The Paris System for Reporting Urinary Cytology (TPS 1.0, published in 2016) is the first standardized, evidence-based reporting system established as an international reporting system for urine specimens after the International Congress of Cytology in Paris. Its primary purpose is to reduce the rate of unnecessary indeterminate diagnoses but maintain the excellent performance of urine cytology, in detecting high-grade urothelial carcinoma. The reporting system comprises six diagnostic categories, as well as each category’s diagnostic criteria, estimated risk of malignancy, and management recommendations. After six years, TPS 2.0 was applied in 2022 upon the unfolding of new data. TPS 2.0 clarifies the diagnosis categories and updates the risk of malignancy in each category and developments of molecular tests. This review provides an updated summary of TPS 2.0. Some diagnostic pitfalls and molecular tests were also discussed.

Pancreatic cancer remains the most malignant type of cancer. Although immunotherapy has shown good efficacy in most solid tumors, it has a poor response in pancreatic cancer. The difficulty in applying immunotherapy to pancreatic cancer lies in the fact that it is an immunologically “cold” tumor. The dense and poorly vascularized microenvironment of pancreatic cancer is not conducive to the infiltration of immune cells, making it difficult to trigger an immune response. Immunogenic cell death is a specific type of cell death that can initiate an adaptive immune response and turn a “cold” tumor into a “hot” one. In this review, we discuss the basis of immunogenic cell death and its inducers in pancreatic ductal adenocarcinoma. The key point is that the manipulation of adjuvant immunogenic cell death inducers can usually synergize with other immunotherapies. This synergetic effect allows for the combination therapy to fully utilize the immune potential of each component, overcome the immune-suppressed microenvironment of pancreatic cancer, and ultimately activate immune responses that result in tumor regression. Clinical trials of therapy based on this strategy may offer hope to patients with pancreatic cancer.

Ovarian cancer (OvCa) is the most deadly gynecological cancer. This study aimed to determine which genes and miRNAs play an important role in OvCa.

We accessed the Gene Expression Omnibus database and downloaded the mRNA microarray dataset. Through the use of GEO2R, we were able to collect data on differentially expressed genes (DEGs) and microRNAs (DEMs). By querying the Enrichr database, we were able to conduct functional and pathway enrichment analysis on DEGs. STRING was used to create a network of protein–protein interactions, and Cytoscape was used to display the networks. Gene Expression Profiling Interactive Analysis and The Cancer Genome Atlas were then used to conduct overall survival and clinical data analyses of hub genes. DEM target predictions were also made using miRnet. For extracellular vesicles confirmation, Exocarta and Vesiclepedia were used.

There were a total of 1,778 DEGs found, and most of them were enriched for terms associated with the cell cycle, mitosis, and the ovulation cycle. There were 141 nodes used in the creation of the protein–protein interaction network. There were 10 genes with a lot of connections between them. Patients with OvCa had a shorter overall survival if they had high expression of four of the 10 genes tested: ATF3, ZEB1, CSF1R, and HSPA8. We found out that the protein–protein interaction network has a significant module. The cell cycle, extracellular matrix receptor, and cell invasion were among the enriched functions and pathways. In addition, we found a total of 20 DEMs. The hsa-let-7 family (hsa-let-15a-3p, hsa-let-18a-5p, and hsa-let-615-5p) may target ZEB1 because its expression is inversely correlated with that of ZEB1.

This study uncovered critical genes that represent promising therapeutic targets in the fight against OvCa.

Hepatic ischemia-reperfusion injury (HIRI) is a key factor leading to complications and poor prognosis after hepatobiliary surgery, but its pathogenesis remains unclear. Hence, it is a very necessary discovery the prevention and treatment methods and pathological mechanism of HIRI.

Our animal experiments indicated that two doses of dogwood alcohol extract (DAX) at 5 g/kg and 2.5 g/kg (crude drug/mouse body mass) could significantly reduce serum alamine aminotransferase (AST) and aspartate aminotransferase (ALT) in HIRI mice. The level of these two transaminases determined the pharmacodynamic effect of DAX on HIRI. Next, we used the results of network pharmacology and transcriptome sequencing to obtain important prevention and cure target genes, and applied molecular docking to simulate receptor and ligand binding. Finally, immunohistochemical method was made use of verifying the results.

When the model group vs control group, administration group vs model group, set padj < 0.05, | log2FoldChange | >1.0 filter condition, the intersection between the obtained transcriptome sequencing data set and the network pharmacological target was only heparin-binding epidermal growth factor (HBEGF). Then DockThor online software was applied to make loganin and ursolic acid, small molecular compounds contained in DAX, form complexes with HBEGF active sites through hydrogen bonding to interfere with HIRI. Meanwhile, immunohistochemical test results showed that HBEGF expression decreased in the administration group compared with the model group (*P < 0.05).

DAX interferes with the occurrence and development of HIRI by down-regulating HBEGF. Our experimental results not only highlight the advantages of traditional Chinese medicine in treating difficult diseases, but also provide a reference for clinical exploration of new methods to prevent and treat HIRI.

Angelica sinensis (Dang gui) has been widely used in traditional Chinese medicine (TCM) clinics and diet therapy for thousands of years. According to TCM theory, A. sinensis can be used for the treatment of breast cancer. As A. sinensis has effects on estrogen, it may have an adverse effect on the prognosis of breast cancer. This article systematically reviews the literature to explore whether breast cancer patients need to avoid taking A. sinensis.

Using the search terms “breast cancer AND Dong-quai”, “breast cancer AND Angelica sinensis”, “breast cancer AND Dang gui” and “breast cancer AND Dang qui”, relevant studies were retrieved from the PubMed database up to December 31, 2022. After excluding irrelevant and repeated studies, the papers were critically reviewed by TCM physicians, and the papers were secondly screened by the impact factor and ranking of the published journals. The included papers were classified into three groups, reporting a “positive”, “negative” or “inconclusive” effect in patients with breast cancer.

A total of 22 articles were identified, which included 9, 5 and 7 positive negative and inconclusive studies, respectively. The results showed that studies advocating that A. sinensis may be safely consumed by patients with breast cancer had a higher evidence hierarchy than those that did not support consumption.

The findings implied that A. sinensis can be prescribed to patients with breast cancer in appropriate doses under TCM treatment theory.

To explore the main action targets and key pathways, along with their mechanisms of action, of Panax ginseng’s special ingredients in the treatment of ulcerative colitis using network pharmacology methods. To provide a theoretical basis for subsequent laboratory experiments and clinical trials.

The main active ingredients of Panax notoginseng were obtained through the TCMSP database and the specific ingredients were screened. The targets of Panax notoginseng-specific components were obtained from the Swiss Target Prediction database. The GeneCards, OMIM, and DisGent databases were used to obtain the targets related to ulcerative colitis. The protein interaction network (PPI) of intersecting targets was constructed using the STRING database. GO function and KEGG pathway enrichment analysis were performed in R language software. Construction of the herb-component-target-disease-KEGG pathway network was achieved using Cytoscape software.

Seven major active ingredients of Panax notoginseng were obtained, and ginsenoside f2 was found to be a special ingredient, corresponding to 16 potential targets. A search of the disease database yielded 5,536 targets for ulcerative colitis. Eight core targets were obtained by protein interaction analysis of the intersecting targets: STAT3, VEGFA, HSP90AA1, FGF2, IL2, MET, BCL2L1, and RORC, respectively. 417 entries were obtained by GO functional enrichment analysis, and 22 statistically significant pathways were obtained by KEGG enrichment analysis.

The mechanism of action of ginsenoside f2 in the treatment of ulcerative colitis features multi-target and multi-pathway interactions. The receptors may be related to STAT3, VEGFA, HSP90AA1, FGF2, IL2, MET, and other targets, and the main signaling pathways may be related to the PI3K-Akt signaling pathway, Th17 cell differentiation, and inflammatory bowel disease among others and this provides a theoretical basis for the next in-depth experimental study.

Studies on the effect of sedated endoscopy on adenoma detection rate (ADR) and advanced adenoma detection rate (AADR) remain scarce. The present study aims to determine whether sedation can help improve ADR and AADR.

Colonoscopies conducted in four endoscopy centers from January 2012 to July 2019 were included to create a propensity score-matched cohort, and compare the endoscopic factors.

The colonoscopies of 216,400 cases were included. The ADR (32.24% vs. 31.63%, p < 0.05), AADR (5.59% vs. 5.39%, p < 0.05), and polyp (20.61% vs. 20.21%, p < 0.05) increased in the sedated endoscopy group, especially for flat adenomas (44.80% vs. 43.95%, p < 0.05) and adenomas of 0–5 mm (66.99% vs. 66.24%, p < 0.05). However, there was no significant difference, in terms of lesion site. Furthermore, the number of biopsies per colonoscopy was significantly higher in the sedated group (0.79 ± 0.93 vs. 0.56 ± 0.80, p < 0.001). Moreover, there was a significant increase in electronic (0.92% vs. 0.83%, p < 0.05) and chemical staining (0.57% vs. 0.45%, p < 0.001) in the sedated group.

The ADR, AADR and polyp detection rate increased for sedated colonoscopy, especially for flat adenomas and adenomas of 0–5 mm. In addition, the frequency of staining, image enhancement techniques, and number of biopsies per colonoscopy increased in sedated colonoscopy.

Pancreatic cancer (PC) is a highly malignant tumor of the digestive system with a poor prognosis. The early diagnosis and accurate screening of PC in high-risk populations are warranted to improve the prognosis of patients. The present study aimed to evaluate the global research characteristics, hotspots, and future trends of the early screening of PC.

A comprehensive search of studies on early screening of PC in the Web of Science core database was performed between 1 January 2003 and 28 December 2022. The information, which included the study population, authorship, journal, contributing institution, country of origin, and keywords, were collected. The Excel, VOSviewer, and Citespace software were used for the bibliometric analytical processing and visualization.

A total of 581 publications were included and analyzed after the screening. For the past 20 years, the annual number of publications exhibited a fluctuating rising trend. The United States contributed more than 40% of the publications. Ralph H. Hruban was the most cited scholar. Pancreas (n = 35), World Journal of Gastroenterology (n = 24), and Pancreatology (n = 18) were the top three journals with the highest number of publications. Keywords related to liquid biopsies, such as “extracellular vesicle”, “dna”, and “circulating tumor cell”, continued to burst until 2022.

Over the past two decades, this area has been gradually gaining attention, with the number of publications rising annually. Liquid biopsy will be the future research trend. These present findings will provide the latest insight into the state of PC early screening, identifying new perspectives for further research.

The transcriptional inhibitor histone methyltransferase enhancer of zeste homolog 2 (EZH2) predominantly targets genes involved in tumor suppression. EZH2 is highly expressed in a variety of human malignancies and promotes carcinogenesis and malignant transformation. Recent research has indicated that altering the tumor microenvironment by focusing on epigenetic variables can improve antitumor immunity. Recent research has also revealed that EZH2 has pleiotropic functions in immune and malignant cells. EZH2 inhibition could be a promising strategy to improve the outcomes of current immunotherapies. Based on the role of EZH2 in the immunomodulation of both immune and tumor cells, we evaluated the effect of EZH2 on tumor immunity in this review. We also highlight improvements in combined EZH2-targeted treatment and immunotherapy.

Delusional disorder (DD), once entrenched, responds poorly to currently available treatment. This calls for community and individual preventive measures. Our goal was to conduct a literature review exploring the possibilities of prevention. This narrative review was based on a search of the PubMed database from its inception until July 2022. While not specific to DD, the search found evidence for primary and secondary strategies used to protect against or ameliorate psychotic illness characterized by prominent delusions. Community preventive strategies included addressing socioeconomic disadvantage and mental health stigma, improving mental health service accessibility, screening for and treating potential precursors to DD, such as sensory and cognitive deficits, and psychiatric symptoms, like depression, anxiety, sleep disturbance, and substance abuse. Secondary community prevention relied on early detection programs and specialized services for early treatment of DD symptoms and their co-morbidities. Individual forms of secondary prevention were interventions geared toward illness denial, treatment nonresponse and antipsychotic refusal. Effective secondary prevention reduced symptom intensity and diminished the risk of fatal outcomes such as suicide. Based mostly on the evidence from related disorders, the implementation of preventive and early treatment strategies held promise for reducing morbidity and facilitating the recovery of patients with DD.

The International Academy of Cytology Yokohama System for Reporting Breast Fine-Needle Aspiration Biopsy Cytology was developed by a group of expert cytopathologists and clinicians in the breast field. Five categories are defined to stratify breast lesions by their risks of malignancy and managed accordingly. Clinical and radiologic information (triple test) are critical for further management. Ultrasound guidance, and rapid on-site evaluation are valuable for improving the rate of definitive diagnosis. Ancillary studies can be tested on cytologic samples to provide prognostic, predictive information as well as diagnostic clues. Based on many published studies in different institutions worldwide, the implementation of the system appears to have been successful. However, further studies are important for improvements and modifications to the current system.

There is limited information available on the evaluation of placebo or nocebo effects on itch. The present study developed a search strategy using PubMed to evaluate literature related to placebo and/or nocebo effects on itch. The search strategy identified 65 articles. After the independent review of each article, 10 studies were selected for inclusion. These studies varied, in terms of methods and outcome measures. Overall, verbal suggestion, conditioning, and/or placebo topical therapies led to placebo and/or nocebo effects on itch. Further understanding the mechanisms of placebo and nocebo effects on verbal suggestion and conditioning can open doors to the development of therapeutic strategies that could ameliorate or improve itch in patients.

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in developed countries, contributing to ∼24% of cases worldwide and includes non-alcoholic steatohepatitis. High-throughput OMICS approaches have been used to characterize NAFLD conditions for the identification of potential molecular signatures or differentially regulated molecules (DEMs). The present study aims to perform a systematic review and meta-analysis from an omics perspective.

We analyzed the publically available data set (accession number: GSE63067) from the Gene Expression Omnibus (GEO) using the GEO2R program. The differentially expressed genes (DEGs) were filtered using the criteria where genes with p-value ≤0.05 and fold-change ≥2.0-fold (upregulated), and fold-change ≤0.5-fold (downregulated).

We identified 264 differentially expressed genes (DEGs) between NAFLD and normal liver tissue samples, where 211 were upregulated and 53 were downregulated in NAFLD. Additionally, we identified novel genes sphingomyelin synthase 2 and WNK lysine deficient protein kinase 3 that were not well understood in the molecular pathophysiology of NAFLD. Further gene ontology-based analysis revealed that among biological processes, cellular components, and molecular functions were also dysregulated in NAFLD.

Our study shows that meta-analysis of publicly available data is useful for the identification of DEGs and indication of dysregulated biological processes in NAFLD, which provide valuable insights into the molecular mechanisms of NAFLD.

Cancer is a hereditary multifactorial disease, and due to its rising incidence in both young people and adults along with its substantial burden, oncological emphasis has been placed more on preventive efforts. It has been suggested that several food and lifestyle choices contribute to the onset of cancer, presumably via complex metabolic and inflammatory pathways. Diet is one of the crucial variables in determining cancer risk. In addition, as research intensifies, a more distinct link between diet and patients’ molecular alterations is emerging and becoming quantifiable, dispelling the previous conventional wisdom that linked phenotypic changes to dietary variation. Although the evidence is not consistent, appropriate doses of vitamin B12, vitamin D, vitamin C, selenium, folic acid, and antioxidants such as carotenoids have shown a preventive effect in certain types of cancer. However, improper use of dietary supplements in well-nourished people provides no effects or even poses harmful effects to increase the risk of some cancer. Contrarily, other factors like alcohol, obesity, certain fatty acids, and some techniques used for food preparation may increase the risk of cancer. It is now appropriate to make dietary modifications that are consistent with suggestions for preventing cancer incidence with an emphasis on lifestyle improvement including proper management of problems associated with diet, nutrition, smoking, and drinking. However, there is currently a need for more clinical research to demonstrate the safety and effectiveness of using various phytochemicals or plant extracts as dietary supplements to prevent primary stages of cancer.

Hepatitis delta virus (HDV) is a defective virus and causes severe liver disease. Several HDV RNA assays have been developed, however the diagnostic efficacy remains unclear.This systematic review and meta-analysis aims to evaluate the diagnostic accuracy of HDV RNA assays to aid in the diagnosis of active hepatitis D.

The PubMed, Embase, and Cochrane Library databases were systematically searched from the beginning to June 31, 2022. Information on the characteristics of the literature and data on sensitivity, specificity, and area under curve (AUC) of the receiver operating characteristic (ROC) were extracted. Stata 14.0 was used for meta-analysis of the combined sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio.

A total of 10 studies were included in the meta-analysis. The summary sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio of HDV RNA assays for HDV diagnosis were 0.92 (95% CI: 0.87–0.95), 0.90 (95% CI: 0.86–0.93), 7.74 (95% CI: 5.31–11.29), 0.10 (95% CI: 0.06–0.18) and 99.90 (95% CI: 47.08–211.99), respectively. The AUC of the pooled ROC curve was 0.95 (95% CI: 0.92–0.96).

The results show that HDV RNA assays had high diagnostic performance. However, that is limited by the number and quality of studies. Standard protocols for the development of assays by manufacturers and larger studies on the use of the assays are needed.

Aging, shifting demographics, and lifestyle changes are some of the underlying factors contributing to an increase in the incidence and prevalence of age-related disorders. Brain health is correlated with cellular senescence and is an important indicator of physiological aging and several age-related diseases. Examining the current state of knowledge of the underlying mechanisms of senescence as well as prospective therapeutic modalities concerning aging and age-related diseases is thus crucial. The senescence-associated secretory phenotype (SASP) of senescent cells (SnCs) results in a secretome, which is primarily composed of growth factors, cytokines/chemokines, and extracellular matrix (ECM) remodeling proteins secreted by the arrested cells. Increasingly, research suggests a causative role of senescence in various diseases such as osteoporosis, neurodegenerative diseases, cardiovascular diseases, and metabolic dysfunction, among others. SnCs promote age-related diseases by affecting the differentiation and proliferation of stem cells. They do so, in part through disruption of the Wingless-related integration site (Wnt) signaling pathways and Yes-associated protein and its ortholog transcriptional coactivators with a PDZ-binding domain (YAP/TAZ) transcriptional regulation, affecting tissue regeneration and a decreased ability for the body to rejuvenate. Senescent cell-induced immune system dysregulation, e.g., immunosenescence, as well as senescent cell-secreted substances also cause persistent, low-grade inflammation in organisms known as inflammaging, which accelerates aging and results in tissue damage. During age-related senescence, key chromatin structural changes take place in the cells that affect nuclear transport, causing genomic instability, changes in nucleosome positioning, post-translational modifications of histones, global histone loss, etc. Elimination of SnCS using senolytics by targeting cellular and molecular pathways has emerged as a potential therapeutic strategy for delaying aging and improving age-related dysfunctions including brain diseases.

The growing knowledge of ferroptosis has suggested the regulatory role of ferroptosis in hepatocellular carcinoma (HCC), but the pertinent molecular mechanisms remain unclear. Herein, this study investigated the mechanistic basis of ferroptosis-related genes (ferrGenes) in the growth of HCC.

Differentially expressed human ferrGenes and tumor-related transcription factors (TFs) were obtained from the The Cancer Genome Atlas (TCGA) dataset and the GTEx dataset. Spearman method-based correlation analysis were conducted to construct TF-ferrGene coexpression regulatory network. Key genes associated with prognosis were singled out with Lasso regression and multivariate Cox analysis to construct the prognostic risk model. Then the accuracy and independent prognostic ability of the model were evaluated. Expression of CENPA and STMN1 was determined in clinical HCC tissues and HCC cells, and their binding was analyzed with dual-luciferase and chromatin immunoprecipitation (ChIP) assays. Furthermore, ectopic expression and knockdown assays were performed in HCC cells to assess the effect of CENPA and STMN1 on ferroptosis and malignant phenotypes.

The prognostic risk model constructed based on the eight TF-ferrGene regulatory network-related genes accurately predicted the prognosis of HCC patients. It was strongly related to the clinical characteristics of HCC patients. Moreover, CENPA/STMN1 might be a key TF-ferrGene regulatory network in ferroptosis of HCC. CENPA and STMN1 were overexpressed in HCC tissues and cells. Additionally, CENPA facilitated STMN1 transcription by binding to STMN1 promoter, thus facilitating the malignant phenotypes and suppressing the ferroptosis of HCC cells.

Taken together, CENPA curbs the ferroptosis of HCC cells by upregulating STMN1 transcription, thereby promoting HCC growth.

Radiotherapy is the most crucial nonsurgical therapeutic method in the multidisciplinary care of patients with non-small cell lung cancer (NSCLC). However, radiation resistance continues to be a significant clinical issue, negatively affecting cancer prognosis in patients. The small molecules that target these RNAs offer therapeutic modulation of multiple biological processes. The study aims to identify the genes and a long non-coding RNA (lncRNA) regulating their expression levels, as well as the binding potential of small volatile inhibitors to the lncRNA to overcome radioresistance in NSCLC.

The non-coding RNA microarray dataset of NSCLC cells was analysed to identify the differentially expressed genes regulated by lncRNA, which drives radioresistance. The study comprises three volatile ligands due to their good pharmacokinetic profile to target the identified lncRNA.

The analysis revealed the dysregulation of the cell cycle, evasion of apoptosis and cancer immune response. A co-expression analysis with a network pharmacology approach revealed an lncRNA ENST00000605056 regulating three highly ranked hub genes. The molecular interaction studies uncovered their high binding affinity to its binding pocket with a preponderance of non-covalent bond interactions between the ligand and the nucleotides. The molecular dynamics simulations revealed the binding stability of ligands to the lncRNA with a very low deviation compared to the control.

This study demonstrates the ability of small molecules to target lncRNA in addressing the global concern of radioresistance among NSCLC patients, thereby facilitating future translational studies.