic. Using shared trauma as a theoretical framework, we analyzed both quantitative and qualitative data. Quantitative results suggested that although these mental health clinicians certainly reported experiencing psychosocial impacts of the pandemic themselves, these shared experiences with client and general populations did not greatly impact how they understood the SCs. Qualitative results helped further contextualize the clinicians’ own personal and professional lives. Implications for clinical practice and further research related to shared trauma are discussed

The Na+/H+ Exchanger Controls Deoxycholic Acid-Induced Apoptosis by a H+-Activated, Na+-Dependent Ionic Shift in Esophageal Cells

Apoptosis resistance is a hallmark of cancer cells. Typically, bile acids induce apoptosis. However during gastrointestinal (GI) tumorigenesis the cancer cells develop resistance to bile acid-induced cell death. To understand how bile acids induce apoptosis resistance we first need to identify the molecular pathways that initiate apoptosis in response to bile acid exposure. In this study we examined the mechanism of deoxycholic acid (DCA)-induced apoptosis, specifically the role of Na+/H+ exchanger (NHE) and Na+ influx in esophageal cells. In vitro studies revealed that the exposure of esophageal cells (JH-EsoAd1, CP-A) to DCA (0.2 mM -0.5 mM) caused lysosomal membrane perturbation and transient cytoplasmic acidification. Fluorescence microscopy in conjunction with atomic absorption spectrophotometry demonstrated that this effect on lysosomes correlated with influx of Na+, subsequent loss of intracellular K+, an increase of Ca2+ and apoptosis. However, ethylisopropyl-amiloride (EIPA), a selective inhibitor of NHE, prevented Na+, K+ and Ca2+ changes and caspase 3/7 activation induced by DCA. Ouabain and amphotericin B, two drugs that increase intracellular Na+ levels, induced similar changes as DCA (ion imbalance, caspase3/7 activation). On the contrary, DCA-induced cell death was inhibited by medium with low a Na+ concentrations. In the same experiments, we exposed rat ileum ex-vivo to DCA with or without EIPA. Severe tissue damage and caspase-3 activation was observed after DCA treatment, but EIPA almost fully prevented this response. In summary, NHE-mediated Na+ influx is a critical step leading to DCA-induced apoptosis. Cells tolerate acidification but evade DCA-induced apoptosis if NHE is inhibited. Our data suggests that suppression of NHE by endogenous or exogenous inhibitors may lead to apoptosis resistance during GI tumorigenesis

Exosomes Released from Mycoplasma Infected Tumor Cells Activate Inhibitory B Cells

Mycoplasmas cause numerous human diseases and are common opportunistic pathogens in cancer patients and immunocompromised individuals. Mycoplasma infection elicits various host immune responses. Here we demonstrate that mycoplasma-infected tumor cells release exosomes (myco+ exosomes) that specifically activate splenic B cells and induce splenocytes cytokine production. Induction of cytokines, including the proinflammatory IFN-γ and the anti-inflammatory IL-10, was largely dependent on the presence of B cells. B cells were the major IL-10 producers. In splenocytes from B cell deficient μMT mice, induction of IFN-γ+ T cells by myco+ exosomes was greatly increased compared with wild type splenocytes. In addition, anti-CD3-stimulated T cell proliferation was greatly inhibited in the presence of myco+ exosome-treated B cells. Also, anti-CD3-stimulated T cell signaling was impaired by myco+ exosome treatment. Proteomic analysis identified mycoplasma proteins in exosomes that potentially contribute to the effects. Our results demonstrate that mycoplasma-infected tumor cells release exosomes carrying mycoplasma components that preferentially activate B cells, which in turn, are able to inhibit T cell activity. These results suggest that mycoplasmas infecting tumor cells can exploit the exosome pathway to disseminate their own components and modulate the activity of immune cells, in particular, activate B cells with inhibitory activity

The Genealogy of the Labor Hoarding Concept

The modern concept of labor hoarding emerged in early 1960s, and soon became a standard part of mainstream economists' explan ation of the working of labor markets. The concept represents the convergence of three importa nt elements: an empirical fi nding that labor productivity was procyclical; a framing of this fi nding as a "puzzle" or anomaly fo r the basic neoclassical theory of the firm, and a proposed resolu tion of the puzzle based on optimizing behavior of the firm in the presence of costs of hiring, firing, and training workers. Th is paper recounts the history of each of these elements, and how they were woven together into the labor hoarding concept. Each history involves people associated with various research traditions and motivated by an array of questions, many of which were unrelated to the qu estions that the modern labor hoarding concept was ultimately created to address

Cholesterol is required for the fusion of single unilamellar vesicles with Mycoplasma capricolum.

Small unilamellar vesicles (SUV) were prepared from the total lipid extract of Mycoplasma capricolum. The SUV were labeled with the fluorescent probe octadecylrhodamine B chloride (R18) to a level at which the R18 fluorescence was self-quenched. At pH 7.4 and 37 degrees C, and in the presence of 5% polyethylene glycol, an increase in the R18 fluorescence with time was observed when the R18-labeled SUV were introduced to a native M. capricolum cell suspension. The fluorescence dequenching resulting from dilution of the R18 into the unlabeled membranes of M. capricolum, was interpreted as a result of lipid mixing during fusion between the SUV and the mycoplasma cells. The presence of cholesterol in the SUV was found to be obligatory to allow SUV-mycoplasma fusion to occur. Adaptation of M. capricolum cells to grow in a medium containing low cholesterol concentration provided cells in which the unesterified cholesterol content was as low as 17 micrograms/mg cell protein. The fusion activity of the adapted cells was very low or nonexistent. Nonetheless, when an early exponential phase culture of the adapted cells was transferred to a cholesterol-rich medium, the cells accumulated cholesterol and regained their fusogenic activity. The cholesterol requirement for fusion in the target mycoplasma membrane was met by a variety of planar sterols having a free beta-hydroxyl group, but differing in the aliphatic side chain, e.g., beta-sitosterol or ergosterol, even though these sterols, having a bulky side chain, are preferentially localized in the outer leaflet of the lipid bilayer. It is suggested that the role of cholesterol in mycoplasma-SUV fusion is not at the level of bulk bilayer viscosity but rather, affecting local lipid-lipid or lipid-protein interactions that are relevant to the fusion event