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Rheumatoid arthritis (RA) is a chronic and inflammatory autoimmune disease. Macrophage pyroptosis, a proinflammatory form of cell death, is critically important in RA; however, the detailed mechanism underlying pyroptosis induction is not yet well understood. Here, we report that DNA polymerase β (Pol β), a key enzyme in base excision repair, plays a pivotal role in RA pathogenesis. Our data shows that Pol β expression is significantly decreased in peripheral blood mononuclear cells (PBMCs) from active RA patients and collagen-induced arthritis (CIA) mice, and Pol β deficiency increases the incidence of RA, macrophage infiltration, and bone destruction in CIA mouse models. In vitro, experiments showed that Pol β deficiency exacerbated macrophage pyroptosis induced by LPS plus ATP, while overexpression of Pol β inhibited macrophage pyroptosis. Further characterization revealed that Pol β knockout resulted in DNA damage accumulation and cytosolic dsDNA leakage, which activated the cGAS-STING-NF-κB signaling pathway and upregulated the expression of NLRP3, IL-1 β, and IL-18. In conclusion, our findings clarify the influence of Pol β on the development of RA and provide a detailed explanation for the STING-NF-κB pathway to induce macrophage pyroptosis.

Camptothecin has been used in tumor therapy for a long time but its antitumor effect is rather limited due to the side effect and the drug resistance. FEN1, a major component of DNA repair systems, plays important roles in maintaining genomic stability via DNA replication and repair. Here we found that FEN1 inhibitor greatly sensitizes cancer cells to low-dose camptothecin. The combinative treatment of FEN1 inhibitor and 1 nM camptothecin induced a synthetic lethal effect, which synergistically suppressed cancer cell proliferation and significantly mediated apoptosis both in vitro and in vivo. Our study suggested that targeting FEN1 could be a potent strategy for tumor-targeting cancer therapy.

Irritable bowel syndrome (IBS) is the most common gastrointestinal disorder significantly decreasing patients’ lives of quality and placing huge economic burden on our society. Existing studies indicated that the therapeutic effects maintained for a period of time after the treatments were discontinued. It is clinically important to assess these post-treatment therapeutic effects (PTTE), which prevent IBS from relapsing. To assess the PTTE in pinaverium treatment and obtain high-quality evidence to justify the use of PTTE for long-term IBS management, we performed this controlled, double blind study on patients with IBS who were randomized to pinaverium 50 mg (n = 132) or placebo (n = 132), three times daily, for 4 weeks, and were followed up for 57 weeks after the treatments. The primary endpoints were abdominal pain and stool consistency. The secondary endpoints were pain frequency and stool frequency. The tertiary endpoints were global overall symptom and adverse events. Three days after pinaverium was discontinued, endpoints rebounded only 23.2–42.8% (P P P’s > 0.05)], during which an average of 51.5–56.4% of patients (pool pinaverium and placebo data together) had IBS symptoms. These results provide clinical insights into efficient and cost-effective management of refractory IBS, and lend support to the IBS management that the selection of a therapy should consider both its effectiveness during treatment and its PTTE after the treatment.Trial registration number: NCT02330029 (16/08/2016).

A 40-year-old man presented with a 3-year duration of intermittent upper abdominal pain. Gastroscopy and endoscopic ultrasonography revealed a tumor in the bottom of the stomach with a homogenous low echogenicity that originated from the gastric serosa. An abdominal contrast-enhanced computed tomography (CT) scan showed that a well-marginated ovoid mass was obviously enhanced homogenously in the arterial period and weakened slightly in the venous period. The diagnosis of a gastric stromal tumor was made. Laparoscopic resection of the gastric tumor was subsequently performed. Surprisingly, postoperative pathological examination of the mass showed the typical structure of a normal splenic tissue. To our knowledge, ectopic splenic tissue originating from the gastric serosa is reported for the first time, showing important clinical significance for the identification of gastric malignant tumors.

Nickel oxide (NiO) hollow fibers were obtained by thermal degradation of nickel alginate fibers (Ni-AF), which was prepared by wet spinning technique. The composition, morphology and microstructure of the as-obtained NiO fibers were investigated by thermal gravimetry (TG), X-ray diffraction (XRD), electron energy-loss spectroscopy (EELS), scanning electron microscopy (SEM), and transmission electron microscopy (TEM). It is found that temperature plays important roles on the final structures and shapes of the NiO nanostructures. NiO hollow fibers (∼ 10 μm) consisting of NiO nanoparticles with diameter about 50 and 80 nm respectively are obtained under 600 and 800 °C in air. The mechanism of Ni-AF thermal degradation and NiO growth were proposed.

Zinc alginate fibers (Zn-AF) were obtained by wet-spinning of sodium alginate into coagulating bath containing an aqueous zinc chloride solution. ZnO nanostructures consisting of nanofibers on the ZnO matrix were prepared from controlled thermal degradation of the as-obtained Zn-AF at 800 °C in air condition when Zn granules were added for extra ZnO source during calcination. The composition and morphology of ZnO nanostructures were investigated by X-ray diffraction (XRD), scanning electron microscopy (SEM) and photoluminescence (PL). The SEM images show that ZnO nanofibers with diameter about 20 nm were formed on the ZnO matrix. The photocatalytic degradation experiment of methylene blue (MB) dye from aqueous solution show that ZnO nanostructures possess good photo catalytic reactivity. The performance of ZnO nanostructures can be attributed to the ZnO nanofibers which facilitate the photocatalytic degradation reaction.