Silver nanoparticles (SNPs) are widely used in the field of biomedicine, but a comprehensive understanding of how SNPs distribute in the body and the induced toxicity remains largely unknown. The present study was designed to investigate the distribution and accumulation of SNPs in rats with subcutaneous injection. Rats were injected with either SNPs or silver microparticles (SMPs) at 62.8 mg/kg, and then sacrificed at predetermined time points. The main organs of the experimental animals were harvested for ultrastructural analysis by transmission electron microscopy (TEM) and for silver content analysis by inductively coupled plasma mass spectrometry (ICP-MS). Results indicated that SNPs translocated to the blood circulation and distributed throughout the main organs, especially in the kidney, liver, spleen, brain and lung in the form of particles. SMPs, however, could not invade the blood stream, or organ tissues. Ultrastructural observations indicate that those SNPs that had accumulated in organs could enter different kinds of cells, such as renal tubular epithelial cells and hepatic cells. Moreover, SNPs also induced blood-brain barrier (BBB) destruction and astrocyte swelling, and caused neuronal degeneration. The results suggest more cautions needed in biomedical applications of SNPs, in particular, the long-term uses.

Silver nanoparticles (SNPs) translocate to the brain through the blood stream after they are implanted in vivo. The aim of this study was to investigate the distribution of SNPs that crossed through the blood-brain barrier (BBB). An in vitro BBB model established by co-cultures of rat brain microvessel vascular endothelial cells (BMVECs) with astrocytes (ACs) was cultured with cell culture medium containing 100 microg/mL of either SNPs or silver microparticles (SMPs). After 4 hours of culture, the ultrastructure and its silver content of BBB was evaluated with transmission electronic microscopy (TEM) and inductively-coupled plasma mass spectrometry (ICP-MS) respectively. Results demonstrated that SNPs crossed the BBB and accumulated inside BMVECs, while the SMPs did not. The data indicated a special distribution of SNPs in the BBB and suggested that SNPs pass the BBB mainly by transcytosis of capillary endothelial cells. Further study would be necessary to evaluate the actual biological effects of SNPs on the brain.

Background: The sensitivity of endoscopy in diagnosing chronic atrophic gastritis is only 42%, and multipoint biopsy, despite being more accurate, is not always available. Aims: This study aimed to construct a convolutional neural network to improve the diagnostic rate of chronic atrophic gastritis. Methods: We collected 5470 images of the gastric antrums of 1699 patients and labeled them with their pathological findings. Of these, 3042 images depicted atrophic gastritis and 2428 did not. We designed and trained a convolutional neural network-chronic atrophic gastritis model to diagnose atrophic gastritis accurately, verified by five-fold cross-validation. Moreover, the diagnoses of the deep learning model were compared with those of three experts. Results: The diagnostic accuracy, sensitivity, and specificity of the convolutional neural network-chronic atrophic gastritis model in diagnosing atrophic gastritis were 0.942, 0.945, and 0.940, respectively, which were higher than those of the experts. The detection rates of mild, moderate, and severe atrophic gastritis were 93%, 95%, and 99%, respectively. Conclusion: Chronic atrophic gastritis could be diagnosed by gastroscopic images using the convolutional neural network-chronic atrophic gastritis model. This may greatly reduce the burden on endoscopy physicians, simplify diagnostic routines, and reduce costs for doctors and patients.

Composite probiotics containing B. infantis might be an effective therapeutic option for IBS patients, which could significantly alleviate the symptoms of IBS without significant adverse effects. However, the efficacy of single probiotic B. infantis on IBS has not been confirmed yet, which needs to be further validated by more large-sized randomized clinical trials.

Seven in absentia homolog 1 (SIAH1) is one of the E3 ubiquitin ligases and plays a key role in regulating target protein degradation. This study was designed to test the hypothesis that Siah1 mediates ethanol-induced apoptosis in NCCs through p38 MAPK-mediated activation of the p53 signaling pathway. We found that exposure of NCCs to ethanol resulted in the increases in the total protein levels of p53 and the phosphorylation of p53 at serine 15. Ethanol exposure also resulted in a significant increase in the phosphorylation of p38 MAPK. Knock-down of Siah1 dramatically reduced the ethanol-induced increase in the phosphorylation of p38 MAPK. Knock-down of Siah1 by siRNA or down-regulation of p38 MAPK by either siRNA or inhibitor significantly diminished ethanol-induced accumulations of p53 and the phosphorylation of p53. In addition, ethanol exposure resulted in a significant increase in the expression of p53 downstream targets and apoptosis in NCCs, which can be significantly diminished by down-regulation of Siah1 with siRNA. Knock-down of p38 MAPK by siRNA also dramatically reduced the ethanol-induced apoptosis. These results demonstrate that Siah1 plays a crucial role in ethanol-induced apoptosis in NCCs and that the up-regulation of Siah1 by ethanol can trigger apoptosis through p38 MAPK-mediated activation of the p53 signaling pathway.