Restenosis is a serious complication for patients with coronary heart disease (CHD) undergoing percutaneous coronary intervention (PCI). In this prospective clinical study, we aimed to investigate the effects of Radix Salviae decoction (RSD) on coronary stenosis and restenosis in CHD patients.

We conducted this study at Guangdong Hospital of Traditional Chinese Medicine (registration No. BF2022-052) and enrolled 60 patients diagnosed with CHD for PCI surgery. The patients were divided into a control group and an RSD treatment group of 30 cases each. The primary outcome was restenosis after PCI, and the secondary outcome was newly increased stenosis (neostenosis).

Fifty-eight of the 60 enrolled patients completed follow-up and were included in the final analysis, with 28 in the control and 30 in the RSD group. A baseline comparison of stenosis location, stenosis degree, and the number of vessels in stenosis before PCI showed comparable results (p > 0.05). Comparison of implanted stents showed similar features in stent diameter and stent length during PCI between the two groups (p > 0.05). For the primary outcome, there was no significant difference in restenosis percentage (p > 0.05) or the number of vessels in restenosis (p > 0.05) of the three arteries between groups. For the secondary outcome, neither the number of nonculprit vessels in neostenosis after PCI nor the percentage of neostenosis of the three arteries showed significant differences between groups (p > 0.05). Although multifactor logistic regression analysis for the incidence of restenosis did not find any statistically significant factors (p > 0.05), the diagnosis of MI/angina (p = 0.031), average stent length (p = 0.010), and alanine transaminase (p = 0.027) were found to be significantly associated with neostenosis occurrence. Safety index measurement indicated that RSD had a good safety profile in clinical treatment.

Although the addition of Radix Salviae decoction for a short period did not significantly change restenosis and neostenosis after PCI, the diagnosis of MI/angina, average stent length and aspartate aminotransferase levels were significantly associated with neostenosis occurrence. This pilot research will help to design future studies in investigating RSD effects on stenosis.

With the development of gene editing technology, its application in tumor diagnosis is becoming increasingly widespread. The CRISPR/Cas system is an important gene editing tool that can significantly improve the early detection rate and precision diagnosis level, enabling high-throughput and high-sensitivity detection of tumors. This article focuses on CRISPR/Cas system for detecting various tumor-related targets and elaborates on its applications in tumor diagnosis from five aspects: (1) detection of tumor-derived exosomes: by recognizing the surface proteins or nucleic acids of exosomes secreted by tumor cells into blood or other samples through adaptors, the CRISPR system is activated, achieving non-invasive liquid biopsy of tumors; (2) detection of circulating tumor DNA tumor cells disseminate DNA into the circulatory system to trigger nucleic acid reactions involving gene editing enzymes, enabling the monitoring of tumor dynamic states; (3) detection of circulating tumor cells (CTCs): by using aptamers to recognize surface proteins of tumor cells or directly detecting tumor-related nucleic acids, the integrated CRISPR system allows for the detection of circulating tumor cells even in trace amounts, achieving precise diagnosis; (4) detection of tumor markers: high sensitivity is achieved through the coupling of various tumor marker aptamers and gene editing systems; (5) detection and identification of tumor microenvironments: by activating gene editing enzyme activity through differential factors in the tumor tissue microenvironment and triggering nucleic acid reactions, the diagnosis and dynamic monitoring of tumors can be achieved. The progress and bottlenecks of the CRISPR/Cas system in tumor diagnosis in the future are also discussed.

Antimicrobial resistance (AMR) poses a significant threat to public health in the 21st century, with bacteria such as Campylobacter jejuni (C. jejuni) exhibiting multidrug resistance due to the presence of AMR genes. Understanding the evolutionary patterns and functional relationships of these genes is crucial for addressing this issue effectively.

We conducted phylogenetic analysis to examine the evolution of AMR genes in C. jejuni. Additionally, we constructed and analyzed a gene interaction network comprising 39 functional relationships. Clustering analysis was employed to identify interconnected clusters associated with AMR processes. Functional enrichment analysis was performed to explore the involvement of cellular components, molecular functions, and biological processes.

Our analysis revealed two interconnected clusters (C1 and C2) closely associated with AMR processes. Furthermore, genes encoding ribosomal proteins (rplE, rplV, rplG, rplK, rplA, rplJ, rpsE, rplB, rpsL, and rpmA) were identified as hub genes within the gene interaction network. These genes interact frequently with their functional counterparts, indicating their significance in AMR mechanisms. Enriched Kyoto Encyclopedia of Genes and Genomes pathway analysis highlighted the importance of the ribosome pathway in understanding antibiotic resistance mechanisms in C. jejuni.

The findings of this study enhance our understanding of the molecular mechanisms underlying AMR in C. jejuni. By elucidating the evolutionary patterns, gene interactions, and pathway enrichment, our study provides valuable insights that may contribute to the development of novel treatments for illnesses caused by this pathogen.

Wilms tumor is the most common renal malignancy in children. miR-146a, a highly conserved small noncoding RNA, plays a critical role in various human diseases. Increasing studies have suggested that rs2910164 C>G polymorphism in miR-146a is associated with susceptibility to cancers. However, miR-146a rs2910164 C>G polymorphism influence on Wilms tumor remains unknown. The aim of this study was to evaluate the relationship between miR-146a rs2910164 C>G polymorphism and Wilms tumor susceptibility in Chinese children.

In the six-center case-control study, we enrolled 1,352 subjects from East China (416 cases and 936 healthy controls). The TaqMan method was adopted to genotype the miR-146a rs2910164 C>G polymorphism. Logistic regression models were utilized to assess the correlation between this polymorphism and the risk of Wilms tumor.

No significant association was observed between miR-146a rs2910164 C>G polymorphism and the susceptibility to Wilms tumor. Further stratification analysis also did not detect a significant relationship.

The present study showed no association of miR-146a rs2910164 C>G polymorphism with the risk of Wilms tumor in the Eastern Chinese population. Subsequent studies with a larger sample size will be required to validate these results.

Both alcohol-associated liver disease (ALD) and metabolic dysfunction-associated steatotic liver disease are leading contributors to chronic liver diseases. These conditions often coexist, exacerbating disease progression. Despite ALD being a leading cause of liver transplantation, many individuals with alcohol use disorder (AUD) do not receive treatment. In this review, we discussed the epidemiology of ALD in AUD, various treatment options for AUD, and their efficacy on liver health. Our critical analysis of current evidence underscores the need for integrated models involving multiple stakeholders to improve ALD management.

The global burden of colorectal cancer (CRC) is a pressing concern, with a substantial impact on public health. Despite advancements in understanding the molecular mechanisms of CRC development, challenges remain in translating this knowledge into effective clinical interventions. Key genetic mutations, notably in the adenomatous polyposis coli (APC) and Kirsten rat sarcoma virus (KRAS) genes, are central to CRC initiation and progression. Current CRC treatments include surgery and chemotherapy, often combined with targeted agents. However, resistance and heterogeneity within CRC patients limit the effectiveness of these therapies. Promisingly, research has focused on targeting APC and KRAS mutations for therapy. Small molecules inhibiting the Wnt pathway and antibodies targeting specific components are under investigation. Targeting KRAS itself is challenging due to its conserved structure, but disrupting its membrane interactions and subcellular localization are potential therapeutic strategies. To address the limitations of single-drug therapy, combination approaches are gaining traction. Combination therapy not only minimizes off-target effects but also tackles drug resistance and diverse genetic alterations within tumors. The intricate interplay of mutations and pathways in CRC necessitates multifaceted therapeutic strategies. Although progress has been made in understanding CRC genetics and developing targeted therapies, there is still work to be done to translate these insights into effective clinical treatments for CRC patients. This review provides crucial information for novel combination treatments for CRC.

Over the past decade, significant progress has been made in managing acute myeloid leukemia (AML). However, refractory disease and relapse continue to pose major challenges. These issues highlight the need for innovative therapeutic options to achieve deeper remission and effectively treat refractory and relapsed diseases, thereby improving survival rates. Natural killer (NK) cell-based therapies have emerged as a promising option. NK cells, a specialized population of innate lymphoid cells, exhibit inherent anti-viral and anti-cancer capabilities. Unlike T cells, NK cells do not require prior antigen sensitization to eliminate their target cells, enhancing their potential as immunotherapeutic agents. However, NK cells often exhibit dysfunction in patients with hematological malignancies. Revitalizing these cells represent another immunotherapeutic strategy. Various NK cell-based therapies have been explored in recent decades, particularly in managing AML. These therapies include chimeric antigen receptor-NK cell therapy, bispecific and trispecific NK cell engagers (bi-specific killer cell engager (BiKEs) and tri-specific killer cell engager (TriKEs), and cytokine-induced memory-like NK cells. These therapies are also associated with fewer adverse events, such as neurotoxicity. Despite their potential for clinical cancer management, challenges such as the in vivo expansion of NK cells remain unresolved. This review summarizes the biology of NK cells and the diverse NK cell-based therapies being developed for the potential management of AML, as evidenced in preclinical studies and clinical trials.

The presence of multinucleated giant cells in fine needle aspiration (FNA) specimens of neuroblastic tumors is not uncommon, but they are often not well-illustrated in the literature. The authors present a case of a 3-year-old boy with a large abdominal mass that was found to have striking multinucleated giant cells on FNA. The FNA specimen showed a cellular smear with a predominance of small, round cells with scant cytoplasm and hyperchromatic nuclei. There were also numerous multinucleated giant cells, some of which had up to 10 to 20 nuclei. The giant cells contained abundant cytoplasm and prominent nucleoli. The patient was subsequently diagnosed with ganglioneuroblastoma. The authors discuss the differential diagnosis of multinucleated giant cells in FNA specimens and argue that these cells can be a helpful diagnostic clue in the diagnosis of ganglioneuroblastoma. The importance of recognizing multinucleated giant cells in FNA specimens of other soft tissue tumors is also discussed.

Prostate cancer (PC) is the second leading cause of death among American men, with most patients receiving androgen deprivation therapy and eventually developing resistance to treatment. The 5-year survival rate from 2015–2020 for men with distant disease was 33%, demonstrating the need for more optimal treatment regimens for patients with distant or metastatic PC. Pharmacogenomic (PGx) testing, a component of precision medicine, focuses on the way a patient’s genome affects drug metabolism. Combining PGx testing with current genetic testing provides an innovative and personalized approach to treating PC while both reducing adverse events and optimizing treatment dosages to fit the patient’s genetic make-up. This review paper describes how clinicians can use PGx testing in combination with genetic testing for PC patients.

The hepatitis E virus (HEV) is a zoonotic disease, and infection with HEV in humans primarily causes acute infections and can progress to chronic manifestation in immunocompromised individuals. Over the past decade, guidelines for diagnosing and treating HEV infection have been developed. This study aimed to systematically assess the quality of current guidelines for diagnosing and treating HEV infection, and we analyzed the differences in guideline quality and primary recommendations and explored possible reasons for these differences.

Guidelines published between 2013 and 2022 were searched, and studies were identified using selection criteria. The study assessed the quality of the included guidelines using the Appraisal of Guidelines for Research and Evaluation tool, extracted the primary recommendations in the guidelines, determined the highest level of evidence supporting the recommendations, and reclassified the evidence using the Oxford Centre for Evidence-Based Medicine grading system.

Seven guidelines were included in the final analysis. The quality of the guidelines varied widely. The discrepancies may have been caused by the lack of external experts, the failure to consider influencing factors in guideline application, and the lack of consideration of the public’s opinion. Analysis of the heterogeneity in primary recommendations revealed differences in algorithms for managing chronic HEV infection, the dosage of ribavirin, and a low level of evidence supporting the primary recommendations.

Guideline quality and primary recommendations vary considerably. Refinement by guideline developers and researchers would facilitate updating and applying guidelines for diagnosing and treating HEV infection.