The pandemic of novel coronavirus disease (COVID-19) has developed as a tremendous threat to global health. Although most COVID-19 patients present with respiratory symptoms, some present with gastrointestinal (GI) symptoms like diarrhoea, loss of appetite, nausea/vomiting and abdominal pain as the major complaints. These features may be attributable to the following facts: (a) COVID-19 is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and its receptor angiotensin converting enzyme 2 (ACE2) was found to be highly expressed in GI epithelial cells, providing a prerequisite for SARS-CoV-2 infection; (b) SARS-CoV-2 viral RNA has been found in stool specimens of infected patients, and 20% of patients showed prolonged presence of SARS-CoV-2 RNA in faecal samples after the virus converting to negative in the respiratory system. These findings suggest that SARS-CoV-2 may be able to actively infect and replicate in the GI tract. Moreover, GI infection could be the first manifestation antedating respiratory symptoms; patients suffering only digestive symptoms but no respiratory symptoms as clinical manifestation have also been reported. Thus, the implications of digestive symptoms in patients with COVID-19 is of great importance. In this review, we summarise recent findings on the epidemiology of GI tract involvement, potential mechanisms of faecal–oral transmission, GI and liver manifestation, pathological/histological features in patients with COVID-19 and the diagnosis, management of patients with pre-existing GI and liver diseases as well as precautions for preventing SARS-CoV-2 infection during GI endoscopy procedures.

Purpose This review aimed to assess whether peroneus longus tendon (PLT) autograft would have comparable functional outcomes and graft survival rates when compared to hamstring tendon (HT) autograft for anterior cruciate ligament (ACL) reconstruction. Methods PubMed, Web of Science, Cochrane Library, Ovid (MEDICINE), and EMBASE databases were queried for original articles from clinical studies including the keywords: ACL reconstruction and PLT autograft. Studies comparing PLT autograft versus HT autograft were included in this analysis and the following data were extracted from studies meeting the inclusion criteria: graft diameter, functional outcomes (Tegner activity scale, Lysholm score, and International Knee Documentation Committee (IKDC) subjective score), knee laxity (Lachman test), and complications (donor site pain or paresthesia, graft failure). Besides, the American Orthopaedic Foot and Ankle Society (AOFAS) scale and the Foot and Ankle Disability Index (FADI) pre-operation and at last follow-up were also compared among patients using PLT autograft. Meta-analysis was applied using Review Manager 5.3 and p < 0.05 was considered statistically signiicant. Results Twenty-three studies including 925 patients with ACL reconstruction met inclusion criteria. Of these, 5 studies included a direct comparison of PLT autograft (164 patients) versus HT autograft (174 patients). No signiicant diference was observed between PLT and HT autografts for Tegner activity scale, Lachman test, donor site pain, or graft failure. However, PLT groups demonstrated better Lysholm score (mean diference between PLT and HT groups, 1.55; 95% CI 0.20-2.89; p = 0.02) and IKDC subjective score (mean diference between PLT and HT groups, 3.24; 95% CI 0.29-6.19; p = 0.03). No diference of FADI was found (n.s.) but AOFAS was slightly decreased at last post-operative follow-up for patients with PLT autograft compared with pre-operative scores (mean diference of 0.31, 95% CI 0.07-0.54, p = 0.01). Conclusion PLT autograft demonstrated comparable functional outcomes and graft survival rates compared with HT autograft for ACL reconstruction. However, a slight decrease in AOFAS score should be considered during surgical planning. Hence, the PLT is a suitable autograft harvested outside the knee for ACL reconstruction to avoid the complication of quadriceps-hamstring imbalance which can occur when harvesting autografts from the knee. Level of evidence Level II.

BackgroundDirect intra-articular injection (DIAI) of mesenchymal stem cells (MSCs) is a promising technique for cartilage repair. However, the repair process was hindered by the absence of scaffold and poor cell–matrix interactions.MethodsIn this study, we developed a pericellular collagen I coating (PCC) on MSCs. The overall performances of MSC-PCC homing, chondrogenic differentiation, and cartilage regeneration have been comprehensively evaluated in a New Zealand rabbit model. Firstly, we examined the morphology and physical characteristics of PCC. Secondly, MSC ex-vivo cartilage slice adhesion and in-vivo cartilage defect homing were observed using multiscale methods. Thirdly, the precartilage condensation of cell pellets formed by aggregation of MSCs was examined to evaluate the cartilage-inducing potential of PCC. Finally, the cartilage regeneration by DIAI of PCC-coated MSCs was observed and scored macroscopically and histologically.ResultsIn general, the cell adhesion and homing assay revealed that PCC facilitated MSC adhesion on cartilage slices, enhancing MSC homing and retention to cartilage defect. This increased homing ratio was accompanied by an increasing cell–cell contact. Compared with naked MSCs, the cell pellets formed by PCC-coated MSCs exhibited more evident appearance of condensation. In pellets, cell–cell interaction has been significantly stimulated, inducing the expression of condensation marker N-cadherin, and subsequent chondrogenic marker collagen II and aggrecan. By 12 weeks after DIAI, cartilage defects have been repaired by MSCs to varying degrees. Overall, PCC significantly enhances the quality of cartilage regeneration judging from macroscopic observation, ICRS score, histological examination, and collagen type I, II, and X immunohistochemical staining.ConclusionsThe capacity and viability of MSCs can be enhanced by collagen I coating, which provides cues for enhancing cell homing and differentiation. Our method provides a novel strategy for stem cell therapy.Electronic supplementary materialThe online version of this article (10.1186/s13287-018-0916-z) contains supplementary material, which is available to authorized users.

The ATPase H+/K+ Transporting Beta Subunit (ATP4B) encodes the β subunit of the gastric H+, K+-ATPase, which controls gastric acid secretion and is therefore a target for acid reduction. Downregulation of ATP4B was recently observed in human gastric cancer (GC) without known mechanisms. In the present study, we demonstrated that ATP4B expression was decreased in human GC tissues and cell lines associated with DNA hypermethylation and histone hypoacetylation of histone H3 lysine 9 at its intragenic region close to the transcriptional start site. The expression of ATP4B was restored in GC cell lines by treatment with the DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine (5-AZA), or histone deacetylase inhibitor, trichostatin A (TSA), with further enhancement by combined treatment with both drugs. In contrast, 5-AZA had no effect on ATP4B expression in human hepatocellular carcinoma (HCC) and pancreatic cancer cell lines, in which ATP4B was silenced and accompanied by intragenic methylation. Chromatin immunoprecipitation (ChIP) showed that, in BGC823 GC cells, histone H3 lysine 9 acetylation (H3K9ac) was enhanced in the intragenic region of ATP4B upon TSA treatment, whereas 5-AZA showed a minimal effect. Additionally, ATP4B expression enhanced the inhibitory effects of chemotherapeutic mediation docetaxel on GC cell growth. Thus, as opposed to HCC and pancreatic cancer cells, the silencing of ATP4B in GC cells is attributable to the interplay between intragenic DNA methylation and histone acetylation of ATP4B, the restoration of which is associated with a favorable anticancer effect of docetaxel. These results have implications for targeting epigenetic alteration at the intragenic region of ATP4B in GC cells to benefit diagnosis and treatment of GC.