Serum concentrations of bilirubin, albumin, and uric acid (UA) play important roles in controlling oxidative stress. Until now, there are few researches related to the relationship between oxidative stress and Crohn's disease (CD); furthermore, no such study has been reported from China. Our aim was to evaluate serum bilirubin, albumin, and UA levels in CD patients and relate them to disease activity.Seventy-one patients diagnosed with CD and 125 sex- and age-matched healthy individuals were retrospectively analyzed during the same period. Clinical characteristics and laboratory parameters were analyzed in CD patients and healthy control groups.Serum levels of bilirubin, albumin, and UA in patients with CD were significantly lower than those in the healthy control group. Correlation analysis demonstrated that serum concentrations of total bilirubin, direct bilirubin, indirect bilirubin, albumin, and UA were negatively related to disease activity in patients with CD (r = −0.620,P < .001;r = −0.304,P < .05;r = −0.623,P < .001;r = −0.408,P < .01; andr = −0.296,P < .05; respectively).Serum bilirubin, albumin and UA levels were significantly lower in CD patients, suggesting potential correlations between serum bilirubin, albumin, and UA levels and disease activity in CD patients. In addition, the noninvasive biochemical index may be potential markers for assessing the disease activity of patients with CD.

Background: Long noncoding RNAs (lncRNAs) have emerged to have irreplaceable roles in the epigenetic regulation of cancer progression, but their biological functions in colorectal cancer (CRC) remain unclear. Methods: LncRNA expression profiles in CRC tissue and their normal counterpart were explored. Through gain and loss of function approaches, the role of lncRNA PTTG3P was validated in relevant CRC cells and subcutaneous tumor model. The correlations of PTTG3P expression with clinical outcomes were assessed. Results: PTTG3P was upregulated in CRC tissues and was closely correlated with unsatisfactory prognosis. PTTG3P facilitated glycolysis and proliferation, and the transcriptional regulator YAP1 was necessary for PTTG3P-induced proliferation. Mechanistically, the N6-methyladenosine (m6A) subunit METTL3 increased PTTG3P expression by influencing its stability, while insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) could identify PTTG3P m6A methylation status and bind to it. IGF2BP2 knockdown partly recovered PTTG3P expression induced by METTL3, indicating that METTL3-regulated PTTG3P expression depended on the presence of IGF2BP2. Finally, rescue assays validated the critical role of the METTL3/PTTG3P/YAP1 axis on CRC proliferation. Conclusions: PTTG3P is an independent prognostic biomarker for CRC. The METTL3/PTTG3P/YAP1 axis promotes the progression of CRC and is a promising treatment target.

Penicillium marneffei, Histoplasma capsulatum, Mucor and Leishmania donovani can lead to penicilliosis marneffei, histoplasmosis, mucormycosis and leishmaniasis, respectively, which, to a certain extent, share similar clinical manifestations. These pathogens are approximately the same size, therefore it is relatively difficult to rapidly diagnose the diseases. The aim of the present study was to explore a novel method that attempts to rapidly identify the pathogens of these diseases. In the Wright‑Giemsa staining, the four pathogens were approximately the same size and mainly existed in macrophages. The multiplying P. marneffei had two nuclei, which were on both sides of the fungus, and had light cross‑walls in the middle. H. capsulatum had a purplish nucleus, which occupied between one‑third and one‑half of the spore. The cytoplasm was light blue. Peripheral spores were observed in the form of an empty, bright ring without color, like a capsule. Generally, Mucor were observed to have a long and lightly stained area, which could be easily confused with the Wright staining of dinuclear P. marneffei. L. donovani exhibited a deep‑staining kinetoplast near the nucleus. In the Periodic Acid Schiff (PAS) staining, the pathogens of P. marneffei and H. capsulatum were distinct and stained red. Differentiation between P. marneffei and H. capsulatum relied on their modes of reproduction: P. marneffei depends on fission, when the pathogens stretch into sausage‑shapes and are split by a cross‑wall, while H. capsulatum depends on budding so that narrow‑necked, single spores can be formed. With PAS staining, the cell walls and intracellular contents of Mucor and L. donovani were not stained, lightly stained or granulated and discontinuous. In conclusion, this method, combining PAS and Wright‑Giemsa staining, is simple and rapid, and may contribute to the effective identification of the four pathogens.

Although human/eukaryotic ribosomal protein L14 (RPL14/eL14) is known to be associated with a variety of cancers, its role in nasopharyngeal carcinoma (NPC) remains unclear. The aim of this study was to explore the impact of RPL14(eL14) in NPC. The results of quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and immunohistochemical staining revealed that the expression of RPL14(eL14) significantly reduced in NPC tissues and cells. Furthermore, the protein expression of RPL14(eL14) was linked to NPC-related clinical pathological features, including the T and N classification of Tumor Node Metastasis (TNM) staging (all p < 0.05). Cell counting kit-8 (CCK-8) assay and colony formation assay revealed that RPL14(eL14) overexpression repressed NPC cell proliferation. In cell cycle assay, RPL14(eL14) overexpression significantly blocked NPC cells in S phase. Overexpression of RPL14(eL14) repressed cell migration and invasion in NPC as shown by transwell assay and cell scratch healing assay. In addition, RPL14(eL14) was closely correlated with the expression of epithelial–mesenchymal transition (EMT) biomarkers, including E-cadherin, N-cadherin, and vimentin as detected by western blot. In conclusion, our results revealed that RPL14(eL14) may be considered as an antioncogene in NPC, which greatly suppresses cancer progression. Graphical Abstract

Bladder cancer originates from bladder tissues and is the ninth most common type of cancer worldwide. The SWI/SNF (SWItch/sucrose non‐ fermentable) complex plays a crucial role in regulating various biological processes, such as cell cycle control, DNA damage repair and transcription regulation. The purpose of this article is to examine the functional studies of the SWI/SNF complex in bladder cancer, highlighting new pathways for creating personalised treatment approaches for bladder cancer patients with mutations in the SWI/SNF complex. By acquiring a comprehensive understanding of the mechanisms of the SWI/SNF complex in bladder cancer, we can offer more precise and effective solutions to treat this disease.