Explore chapters and articles related to this topic
Physical Patient Ergonomics
Published in Richard J. Holden, Rupa S. Valdez, The Patient Factor, 2021
Linsey M. Steege, Lora Cavuoto, Barbara J. King
Other research has explored how the design of consumer products impacts posture and physical forces required to complete ADLs. For example, a study by Hensler et al. (2015) evaluated a new food packaging design for ease of opening by patients with hand osteoarthritis. Patients reported that food package design differentially influenced the force required, tear tab size, and palpability, which may reduce physical demands for patients with decreased hand strength and dexterity completing feeding tasks. In other work, Roda-Sales et al. (2019) investigated the effects of commercially available assistive devices on hand and arm posture, precision grasps, and contact forces during meal preparation (opening cans or bottles, pouring), eating (utensil use and drinking), or grooming (brushing teeth and hair, and dressing) ADLs. Physical ergonomics can support selection of appropriate assistive devices, for example, which type of fork design will result in minimal postural deviation and allow for the best reach during eating, and inform the design of new products (e.g., a new utensil design) to support this type of patient work.
Ecology
Published in Paul Pumpens, Single-Stranded RNA Phages, 2020
Because of this rather high sensitivity as compared to the pathogenic viruses, the phage MS2 was considered a non-suitable indicator for the ionizing irradiation treatment. The phage MS2 was significantly more sensitive to ionizing radiation than E. coli (Gehringer et al. 2003). The inactivation rate of the phage MS2 was comparable but nevertheless different from those for feline and canine caliciviruses by ionizing, as well as nonionizing, radiation treatment (De Roda Husman et al. 2004). Later, the phage MS2 appeared as the most resistant organism against ionizing radiation when it was compared with E. coli, feline calicivirus, and poliovirus (Tree et al. 2005).
Birth choices in Eastern Europe and Russia
Published in Hannah Dahlen, Bashi Kumar-Hazard, Virginia Schmied, Birthing Outside the System, 2020
Daniela Drandić, Nicholas Rubashkin, Tamara Sadovaya, Svetlana Illarionova
I (Daniela) am a pro-choice researcher and advocate at Croatia’s largest non-profit organisation representing parents: RODA – Parents in Action. I work to improve maternity care in Croatia and in the Central and Eastern European Region. I am passionate about antenatal education, maternal choice and autonomy. I am also a board member of Human Rights in Childbirth and have headed campaigns on improving maternity care in Croatia, including #PrekinimoŠutnju (Break the Silence), a campaign featured in international media reports in 2015. In 2019, I coordinated the development and launch of Expecting, a mobile application for pregnant families. I live in Croatia with my partner and three children.
Association of Tear Cytokine Concentrations with Symptoms and Signs of Dry Eye Disease: Baseline Data from the Dry Eye Assessment and Management (DREAM) Study
Published in Current Eye Research, 2023
Neeta S. Roy, Yi Wei, Gui-Shuang Ying, Maureen G. Maguire, Penny A. Asbell
Past reports on tear cytokines have shown mixed results. McDonnell et al. study34 with analysis of 217 tear samples, showed no difference between controls and subjects with mild to moderate DED for levels of the cytokines IL-1β, IL-6, IL-17A, IFNγ, TNFα, IL-2, IL-4, IL-8, and IL-13, among others. These results are in contrast with Roda et al.39 a meta-analysis of tear cytokine studies in DED showed overall that higher levels of Il-1B, Il-6, Il-8, Il-10, IFNγ, TNFα in DED compared to tears from controls. Key issues that were noted in this review were the lack of consistency of cytokines findings between studies and no guidelines for cutoff values to differentiate abnormal from normal tear cytokine tear concentrations. The lack of a standardized approach to tear analysis was emphasized by the observation that of the 118 studies that met the most basic search criteria, only 13 met the inclusion criteria which included (1) study type: case-control; (2) population: patients having DED of any etiology; (3) purpose: measurement of pro-inflammatory mediator concentrations in tears; (4) outcome variables for qualitative synthesis: to report the different concentrations of tear cytokines between non-DED control subjects and DED patients.
Elevated internalization and cytotoxicity of polydispersed single-walled carbon nanotubes in activated B cells can be basis for preferential depletion of activated B cells in vivo
Published in Nanotoxicology, 2019
Taru S. Dutt, Md. Babu Mia, Rajiv K. Saxena
While the killing of B cells by AF-SWCNTs is not restricted to activated B cells as clearly shown by our in vitro data (Figure 4) as well as the fact that B cell proportion did fall (albeit to lesser extent), in control mice treated with AF-SWCNTs, activated B cells nonetheless seem to be significantly more susceptible to AF-SWCNTs than resting B cells. There are many situations (e.g. autoimmunity and B cell proliferative diseases) where overactive B cells need to be eliminated. Our results show that AF-SWCNTs could be a possible candidate agent to be further examined for this purpose. Many studies have examined the toxic effect of functionalized carbon nanotubes and in general have shown that generalized toxicity of carbon nanotubes is significantly reduced upon functionalization (Tang et al. 2012; Bari et al. 2013; Coccini, Manzo, and Roda 2013). A clear consensus about the toxic effects of carbon nanotubes toward different components of the immune system has not yet emerged. Even if AF-SWCNTs may turn out to be toxic in vivo to a certain extent, their short-term use for ablating activated B cells may out-weigh their general toxic effect in this time frame. A large number of toxic drugs are routinely used for deriving short-term treatments advantages. In this context, short-term use of AF-SWCNTs for depleting activated B cells in vivo may be worth examining.
Laboratory biomarkers in the diagnosis and follow-up of treatment of allergic bronchopulmonary aspergillosis in cystic fibrosis
Published in Critical Reviews in Clinical Laboratory Sciences, 2023
Sophie Steels, Marijke Proesmans, Xavier Bossuyt, Lieven Dupont, Glynis Frans
A schematic presentation of the pathophysiology of ABPA in CF is depicted in Figure 1. The conidia of Af are immunologically inactive because of the presence of a surface hydrophobin, RodA, which prevents immune recognition of the fungi by the host [16]. In hosts with impaired inflammatory response and defective clearance of conidia in the airways, e.g. asthma patients genetically predisposed to develop ABPA and CF patients, conidia can germinate into hyphae [9]. The germinating conidia shed their rodlet layer. This exposes fungal proteins like β-D-glucan and galactomannan [17]. The subsequent fungal growth causes exocytosis of several proteins, which is followed by the release of chemokines and cytokines and the activation of adaptive immune responses by T helper cells (Th) cells [17]. Dectin-1, a beta-glucan receptor expressed by dendritic cells and macrophages, is involved in innate immune recognition and triggers the pro-inflammatory cytokine and chemokine responses [18]. In normal circumstances, Aspergillus fungi are then eliminated by Th1 CD4+ T cell response, leading to macrophage and neutrophil-mediated phagocytosis [9]. In ABPA patients, the innate immune cells located in the lung (including epithelium, dendritic cells, and macrophages) recognize fungal pathogen-associated molecular patterns (beta-glucan, galactomannan and glycosaminogalactan) through pattern recognition receptors like Toll-like receptors (TLR) 2/4 and nucleotide-binding oligomerization domain-like receptors [9,17,19,20]. Activation of these receptors leads to the release of several chemo- and cytokines that then lead to a Th2 CD4+ T cell response in ABPA patients. The most important chemo- and cytokines released during this process by both innate and Th2-cells are chemokine ligand (CCL) 17, CCL22, thymal stromal lymphopoetin, interleukin (IL)-4, IL-5, and IL-13 [9,12,21,22]. CCL17 (historically called thymus- and activation-regulated chemokine, TARC) also attracts regulatory T cells via binding to C-C chemokine receptor type 4 (CCR4) and suppressing the protective Th1 response and macrophage activation that contribute to impaired fungal killing [21]. The continuous release of Th2-type cytokines causes a devastating inflammatory reaction through a combination of IgE production, mast cell degranulation, and the influx of neutrophils and eosinophils [9,21]. Besides raising the levels of total and Af-specific IgE (sIgE), the Th2 CD4+ T cell humoral response also leads to a polyclonal antibody response with the production of Af-specific IgG (sIgG) and IgA [19,23]. Granulocytic luminal mucus plugging and bronchocentric mucosal inflammation occur because of this immunological cascade, which eventually leads to bronchiectasis and may further progress to fibrosis if the condition remains untreated [21].