[A new cucurbitane glycoside from Picrorhiza scrophulariiflora].

Chemical constituents from the ethanol extract of Picrorhiza scrophulariiflora were isolated and purified by column chromatography. Their structures were identified by HR-MS, 1D and 2D-NMR, and their cytotoxicity was assessed by CCK-8 assay. Four compounds were isolated and identified as follows: 2ß-D-glucosyloxy-3ß,16α,20ß-trihydroxy-9-methyl-19-norlanosterol-5,25-diene-22-one(1), 2ß-D-glucosyloxy-3ß,16α,20ß-trihydroxy-9-methyl-19-norlanosta-5,24-diene-22-one(2), 25-acetoxy-2ß-glucosyloxy-3ß,16α,20ß-trihydroxy-9-methyl-19-norlanosta-5-ene-22-one(3) and 25-acetoxy-2ß-glucosyloxy-3ß,16α,20ß-trihydroxy-9-methyl-19-norlanosta-5,23-(E)-diene-22-one(4). Compound 1 represents a new cucurbitane glycoside. The half inhibitory concentrations of the 4 compounds exceeded 100 µmol·L~(-1) against four tumor cell lines, indicating no significant cytotoxicity.

Exosomal EGFR and miR-381-3P Mediate HPV-16 E7 Oncoprotein-Induced Angiogenesis of Non-Small Cell Lung Cancer.

BACKGROUND: It has been demonstrated that exosomes derived from HPV-16 E7-over-expressiong non-small cell lung cancer (NSCLC) cells (E7 Exo) trigger increased levels of epidermal growth factor receptor (EGFR) and miR-381-3p. The purpose of this investigation was to examine the role of E7 Exo in NSCLC angiogenesis, and to analyze the contribution of exosomal EGFR and miR-381-3p to it. METHODS: The influence of E7 Exo on the proliferation and migration of human umbilical vein endothelial cells (HUVECs) was assessed using colony formation and transwell migration assays. Experiments on both cells and animal models were conducted to evaluate the angiogenic effect of E7 Exo treatment. The involvement of exosomal EGFR and miR-381-3p in NSCLC angiogenesis was further investigated through suppressing exosome release or EGFR activation, or by over-expressing miR-381-3p. RESULTS: Treatment with E7 Exo increased the proliferation, migration, and tube formation capacities of HUVECs, as well as angiogenesis in animal models. The suppression of exosome release or EGFR activation in NSCLC cells decreased the E7-induced enhancements in HUVEC migration and tube formation, and notably reduced vascular endothelial growth factor A (VEGFA) and Ang-1 levels. HUVECs that combined miR-381-3p mimic transfection and E7 Exo treatment exhibited a more significant tube-forming capacity than E7 Exo-treated HUVECs alone, but were reversed by the miR-381-3p inhibitor. CONCLUSION: The angiogenesis induced by HPV-16 E7 in NSCLC is mediated through exosomal EGFR and miR-381-3p.

Revolutionizing Gastric Cancer Prevention: Novel Insights on Gastric Mucosal Inflammation-Cancer Transformation and Chinese Medicine.

The progression from gastric mucosal inflammation to cancer signifies a pivotal event in the trajectory of gastric cancer (GC) development. Chinese medicine (CM) exhibits unique advantages and holds significant promise in inhibiting carcinogenesis of the gastric mucosa. This review intricately examines the critical pathological events during the transition from gastric mucosal inflammation-cancer transformation (GMICT), with a particular focus on pathological evolution mechanisms of spasmolytic polypeptide-expressing metaplasia (SPEM). Moreover, it investigates the pioneering applications and advancements of CM in intervening within the medical research domain of precancerous transformations leading to GC. Furthermore, the analysis extends to major shortcomings and challenges confronted by current research in gastric precancerous lesions, and innovative studies related to CM are presented. We offer a highly succinct yet optimistic outlook on future developmental trends. This paper endeavors to foster a profound understanding of forefront dynamics in GMICT research and scientific implications of modernizing CM. It also introduces a novel perspective for establishing a collaborative secondary prevention system for GC that integrates both Western and Chinese medicines.

MiRNA-296-5p promotes the sensitivity of nasopharyngeal carcinoma cells to cisplatin via targeted inhibition of STAT3/KLF4 signaling axis.

Improving drug sensitivity is an important strategy in chemotherapy of cancer and accumulating evidence indicates that miRNAs are involved in the regulation of drug sensitivity, but the specific mechanism is still unclear. Our previous study has found that miR-296-5p was significantly downregulated in nasopharyngeal carcinoma (NPC). Here, we aim to explore whether miR-296-5p is involved in regulating cisplatin sensitivity in NPC by regulating STAT3/KLF4 signaling axis. The cell proliferation and clonogenic capacity of NPC cells were evaluated by CCK8 Assay and plate colony assay, respectively. The Annexin V-FITC staining kit was used to determine and quantify the apoptotic cells using flow cytometry. The drug efflux ability of NPC cells were determined by Rhodamine 123 efflux experiment. The expression of miR-296-5p, apoptosis-related genes and protein in NPC cell lines were detected by qPCR and Western blot, respectively. Animal study was used to evaluate the sensitivity of NPC cells to DDP treatment in vivo. Our results showed that elevated miR-296-5p expression obviously promoted the sensitivity of NPC cells to DDP by inhibiting cell proliferation and clonogenic capacity, and inducing apoptosis. In addition, we found that miR-296-5p inhibited the expression of STAT3 and KLF4 in NPC cells, while overexpression of exogenous STAT3 reversed miR-296-5p-mediated enhancement in cell death of DDP-treated NPC cells. In vivo studies further confirmed that miR-296-5p promotes the sensitivity of NPC cells to DDP treatment. miRNA-296-5p enhances the drug sensitivity of nasopharyngeal carcinoma cells to cisplatin via STAT3/KLF4 signaling pathway.

The Function of Different Subunits of the Molecular Chaperone CCT in the Microsporidium Nosema bombycis: NbCCTζ Interacts with NbCCTα.

Chaperonin containing tailless complex polypeptide 1 (CCT) is a molecular chaperone protein that consists of eight completely different subunits and assists in the folding of newly synthesized peptides. The zeta subunit of CCT is a regulatory factor for the folding and assembly of cytoskeletal proteins as individuals or complexes. In this study, the zeta subunit of Nosema bombycis (NbCCTζ) is identified for the first time. The complete ORF of the NbCCTζ gene is 1533 bp in length and encodes a 510 amino acid polypeptide. IFA results indicate that NbCCTζ is colocalized with actin and ß-tubulin in the cytoplasm during the proliferative phase and that NbCCTζ is completely colocalized with NbCCTα in the cytoplasm of N. bombycis throughout the entire life cycle. Furthermore, the yeast two-hybrid assay revealed that the NbCCTζ interacts with NbCCTα. The transcriptional level of NbCCTζ is significantly downregulated by knocking down the NbCCTα gene, while the transcriptional level of NbCCTα is downregulated after knocking down the NbCCTζ gene. These results suggest that NbCCTζ may play a vital role in the proliferation of N. bombycis by coordinating with NbCCTα.

Targeted delivery of Fc-fused PD-L1 for effective management of acute and chronic colitis.

The PD-1/PD-L1 pathway in mucosal immunity is currently actively explored and considered as a target for inflammatory bowel disease (IBD) treatment. However, systemic PD-L1 administration may cause unpredictable adverse effects due to immunosuppression. Here we show that reactive oxygen species (ROS)-responsive nanoparticles enhance the efficacy and safety of PD-L1 in a mouse colitis model. The nanoparticles control the accumulation and release of PD-L1 fused to Fc (PD-L1-Fc) at inflammatory sites in the colon. The nanotherapeutics shows superiority in alleviating inflammatory symptoms over systemic PD-L1-Fc administration and mitigates the adverse effects of PD-L1-Fc administration. The nanoparticles-formulated PD-L1-Fc affects production of proinflammatory and anti-inflammatory cytokines, attenuates the infiltration of macrophages, neutrophils, and dendritic cells, increases the frequencies of Treg, Th1 and Tfh cells, reshapes the gut microbiota composition; and increases short-chain fatty acid production. In summary, PD-L1-Fc-decorated nanoparticles may provide an effective and safe strategy for the targeted treatment of IBD.

Ssn6 Interacts with Polar Tube Protein 2 and Transcriptional Repressor for RNA Polymerase II: Insight into Its Involvement in the Biological Process of Microsporidium Nosema bombycis.

Nosema bombycis is a representative species of Microsporidia, and is the pathogen that causes pebrine disease in silkworms. In the process of infection, the polar tube of N. bombycis is injected into the host cells. During proliferation, N. bombycis recruits the mitochondria of host cells. The general transcriptional corepressor Ssn6 contains six tetratricopeptide repeats (TPR) and undertakes various important functions. In this study, we isolated and characterized Nbssn6 of the microsporidium N. bombycis. The Nbssn6 gene contains a complete ORF of 1182 bp in length that encodes a 393 amino acid polypeptide. Indirect immunofluorescence assay showed that the Ssn6 protein was mainly distributed in the cytoplasm and nucleus at the proliferative phase of N. bombycis. We revealed the interaction of Nbssn6 with polar tube protein 2 (Nbptp2) and the transcriptional repressor for RNA polymerase II (Nbtrrp2) by Co-IP and yeast two-hybrid assays. Results from RNA interference further confirmed that the transcriptional level of Nbptp2 and Nbtrrp2 was regulated by Nbssn6. These results suggest that Nbssn6 impacts the infection and proliferation of N. bombycis via interacting with the polar tube protein and transcriptional repressor for RNA polymerase II.

Safety and efficacy of waterjet debridement vs. conventional debridement in the treatment of extremely severe burns: A retrospective analysis.

INTRODUCTION: Patients with extremely severe burns often require rapid wound closure with a tangential excision or escharectomy combined with a skin graft to reduce life-threatening complications such as infection. Traditional tangential excision surgery using the Watson or Humby knife does not allow accurate excision of necrotic tissue and often removes too much active tissue, which is detrimental to the rapid healing of the wound. Importantly, the Versajet hydrosurgical system, with its smaller handle, allows for more precise excision of necrotic burn tissue and preserves more active dermal tissue, positively affecting wound healing and scarring. This study compared the safety and efficacy of hydrosurgical combined with autologous skin grafting to conventional excision combined with autologous skin grafting in patients with extremely severe burn. METHODS: Information of sixty burn patients with total body surface area (TBSA) > 50 % treated at the first affiliated hospital of Anhui Medical University from January 2019 to August 2022 were analyzed. The patients were divided into a conventional debridement group (n = 37) and a hydrosurgical debridement group (n = 23) according to the approach used. The hydrosurgical debridement group and the conventional debridement group were compared from the difference between the duration of the first debridement surgery, wound healing time, the changes of red blood cells and hemoglobin concentration postoperative, total blood transfusion, hospitalization cost, skin grafting frequency, procalcitonin, wound bacterial culture, albumin and prealbumin. RESULTS: Information on age, gender, weight, inhalation injury, hypovolemic shock, preoperative procalcitonin, preoperative albumin, preoperative prealbumin, the operation frequency (n ≥ 3), preoperative trauma culture and postoperative trauma culture were compared between both groups (P > 0.05). Operative time and wound healing time were significantly shorter in patients with hydrosurgical debridement combined with autologous skin grafting than those in the control group (P < 0.05), while hospitalization costs were not significantly different between the two groups (P > 0.05). The changes of red blood cells and hemoglobin concentration during the postoperative period in the hydrosurgical debridement group were less significantly than those in the conventional debridement group (P < 0.05). The total amount of red blood cells transfused during hospitalization was significantly lower in the hydrosurgical debridement group than that in the conventional debridement group (P < 0.05), but the total amount of fresh frozen plasma transfused during hospitalization was not statistically significant between the two groups (P > 0.05). Albumin on the third day after surgery and prealbumin on the first, third and fifth day after surgery improved more significantly than those in the control group(P < 0.05), however, there were no significant differences between the two groups in albumin on the first and fifth postoperative days (P > 0.05). The PCT level in the conventional debridement group was significantly higher than that in the hydrosurgical debridement group on the first, third and fifth days after surgery(P < 0.05). CONCLUSION: The hydrosurgical debridement group presented with shorter operative time, less blood loss during surgery, faster postoperative nutritional recovery, less postoperative inflammatory response and faster wounds healing, and did not increase the hospitalization cost, postoperative bacterial culture of the wounds and the number of skin grafting surgeries. In patients with extremely severe burn, hydrosurgical debridement combined with autologous skin grafting group is safer and more effective than those in the conventional debridement combined with autologous skin grafting group.

Treatment of refractory or relapsed myelodysplastic neoplasms with luspatercept: a multicenter Chinese study.

Few effective therapies are available to treat patients with relapsed/refractory myelodysplastic neoplasms (MDS). Luspatercept was shown to display good efficacy in a phase 3 clinical trial for lower-risk MDS (LR-MDS) patients, yet real-world data are limited, especially in China. Therefore, data from patients diagnosed as having MDS with low blasts and SF3B1 mutation (MDS-SF3B1) and MDS with SF3B1 mutation and thrombocytosis were retrospectively analyzed. Of the 23 enrolled patients, 17 (73.9%) were males (median age 67 years: range 29 to 80 years). Previously, a total of 22 (95.7%) patients had received recombinant human erythropoietin (rhEPO), 9 (39.1%) roxadustat, 7 (30.4%) lenalidomide and 3 (13.0%) hypomethylating agents (HMA). The median treatment time was 22.9 weeks (9.0-32.4). At week 12, 60.9% (14/23) of the patients achieved a hematologic improvement-erythroid (HI-E) response. Red blood cell transfusion independence (RBC-TI) for ≥ 8 weeks was found in 57.1% (8/14) of transfusion-dependent patients. The median hemoglobin concentration was 84 g/L, and patients had significantly higher hemoglobin concentrations after 12 weeks of treatment (P < 0.001). It is noteworthy that responders had a greater reduction in serum ferritin (P = 0.021). Those with serum EPO < 500 IU/L at baseline tended to have a higher HI-E rate (P = 0.081), but only patients in non-transfusion and low transfusion burden (LTB) subgroups had statistical differences (P = 0.024). The most commonly occurring adverse events were blood bilirubin increase (17.4%), fatigue (13.0%) and dizziness (13.0%). Luspatercept was effective and tolerated well in refractory LR-MDS-SF3B1 patients. In particular, baseline non-transfusion and LTB patients exhibited a greater response rate to treatment.

MicroRNA-199a-3p suppresses the invasion and metastasis of nasopharyngeal carcinoma through SCD1/PTEN/AKT signaling pathway.

MicroRNAs (miRs) are 18-25 nucleotides non-coding RNAs, which contribute to tumorigenesis. Previous studies have demonstrated that miR-199a-3p is dysregulated in human nasopharyngeal carcinoma (NPC), but its role in NPC progression still largely unknown. The current study aimed to determine the potential role of miR-199a-3p in NPC progression and the underlying mechanisms. In this study, miR-199a-3p was found to be prominently down-regulated in NPC tissues and cells. The cellular assay showed that transfection of miR-199a-3p markedly repressed the migration, invasion and induced epithelial-mesenchymal transition (EMT) in both 5-8F and CNE-2 cell lines. By dual-luciferase reporter, western blotting and gas chromatography assays, we found that SCD1 is not only highly expressed in NPC tissues and negatively associated with the prognosis of NPC patients but also can be apparently downregulated by miR-199a-3p in NPC cells, suggesting that SCD1 is a direct target gene of miR-199a-3p. Moreover, inhibition of miR-199a-3p expression activated PI3K/Akt signaling and up-regulated the expression of MMP-2. With tumor xenograft models in nude mice, we also showed that miR-199a-3p repressed tumor growth in vivo. Our study demonstrated that miR-199a-3p inhibited migration and invasion of NPC cells through downregulating SCD1 expression, thus providing a potential target for the treatment of NPC.

Jian-Pi-Yin decoction attenuates lactose-induced chronic diarrhea in rats by regulating GLP-1 and reducing NHE3 ubiquitination and phosphorylation.

Objectives: Jian-Pi-Yin decoction (JPY), a prescription derived from the traditional Chinese medicine Shen-Ling-Bai-Zhu-San, has shown good clinical efficacy in the treatment of diarrhea caused by lactose intolerance. However, the mechanism of action of JPY in the treatment of diarrhea is not fully understood. Design: In this study, a rat diarrhea model was induced by high lactose feeding combined with standing on a small platform to investigate the ameliorating effect of JPY on hyper lactose-induced diarrhea in rats and its possible mechanism. Methods: The rat model of hyper lactose diarrhea was given high, medium, and low doses of JPY and the positive control drug Smida by gavage for 1 week. At the same time, NA+-H+ exchanger 3 (NHE3) inhibitor Tenapanor was administered orally for 3 weeks. Body weight, food intake, water intake, grip strength, and severity of diarrhea symptoms were measured in rats throughout the study. The serum, colon, and jejunum tissues of the model and drug-treated rats were collected for histopathological examination and analysis of relevant indicators. Results: JPY significantly alleviated the symptoms of fatigue, diet reduction and diarrhea in the model group. Glucagon-like peptide-1 (GLP-1) and cyclic adenosine monophosphate (cAMP) expression were also down-regulated after JPY treatment. JPY can significantly promote NHE3 in intestinal tissues of rats with diarrhea, and the mechanism is related to the decrease of GLP-1, inhibition of cAMP/PKA pathway activation, an increase of ubiquitin-specific protease 7 (USP7) and USP10 expression, and decrease of NHE3 ubiquitination and phosphorylation. Conclusion: JPY can reduce the expression of GLP-1, reduce the ubiquitination and phosphorylation of NHE3, regulate the expression of NHE3, at least partly improve ion transport in the intestinal epithelium, and improve the imbalance of electrolyte absorption, thus significantly reducing the diarrhea symptoms of rats with high lactose combined with small platform standing. Innovation: In this study, we explored the mechanism of intestinal GLP-1 activation of cAMP/PKA signaling pathway from multiple dimensions, and increased its expression by reducing phosphorylation and ubiquitination of NHE3, thereby treating chronic diarrhea associated with lactose intolerance.

[Corrigendum] Endophytic fungi from mangrove inhibit lung cancer cell growth and angiogenesis in vitro.

Subsequently to the publication of the above article, the authors have drawn to the attention of the Editorial Office that a few inadvertent errors were made during the assembly of Fig. 6 on p. 1802. In the first instance, the images selected to represent the A549 cell line in Fig. 6A were inadvertently shown as the data for the NCI­H460 cell line in Fig. 6C and vice versa, and so the data shown for Fig. 6A and C have been interchanged in the revised version of this figure. Moreover, the representative image for panel '3' in Fig. 6A of the above article (and so, now panel '3' in Fig. 6C of the corrected version) was wrongly copied across from that of panel '2' in Fig. 6C (now, panel '2' in Fig. 6A of the corrected version). The authors were able to re­examine their original data files, and realize how the errors were made during the assembly of this figure. The revised version of Fig. 6, with the data originally shown in Fig. 6A and C now interchanged, also showing the correct data for panel '3' in Fig. 6C, is shown on the next page. Note that the errors made in assembling this figure did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and all the authors agree with its publication. They also apologize to the readership for any inconvenience caused. [Oncology Reports 37: 1793­1803, 2017; DOI: 10.3892/or.2017.5366].

[Corrigendum] Epigallocatechin­3­gallate inhibits nicotine­induced migration and invasion by the suppression of angiogenesis and epithelial­mesenchymal transition in non­small cell lung cancer cells.

Subsequently to the publication of the above paper, the authors have drawn to the attention of the Editorial Office that a pair of the data panels showing the results of wound­healing assay experiments (in Fig. 1A) and Transwell invasion assays (in Fig. 1B) on p. 2975 were inadvertently featured incorrectly in this figure. Specifically, in Fig. 1A, the 'nicotine + 25 µM EGCG / 0 h' data panel was erroneously copied across to represent the 'nicotine + 0 µM EGCG / 0 h' image, whereas in Fig. 1B, the representative invasion image for the 'nicotine + 10  µM  EGCG' experiment was also incorrectly placed. The authors were able to re­examine their original data files, and realize how the errors were made during the assembly of this figure. The revised version of Fig. 1, showing the correct data for the 'nicotine + 0 µM EGCG / 0 h' in Fig. 1A and the 'nicotine + 10  µM  EGCG' experiment in Fig. 1B, is shown on the next page. Note that the errors made in assembling this figure did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and all the authors agree with its publication. They also apologize to the readership for any inconvenience caused. [Oncology Reports 33: 2972­2980, 2015; DOI: 10.3892/or.2015.3889].

Erratum: PI3K/Akt/HIF-1α signaling pathway mediates HPV-16 oncoprotein-induced expression of EMT-related transcription factors in non-small cell lung cancer cells: Erratum.

[This corrects the article DOI: 10.7150/jca.26112.].

GPER governs the immune infiltration of gastric cancer and activates the NF-κB/ROS/Apoptosis pathway in gastric mucosal epithelium.

BACKGROUND: Gastric cancer (GC) is with high mortality and morbidity. The GC morbidity of males is twice as high as that of females. G-protein estrogen receptor (GPER) bears on this phenomenon. METHODS: Networks and experiments assessed the GPER expression in different validity and content. The evidence-based practice involved accessing the clinical relevance of GPER by UALCAN and Kaplan-Meier plotter. Enrichment analyses contributed to guide further experimental validations. Activation of the NF-κB/ROS/Apoptosis pathway was analyzed by WB, immunofluorescence (IF), microplate reader and flow cytometry. TISIDB and TIMER identified the immune infiltration investigations, with credibility boosted by the Kaplan-Meier plotter. RESULTS: The appraisers revealed that GPER significantly decreased in GC at both gene and protein levels with highly approved prognosis value (P < 0.05). GPER was a significant fate determinant governing the inner part of gastric glands. NF-κB pathway and the following ROS in gastric cells were activated after MNU stimulation (20 µM, 24 h), and the GPER antagonist G15 strengthened the effect of MNU. Furthermore, GPER expression positively correlated with immune cells and various immune markers in GC patients, with highly approved clinical relevance. For example, type-2 helper cells enriched GC patients had a lower survival rate in the GPER-high expression group (P < 0.05). CONCLUSION: We demonstrated that GPER governs the GC progression by activating the NF-κB/ROS/Apoptosis pathway in gastric cells and regulating the immune environment around them.

Diagnostic value of procalcitonin and red blood cell distribution width at admission on the prognosis of patients with severe burns: A retrospective analysis.

The plasma procalcitonin (PCT) concentration and red blood cell distribution (RDW) value after severe burns can be used as prognostic indicators, but at present, it is difficult to give consideration to sensitivity and specificity in diagnosing the prognosis of severe burns with a single indicator. This study analysed the diagnostic value of plasma PCT concentration and RDW value at admission on the prognosis of severe burn patients to improve its sensitivity and specificity. A total of 205 patients with severe burns who were treated in the First Affiliated Hospital of Anhui Medical University from November 2017 to November 2022 were retrospectively analysed. The optimal cut-off values of plasma PCT concentration and RDW were analysed and counted through the subject curve (ROC curve). According to the cut-off value, patients were divided into high PCT group and low PCT group, high RDW group and low RDW group. The independent risk factors of severe burns were analysed by single-factor and multiple-factor COX regression. Kaplan-Meier survival was used to analyse the mortality of high PCT group and low PCT group, high RDW group and low RDW group. The area under the curve of plasma PCT concentration and RDW value at admission was 0.761 (95% CI, 0.662-0.860, P < .001), 0.687 (95% CI, 0.554-0.820, P = .003) respectively, and the optimal cut-off values of serum PCT concentration and RDW were 2.775 ng/mL and 14.55% respectively. Cox regression analysis found that age, TBSA, and RDW were independent risk factors for mortality within 90 days after severe burns. Kaplan-Meier survival analysis showed that there was a significant difference in the 90-day mortality rate of severe burns between the PCT ≥ 2.775 ng/mL group and the PCT < 2.775 ng/mL group (log-rank: 24.162; P < .001), with the mortality rate of 36.84% versus 5.49%, respectively. The 90-day mortality rate of severe burns was significantly different between the RDW ≥ 14.55% group and the RDW < 14.55% group (log-rank: 14.404; P < .001), with the mortality rate of 44% versus 12.2% respectively. The plasma PCT concentration and RDW value at admission are both of diagnostic value for the 90-day mortality of severe burns, but the plasma PCT concentration has higher sensitivity and the RDW value has higher specificity. Age, TBSA, and RDW were independent risk factors for severe burns, and then plasma PCT concentration was not independent risk factors.

Identifying biomarkers associated with the diagnosis of ulcerative colitis via bioinformatics and machine learning.

BACKGROUND: Ulcerative colitis (UC) is an idiopathic inflammatory disease with an increasing incidence. This study aimed to identify potential UC biomarkers and associated immune infiltration characteristics. METHODS: Two datasets (GSE87473 and GSE92415) were merged to obtain 193 UC samples and 42 normal samples. Using R, differentially expressed genes (DEGs) between UC and normal samples were filtered out, and their biological functions were investigated using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses. Promising biomarkers were identified using least absolute shrinkage selector operator regression and support vector machine recursive feature elimination, and their diagnostic efficacy was evaluated through receiver operating characteristic (ROC) curves. Finally, CIBERSORT was used to investigate the immune infiltration characteristics in UC, and the relationship between the identified biomarkers and various immune cells was examined. RESULTS: We found 102 DEGs, of which 64 were significantly upregulated, and 38 were significantly downregulated. The DEGs were enriched in pathways associated with interleukin-17, cytokine-cytokine receptor interaction and viral protein interactions with cytokines and cytokine receptors, among others. Using machine learning methods and ROC tests, we confirmed DUOX2, DMBT1, CYP2B7P, PITX2 and DEFB1 to be essential diagnostic genes for UC. Immune cell infiltration analysis revealed that all five diagnostic genes were correlated with regulatory T cells, CD8 T cells, activated and resting memory CD4 T cells, activated natural killer cells, neutrophils, activated and resting mast cells, activated and resting dendritic cells and M0, M1 and M2 macrophages. CONCLUSIONS: DUOX2, DMBT1, CYP2B7P, PITX2 and DEFB1 were identified as prospective biomarkers for UC. A new perspective on understanding the progression of UC may be provided by these biomarkers and their relationship with immune cell infiltration.

Erratum: Cytochalasin H isolated from mangrove-derived endophytic fungus inhibits epithelial-mesenchymal transition and cancer stemness via YAP/TAZ signaling pathway in non-small cell lung cancer cells: Erratum.

[This corrects the article DOI: 10.7150/jca.50512.].

Bacteria-targeted delivery of black phosphorus quantum dots facilitates photothermal therapy against hypoxic tumors and complementary low-dose radiotherapy.

Many approaches have been employed to relieve hypoxia in solid tumors to enhance sensitivity to radiotherapy (RT), including O2 delivery or hydrogen peroxide (H2O2) decomposition strategies. To date, however, these modalities have been restricted by poor O2 loading, rapid O2 leakage, and limited endogenous H2O2 levels. To overcome these limitations, we therefore sought to develop an effective approach for the oxygen-independent treatment of hypoxic tumors. In this study, we designed a novel black phosphorus quantum dot (BPQD)/Escherichia coli (E. coli) hybrid system (BE) capable of facilitating the photothermal therapy (PTT) of hypoxic tumors. A simple electrostatic adsorption approach was used to conjugate BPQDs to E. coli. BE is capable of reliably targeting hypoxic tumors and mediating PTT. BPQDs in BE can directly facilitate X-ray-mediated radiosensitization of tumors, thereby achieving significant RT efficacy in response to lower doses of radiation, effectively and specifically damaging hypoxic tumor tissues to suppress the growth of tumors. Our results highlight this BE system as a novel approach to tumor radiosensitization with great potential for clinical application.

Erratum: Cytochalasin H Inhibits Angiogenesis via the Suppression of HIF-1α Protein Accumulation and VEGF Expression through PI3K/AKT/P70S6K and ERK1/2 Signaling Pathways in Non-Small Cell Lung Cancer Cells: Erratum.

[This corrects the article DOI: 10.7150/jca.29933.].