Vitamin D (VitD) has a role in the regulation of calcium and phosphate metabolism and in addition impacts the activity of the immune system. VitD deficiency might be linked to increased susceptibility to respiratory tract infection. The aim of the present study was to characterize the impact of VitD deficiency on the susceptibility to bacterial infection in murine models. C57BL/6N mice were fed a diet with or without VitD for 10 weeks. The VitD-deficient or -sufficient mice were infected with Pseudomonas aeruginosa or Streptococcus pneumoniae The colonization and inflammatory response in the lung were analyzed at defined time points. The serum 25-hydroxy-VitD concentration was significantly lower in mice on the VitD-deficient diet. In infection experiments with Pseudomonas aeruginosa or Streptococcus pneumoniae, no differences could be observed in the numbers of viable bacteria or in differential cell counts in the bronchoalveolar lavage fluids. Measurements of inflammatory cytokines (KC and interleukin-1β [IL-1β]) did not show significant differences between the groups. In conclusion, VitD-deficient animals did not show significantly increased susceptibility to infection or an altered course of infection. The immune systems of humans and mice likely respond differently to VitD. Murine models are likely not appropriate for drawing conclusions on the role of VitD in human pulmonary host defense.
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http://dx.doi.org/10.1128/IAI.00282-16 | DOI Listing |
Curr Top Med Chem
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Department of Chemistry, University of Swabi, Anbar 23561, Khyber Pakhtunkhwa, Pakistan.
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Department of Biomedical Engineering, Duke University, Durham, North Carolina, USA.
With the goal of studying skin wound healing and testing new drug treatments to enhance wound healing in rodent models, there is a clear need for improved splinting techniques to increase surgical efficiency and support routine wound monitoring. Splinted wound healing models humanize wound healing in rodents to prevent contraction and instead heal through granulation tissue deposition, increasing the relevance to human wound healing. Current technologies require suturing and heavy wrapping, leading to splint failure and cumbersome monitoring of the wound.
View Article and Find Full Text PDFJACS Au
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School of Chemistry and Chemical Engineering, Chemistry and Biomedicine Innovation Center (ChemBIC), State Key Laboratory of Coordination Chemistry, Najing University, Nanjing 210023, PR China.
Cancer cells often upregulate ribosome biogenesis to meet increased protein synthesis demands for rapid proliferation; therefore, targeting ribosome biogenesis has emerged as a promising cancer therapeutic strategy. Herein, we introduce two Pt complexes, ataluren monosubstituted platinum(IV) (SPA, formula: c,c,t,-[Pt(NH)Cl(OH)(CHFNO)], where CHFNO = ataluren) and ataluren bisubstituted platinum(IV) complex (DPA, formula: c,c,t,-[Pt(NH)Cl(CHFNO)], where CHFNO = ataluren), which effectively suppress ribosome biogenesis by inhibiting 47s pre-RNA expression. Furthermore, SPA and DPA induce nucleolar stress by dispersing nucleolar protein NPM1, ultimately inhibiting protein generation in tumor cells.
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Hospital Universitario de Gran Canaria Dr. Negrín, Respiratory Service, Las Palmas de Gran Canaria, Spain.
Eosinophils are polymorphonuclear cells that have progressively gained attention due to their involvement in multiple diseases and, more recently, in various homeostatic processes. Their well-known roles range from asthma and parasitic infections to less prevalent diseases such as eosinophilic granulomatosis with polyangiitis, eosinophilic esophagitis, and hypereosinophilic syndrome. In recent years, various biological therapies targeting these cells have been developed, altering the course of eosinophilic pathologies.
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