Vitamin A Insufficiency in Current and Former Smokers and Lung Cancer Risk: A Case-Control Approach

Background: Adequate dietary intakes of vitamin A are protective against lung cancer, but little is known about the risk of lung cancer when intakes of the vitamin are below minimum physiological requirements. Further investigation into this relationship is needed considering established relationships between smoking, vitamin A deficiency (VAD), and lung cancer risk. Objective: The objective of this study was to determine whether intakes of vitamin A below the minimal physiological threshold increased the likelihood of lung cancer. We hypothesized vitamin A intakes above the minimal physiological threshold would reduce the likelihood of lung cancer. Methods: A case-control approach was used, utilizing data from eight cycles of NHANES surveys. Cancer-free, everyday cigarette smokers were matched on a 1:1 basis to cases with lung cancer by smoking duration, sex, and age. Paired sample T-tests were used to test differences in mean intakes of retinoids between groups, while an Exact McNemar test was used to assess differences between categorical variables. Conditional logistic regression was used to model the relationship between vitamin A insufficiency and lung cancer incidence, before and after adjustment. Results: A covariate in our adjusted model, milk consumption was significantly associated with increased odds of lung cancer (OR = 2.38, CI = 1.04 – 5.43). Contrary to our hypothesis, intakes of vitamin A at or above the minimal physiological threshold increased the odds of lung cancer, though confounding effects of several covariates, such as the age of smoking initiation, could not be ruled out (OR = 5.49, CI = 0.82 – 36.96). Conclusions: While mean intakes of vitamin A and subtypes did not significantly differ between case and control, only 20.4 % of individuals across our sample consumed intakes at or above gender-specific RDAs. As we did not collect data on food-specific micro/macronutrients, more research into dietary contributions of micro/macronutrients from foods known to be implicated in lung cancer prevention or risk, such as vitamin A, vitamin A, calcium, and fatty acids, could prove to be important areas for future research

Blockade of interleukin-6 signaling inhibits the classic pathway and promotes an alternative pathway of macrophage activation after spinal cord injury in mice

Background Recent in vivo and in vitro studies in non-neuronal and neuronal tissues have shown that different pathways of macrophage activation result in cells with different properties. Interleukin (IL)-6 triggers the classically activated inflammatory macrophages (M1 phenotype), whereas the alternatively activated macrophages (M2 phenotype) are anti-inflammatory. The objective of this study was to clarify the effects of a temporal blockade of IL-6/IL-6 receptor (IL-6R) engagement, using an anti-mouse IL-6R monoclonal antibody (MR16-1), on macrophage activation and the inflammatory response in the acute phase after spinal cord injury (SCI) in mice. Methods MR16-1 antibodies versus isotype control antibodies or saline alone were administered immediately after thoracic SCI in mice. SC tissue repair was compared between the two groups by Luxol fast blue (LFB) staining for myelination and immunoreactivity for the neuronal markers growth-associated protein (GAP)-43 and neurofilament heavy 200 kDa (NF-H) and for locomotor function. The expression of T helper (Th)1 cytokines (interferon (IFN)-? and tumor necrosis factor-a) and Th2 cytokines (IL-4, IL-13) was determined by immunoblot analysis. The presence of M1 (inducible nitric oxide synthase (iNOS)-positive, CD16/32-positive) and M2 (arginase 1-positive, CD206-positive) macrophages was determined by immunohistology. Using flow cytometry, we also quantified IFN-? and IL-4 levels in neutrophils, microglia, and macrophages, and Mac-2 (macrophage antigen-2) and Mac-3 in M2 macrophages and microglia. Results LFB-positive spared myelin was increased in the MR16-1-treated group compared with the controls, and this increase correlated with enhanced positivity for GAP-43 or NF-H, and improved locomotor Basso Mouse Scale scores. Immunoblot analysis of the MR16-1-treated samples identified downregulation of Th1 and upregulation of Th2 cytokines. Whereas iNOS-positive, CD16/32-positive M1 macrophages were the predominant phenotype in the injured SC of non-treated control mice, MR16-1 treatment promoted arginase 1-positive, CD206-positive M2 macrophages, with preferential localization of these cells at the injury site. MR16-1 treatment suppressed the number of IFN-?-positive neutrophils, and increased the number of microglia present and their positivity for IL-4. Among the arginase 1-positive M2 macrophages, MR16-1 treatment increased positivity for Mac-2 and Mac-3, suggestive of increased phagocytic behavior. Conclusion The results suggest that temporal blockade of IL-6 signaling after SCI abrogates damaging inflammatory activity and promotes functional recovery by promoting the formation of alternatively activated M2 macrophages

An overview of tissue engineering approaches for management of spinal cord injuries

Severe spinal cord injury (SCI) leads to devastating neurological deficits and disabilities, which necessitates spending a great deal of health budget for psychological and healthcare problems of these patients and their relatives. This justifies the cost of research into the new modalities for treatment of spinal cord injuries, even in developing countries. Apart from surgical management and nerve grafting, several other approaches have been adopted for management of this condition including pharmacologic and gene therapy, cell therapy, and use of different cell-free or cell-seeded bioscaffolds. In current paper, the recent developments for therapeutic delivery of stem and non-stem cells to the site of injury, and application of cell-free and cell-seeded natural and synthetic scaffolds have been reviewed