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Cadmium (Cd), a common environmental pollutant, seriously threatens the health of intestine. This research aimed to investigate the effects of compound probiotics (CP) on intestinal dysfunction and cecal microbiota dysregulation induced by Cd in broilers. A total of 240 1-day-old Arbor Acre (AA) broilers were randomly assigned to four groups. After 120 days of feeding, the jejunum tissues and cecal contents were sampled for jejunum histopathological observation, the intestinal barrier and inflammatory factors related mRNA and proteins examinations, and intestinal microbiota analysis. The results showed that Cd could cause jejunal villus damage and inflammatory cells infiltration, down-regulate the mRNA levels of intestinal barrier related genes (ZO-1, ZO-2, ZO-3, Claudin1, Claudin3, Claudin4, Occludin, and E-cadherin) and inflammatory factor related genes (IL-1β, IL-18, IFN-γ, NF-κB), and the protein levels of Claudin1, ZO-1, Occludin, but up-regulate the Claudin2, IL-2, IL-4 and IL-10 mRNA levels. However, the addition of CP could effectively improve these changes. In addition, 16S rRNA gene sequencing analysis showed that compared with the Cd group, supplementation CP increased the abundance of Lactobacillales , Clostridiales, Firmicutes , together with regulations on the pathways responsible for energy metabolism, translation and amino acid metabolism. In conclusion, CP could improve intestinal barrier damage and intestinal microbiota disturbance induced by Cd. [Display omitted] • Cadmium (Cd) damaged intestinal barrier and caused microbiota disorders in broilers. • Compound probiotics (CP) alleviated intestinal damage and inflammation induced by Cd. • CP increased the colonization of beneficial bacteria in the cecum. • CP alleviated microbiota disorders induced by Cd. [ABSTRACT FROM AUTHOR]

As an emerging pollutant, uranium poses serious concerns to ecological and human health. The kidney has been established as a major deposition site and the most sensitive target organ for uranium poisoning, and the underlying toxicological mechanisms have been associated with oxidative stress and mitochondrial respiration. However, the identities of key molecular targets in uranium-induced toxicity remain elusive. In this study, we comprehensively evaluated the in vitro effects of uranium on ten critical enzymes in the mitochondrial respiration pathway and discovered that respiratory chain complex IV (cytochrome c oxidase) and complex V (ATP synthase) were strongly inhibited. The inhibitory effects were validated with mitochondria from human renal proximal tubule cells—the most affected renal site in uranium poisoning. The IC 50 values (around 1 mg/L) are physiologically relevant, as they are comparable to known kidney accumulation levels in uranium poisoning. In addition, these inhibitory effects could explain the well-documented uranium-induced reactive oxygen species generation and mitochondrial alterations. In conclusion, cytochrome c oxidase and ATP synthase are possibly key molecular targets underlying the toxic effects of uranium. Image 1 • Effects of uranium on mitochondrial respiration are comprehensively evaluated. • Uranium inhibits human mitochondrial cytochrome c oxidase and ATP synthase. • The IC 50 values (around 1 mg/L) are comparable to renal levels in uranium poisoning. Mitochondrial cytochrome c oxidase and ATP synthase are identified as potential molecular targets underlying the nephrotoxicity of uranium. [ABSTRACT FROM AUTHOR]

There have been increasing numbers of reports that anti-osteoporosis drugs cause osteonecrosis. A typical example is medication-related osteonecrosis of the jaws (MRONJ) which can cause massive necrosis and defects of the jaws. Thus, the dosage and effects of anti-osteoporosis drugs should be re-examined. Our hypothesis is that primary moderate osteoporosis itself is beneficial for bones and should not be excessively treated other than vitamin D, calcium supplementation and functional exercises. The self-repair and anti-infection abilities of bone depend on its organic tissues including stem cells, blood vessels, osteoclastic and osteogenic factors in bone, which jointly fight against invading pathogens and repair bone damage. Recent evidence supports age-related changes in mesenchymal stem cell including loss of self-renewal and increases in senescent cell numbers. Thus, the number of MSCs and vessels need to be increased to achieve functions similar to those in young people. This requires dissolving a portion of inorganic materials and providing extra space to hold more cells and blood vessels. In contrast, anti-osteoporosis drugs prevent bone destruction, and increase mineralization that occupies the space of organic materials, reduces bone immunity and self-repair. Moreover, long term use of anti-osteoporosis drugs also have negative effects on long bones and cartilages. Therefore, moderate age-related osteoporosis is natural in humans to protect bones. Excessive treatment of osteoporosis weakens immunity and self-repair. [ABSTRACT FROM AUTHOR]

Summary: Lung cancer continues to be the leading cause of cancer deaths worldwide. Cigarette smoking is the predominant cause of lung cancer. Researchers found that tobacco-induced molecular changes in the oral epithelium are similar to those in the lung epithelium. Furthermore, there has been considerable progress in investigating the tumorigenesis of oral epithelium using molecular markers. These results offer hope that we can predict lung cancer in smokers by oral examination, which is much easier and more practical than lung biopsy. The hypothesis is to collect oral epithelial cells by gently scraping the oral mucosa, and analyze the DNA variation in these cells using molecular biological methods. Therefore, the oral epithelium is serving as a surrogate tissue for assessing smoking-induced molecular damage to the lungs and thus have important implications for early detection of lung cancer. [Copyright &y& Elsevier]