Bacterial determination, emerging as a critical step in the understanding of increasingly serious bacterial contaminations, remains a major challenge. Herein, a novel chemiluminescence biosensor was exploited for the ultrasensitive determination of nuclease activity and bacteria, in which, hemin, the chemiluminescent (CL) tag molecule was encapsulated into ordered mesopores of mesoporous silica nanoparticles with a specific DNA gate. The capped DNA could be specifically switched upon exposure to the DNA nuclease or bacterial lysate and allowed for an increased release of the encapsulated hemin, which therefore resulted in an obviously enhanced CL signal for the luminol−H 2 O 2 system. Attributed to this unique behavior with the linear or sigmoidal relationship between CL intensity and DNA nuclease or bacterial concentration, the as-prepared CL biosensor could detect S1 nuclease activity in the concentration range 0.01−10.0 U with a detection limit of 0.1 mU, and Escherichia coli O157:H7 (E. coli) or Staphylococcus aureus (S. aureus) in the concentration ranges 10 1 to 10 9 cfu mL −1 . The detection limit of E. coli and S. aureus was calculated to be 3.0 and 2.5 cfu mL −1 , respectively, which was comparable or even better than that of previous studies. Thus, this detection method could achieve detectable levels without cell enrichment overnight. Moreover, the proposed biosensing system could be conducted in the homogeneous solution without separation and washing, greatly improving the reaction efficiency and simplifying the procedure. As expected, the novel CL biosensor promised a great potential for simple and convenient detection of nuclease and bacteria in fields such as food bacterial contamination, pharmaceuticals, and clinical analysis.

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Slow transit constipation (STC) is a common disease characterized by markedly delayed colonic transit time as a result of colonic motility dysfunction. It is well established that STC is mostly caused by disorders of relevant nerves, especially the enteric nervous system (ENS). Colonic electrical stimulation (CES) has been regarded as a valuable alternative for the treatment of STC. However, little report focuses on the underlying nervous mechanism to normalize the delayed colonic emptying and relieve symptoms. In the present study, the therapeutic effect and the influence on ENS triggered by CES were investigated in STC beagles. The STC beagle model was established by oral administration of diphenoxylate/atropine and alosetron. Histopathology, electron microscopy, immunohistochemistry, Western blot analysis and immunofluorescence were used to evaluate the influence of pulse train CES on myenteric plexus neurons. After 5 weeks of treatment, CES could enhance the colonic electromyogram (EMG) signal to promote colonic motility, thereby improving the colonic content emptying of STC beagles. HE staining and transmission electron microscopy confirmed that CES could regenerate ganglia and synaptic vesicles in the myenteric plexus. Immunohistochemical staining showed that synaptophysin (SYP), protein gene product 9.5 (PGP9.5), cathepsin D (CAD) and S-100B in the colonic intramuscular layer were up-regulated by CES. Western blot analysis and immunofluorescence further proved that CES induced the protein expression of SYP and PGP9.5. Taken together, pulse train CES could induce the regeneration of myenteric plexus neurons, thereby promoting the colonic motility in STC beagles.

Background The water extract of Quercuse infectoria galls (QIG) is the active ingredient of Uyghur medicine Xipayi Kui Jie’an (KJA) which has promising therapeutic effects on Ulcerative Colitis (UC) as an alternative medicine. Considering the relationship between UC and the development of colorectal cancer (CRC), the present work aims to explore the direct anti-CRC activity of QIG extract. Methods CCK8 assay and flow cytometry were used to detect cytotoxicity and apoptosis. Transmission electron microscopy (TEM), flow cytometry, laser confocal and western blotting were performed to examine autophagy. We also adopted Reactive Oxygen Assay kit, as well as transwell and wound healing tests to study the underlying mechanism of QIG against CRC cells. Results First, we found that QIG extract could suppress the viability of CRC cells and trigger caspases-dependent apoptosis. Subsequently, we proved for the first time that QIG extract also triggered autophagic cell death in CRC cells, which together with apoptosis contributed to the cytotoxic effect on CRC cells. Further investigation revealed that QIG-induced cytotoxicity associated with intracellular ROS accumulation which could suppress the AKT/mTOR signaling pathway, and then induce autophagy and inhibit cell growth. Besides, Erk signaling pathway was also involved in the process of autophagic cell death. Moreover, QIG extract also influenced EMT process and inhibited CRC cell migration. Conclusion Altogether, this study provides a basis for the utilization of QIG as an alternative medicine for CRC prevention and treatment.