Musculoskeletal pain intensity in different body regions and risk of disability pension among female eldercare workers: prospective cohort study with 11-year register follow-up

Background Musculoskeletal pain is a risk factor for leaving the labour market temporarily and permanently. While the presence of multi-site pain increases the risk of disability pension, we lack detailed knowledge about pain intensity as a risk factor. This study investigated the association between musculoskeletal pain intensity in different body regions and risk of future disability pension among eldercare workers. Methods Eight thousand seven hundred thirty-one female eldercare workers replied to a questionnaire on work and health in 2005 and were followed for 11 years in the Danish Register for Evaluation of Marginalization. Time-to-event analyses estimated hazard ratios (HR) for disability pension from pain intensities (0-9 numeric rating scale (NRS)) in the low-back, neck/shoulders, and knees during the previous 3 months. Analyses were mutually adjusted for pain regions, age, education, lifestyle, psychosocial work factors, and physical exertion at work. Results During 11-year follow-up, 1035 (11.9%) of the eldercare workers received disability pension. For all body regions among all eldercare workers, dose-response associations were observed between higher pain intensity and risk of disability pension (p = 7 points on the 0-9 NRS) in the low-back (HR 2.19, 95% CI 1.70-2.82), neck/shoulders (HR 2.34, 95% CI 1.88-2.92), and knees (HR 1.89, 95% CI 1.44-2.47). Population attributable risks (PAR) were 15.5, 23.2, and 9.6% for pain > 2 on NRS in the low-back, neck/shoulders, and knees, respectively, indicating that 15.5, 23.2, and 9.6% fewer eldercare workers would likely receive disability pension if the pain intensity was reduced to 2 or less. For workers 45 years, PAR was highest for neck/shoulder pain (27.6%) and low-back pain (18.8%), respectively. Conclusions The present study found positive dose-response associations between pain intensity in the low-back, neck/shoulders, and knees, and risk of disability pension during 11-year follow-up. Moderate to very high levels of musculoskeletal pain in eldercare workers should, therefore, be considered an early warning sign of involuntary premature exit from the labour market. These findings underscore the importance of preventing, managing, and reducing musculoskeletal pain to ensure a long and healthy working life

Whipworm and roundworm infections

Trichuriasis and ascariasis are neglected tropical diseases caused by the gastrointestinal dwelling nematodes Trichuris trichiura (a whipworm) and Ascaris lumbricoides (a roundworm), respectively. Both parasites are staggeringly prevalent, particularly in tropical and subtropical areas, and are associated with substantial morbidity. Infection is initiated by ingestion of infective eggs, which hatch in the intestine. Thereafter, T. trichiura larvae moult within intestinal epithelial cells, with adult worms embedded in a partially intracellular niche in the large intestine, whereas A. lumbricoides larvae penetrate the gut mucosa and migrate through the liver and lungs before returning to the lumen of the small intestine, where adult worms dwell. Both species elicit type 2 anti-parasite immunity. Diagnosis is typically based on clinical presentation (gastrointestinal symptoms and inflammation) and the detection of eggs or parasite DNA in the faeces. Prevention and treatment strategies rely on periodic mass drug administration (generally with albendazole or mebendazole) to at-risk populations and improvements in water, sanitation and hygiene. The effectiveness of drug treatment is very high for A. lumbricoides infections, whereas cure rates for T. trichiura infections are low. Novel anthelminthic drugs are needed, together with vaccine development and tools for diagnosis and assessment of parasite control in the field

Analysis of norfloxacin ecotoxicity and the relation with its degradation by means of electrochemical oxidation using different anodes

[EN] In this work, ecotoxicological bioassays based on Lactuca sativa seeds and bioluminescent bacterium (Vibrio fischeri) have been carried out in order to quantify the toxicity of Norfloxacin (NOR) and sodium sulfate solutions, before and after treating them using electrochemical advanced oxidation. The effect of some process variables (anode material, reactor configuration and applied current) on the toxicity evolution of the treated solution has been studied. A NOR solution shows an EC50 (5 days) of 336 mg L-1 towards Lactuca sativa. This threshold NOR concentration decreases with sodium sulfate concentration, in solutions that contain simultaneously Norfloxacin and sodium sulfate. In every case considered in this work, the electrochemical advanced oxidation process increased the toxicity (towards both Lactuca sativa and Vibrio fischeri) of the solution. This toxicity increase is mainly due to the persulfate formation during the electrochemical treatment. From a final solution toxicity point of view, the best results were obtained using a BDD anode in a divided reactor applying the lowest current intensity.The authors are very grateful to the Ministerio de Economia y Competitividad (Projects CTQ2015-65202-C2-1-R and RTI2018-101341-B-C21) for their economic support.Montañés, M.; García Gabaldón, M.; Roca-Pérez, L.; Giner-Sanz, JJ.; Mora-Gómez, J.; Pérez-Herranz, V. (2020). Analysis of norfloxacin ecotoxicity and the relation with its degradation by means of electrochemical oxidation using different anodes. Ecotoxicology and Environmental Safety. 188:1-10. https://doi.org/10.1016/j.ecoenv.2019.109923S110188Banks, M. K., & Schultz, K. E. (2005). Comparison of Plants for Germination Toxicity Tests in Petroleum-Contaminated Soils. Water, Air, and Soil Pollution, 167(1-4), 211-219. doi:10.1007/s11270-005-8553-4Barreto, J. P. d. P., Araujo, K. C. d. F., de Araujo, D. M., & Martinez-Huitle, C. A. (2015). 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Regulatory T Cell Induction during Plasmodium chabaudi Infection Modifies the Clinical Course of Experimental Autoimmune Encephalomyelitis

BACKGROUND: Experimental autoimmune encephalomyelitis (EAE) is used as an animal model for human multiple sclerosis (MS), which is an inflammatory demyelinating autoimmune disease of the central nervous system characterized by activation of Th1 and/or Th17 cells. Human autoimmune diseases can be either exacerbated or suppressed by infectious agents. Recent studies have shown that regulatory T cells play a crucial role in the escape mechanism of Plasmodium spp. both in humans and in experimental models. These cells suppress the Th1 response against the parasite and prevent its elimination. Regulatory T cells have been largely associated with protection or amelioration in several autoimmune diseases, mainly by their capacity to suppress proinflammatory response. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we verified that CD4(+)CD25(+) regulatory T cells (T regs) generated during malaria infection (6 days after EAE induction) interfere with the evolution of EAE. We observed a positive correlation between the reduction of EAE clinical symptoms and an increase of parasitemia levels. Suppression of the disease was also accompanied by a decrease in the expression of IL-17 and IFN-γ and increases in the expression of IL-10 and TGF-β1 relative to EAE control mice. The adoptive transfer of CD4(+)CD25(+) cells from P. chabaudi-infected mice reduced the clinical evolution of EAE, confirming the role of these T regs. CONCLUSIONS/SIGNIFICANCE: These data corroborate previous findings showing that infections interfere with the prevalence and evolution of autoimmune diseases by inducing regulatory T cells, which regulate EAE in an apparently non-specific manner

Concurrent Helminthic Infection Protects Schoolchildren with Plasmodium vivax from Anemia

malaria in rural areas in the municipality of Careiro, in the Western Brazilian Amazon. (n = 9). In children without intestinal helminthes, a significant decrease in the hemoglobin during the malarial attack was seen as compared to the baseline concentration. In the survival analysis, no difference was seen in the time (in days) from the baseline cross-sectional to the first malarial infection, between parasitized and non-parasitized children.

Induction of CD4+CD25+FOXP3+ Regulatory T Cells during Human Hookworm Infection Modulates Antigen-Mediated Lymphocyte Proliferation

Hookworm infection is considered one of the most important poverty-promoting neglected tropical diseases, infecting 576 to 740 million people worldwide, especially in the tropics and subtropics. These blood-feeding nematodes have a remarkable ability to downmodulate the host immune response, protecting themselves from elimination and minimizing severe host pathology. While several mechanisms may be involved in the immunomodulation by parasitic infection, experimental evidences have pointed toward the possible involvement of regulatory T cells (Tregs) in downregulating effector T-cell responses upon chronic infection. However, the role of Tregs cells in human hookworm infection is still poorly understood and has not been addressed yet. In the current study we observed an augmentation of circulating CD4+CD25+FOXP3+ regulatory T cells in hookworm-infected individuals compared with healthy non-infected donors. We have also demonstrated that infected individuals present higher levels of circulating Treg cells expressing CTLA-4, GITR, IL-10, TGF-β and IL-17. Moreover, we showed that hookworm crude antigen stimulation reduces the number of CD4+CD25+FOXP3+ T regulatory cells co-expressing IL-17 in infected individuals. Finally, PBMCs from infected individuals pulsed with excreted/secreted products or hookworm crude antigens presented an impaired cellular proliferation, which was partially augmented by the depletion of Treg cells. Our results suggest that Treg cells may play an important role in hookworm-induced immunosuppression, contributing to the longevity of hookworm survival in infected people