Objective This study aims to utilize the CRISPR / Cas9 system to achieve β-cell specific gene knockout in the pancreas through adeno-associated virus ( AAV8 ) carrying guide RNA ( gRNA ) targeting the Adra2a gene. Methods  RIP2 ( rat insulin Ⅱ promoter ) -Cre; Cas9KI / + mice were used to achieve β-cell-specific gene editing. In this model, the RIP2 promoter drives Cre recombinase expression selectively in pancreatic β cells, resulting in targeted activation of Cas9 in these cells. To enable efficient editing of the Adra2a gene, adeno-associated virus serotype 8, a low-immunogenic vector, was used to deliver gene-specific guide RNAs. AAV8 particles carrying gRNAs targeting Adra2a were injected via the pancreatic duct, enabling precise geneknockout in β cells. Results   Successful β-cell-specific gene knockout was achieved in the pancreas, confirmed by tissue analysis, PCR, and protein expression analysis. GFP expression was observed in the pancreas, and the targeted gene was successfully disrupted in β cells. Conclusion  The use of AAV carrying gRNA in the RIP2-Cre; Cas9KI / + mouse model provides an effective method for β-cell-specific gene knockout, offering a valuable tool for future studies of islet gene function.

Objective To investigate how miR-181c influences cardiopulmonary recovery afterlung transplantation in mice by targeting mitochondrial calcium uniporter 1 (MICU1) . Methods Fifty-four adult male C57BL / 6 mice were randomly assigned to six groups (n = 9 each): Normalgroup, Lung Transplantation group, Lung Transplantation + inhibitor-NC group, Lung Transplantation + miR-181c-inhibitor group, Lung Transplantation + miR-181c-inhibitor + si-NC group, andLung Transplantation + miR-181c-inhibitor + si-MICU1 group. The Normal group underwent anesthesia and thoracotomy only; the other groups received autologous left lung orthotopic transplantation,followed by weekly tail-vein injections (0. 2 mL) of saline or 10 nmol / mL inhibitor / siRNA for 60days. qRT-PCR and Western blotting were use to detect miR-181c and MICU1 mRNA and protein expression levels. Dual-luciferase gene reporter assay was performed to verify the targeting relationship between miR-181c and MICU1. Pulmonary pathology was assessed by hematoxylin-eosin (HE) staining. Pulmonary function was assessed using a small animal pulmonary function test system [0. 15 s forced expiratory volume as a percentage of forced vital capacity ( FEV0. 15 / FVC), peak expiratory flow (PEF), maximum ventilation volume ( MVV), diffusing capacity of the lung for carbon monoxide ( DLCO), and residual volume ( RV)] . Cardiac function was detected using small animal ultrasound imaging technology [ left ventricular ejection fraction ( LVEF), left ventricular fractional shortening (LVFS), left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter ( LVESD), left ventricular end-diastolic volume ( LVEDV), and left ventricular end-systolic volume (LVESV)] . Results The expression level of miR-181c was elevated and that of MICU1 was reduced in the Lung transplantation group versus those in the Normalgroup (P< 0. 05), with a significant negative correlation (r = - 0. 378, P = 4. 21 × 10 - 4 ) . miR- 181c mimic suppressed MICU1-3′ UTR-WT luciferase activity ( P < 0. 05 ) but not 3′ UTRMUT. Inhibition of miR-181c expression restored MICU1 expression, and reduced lung lesions, and improved FEV0. 15 / FVC, PEF, MVV, DLCO, LVEF, LVFS, and decreased RV, LVESD, LVEDV, LVESV ( all P < 0. 05) . These gains were abolished by co-silencing MICU1 and miR-181c (P< 0. 05) . Conclusion miR-181c impairs cardiopulmonary recovery after lung transplantation bytargeting MICU1. miR-181c inhibition enhances post-transplant function.

Objective To investigate the use of quantitative real-time PCR as an alternative tothe screening plate culture method for the detection of salmonella and shigella in pre-employmenthealth examinations, comparing the two methods in terms of detection rate, cost, and duration oftesting. Methods Compare the screening test results of salmonella and shigella detection using thebacterial screening plate culture method in 10 100 cases in 2023 with the screening test results ofsalmonella and shigella detection using the quantitative real-time PCR method in 9 842 cases in2024. Results Quantitative real-time PCR method demonstrated a high level of screening power(91 / 9 842 in 2024 vs. 0 / 10 100 in 2023) with a lower total cost (4. 4 yuan / sample in 2004 vs. 6. 9 yuan / sample in 2023) . In addition, quantitative real-time PCR can be implemented without increasing the testing duration and is easy to carry out. Conclusion Quantitative real-time PCR can be usedas a screening test for salmonella and shigella detection in pre-employment health examinations.

Regulatory T cells ( Tregs) play multifaceted roles in hepatic inflammatory injury. On one hand, Tregs can migrate to inflamed hepatic tissues via chemokine-mediated chemotaxis, exerting immunosuppressive functions and promoting tissue repair. On the other hand, during the fibrotic process induced by inflammatory injury, the interactions between Tregs and other immune cells can counteract fibrogenesis. This review focuses on the classification and functions of Tregs, their specific roles in hepatic inflammatory injury diseases, and the underlying mechanisms mediating their actions in hepatic inflammation and injury, to elucidate the intricate mechanisms by which Tregs modulate hepatic inflammatory injury and further clarify the complexity of hepatic immune cell interactions.

Helicobacter pylori (HP) is a major pathogen responsible for various gastrointestinaldiseases, and its eradication plays a critical role in preventing gastric cancer. The resistance of HP to clarithromycin has become a key issue affecting its eradication. This article reviews the main molecular mechanisms of HP resistance to clarithromycin, aiming to provide a theoretical foundation for optimizing treatment strategies and future antimicrobial research.

Influenza, also known as the flu, is an acute respiratory infectious disease causedby the influenza virus. It has a high incidence rate and can lead to patient mortality. To create a suitable environment for replication and proliferation, the influenza virus engages in complex interactions with the host, including the regulation of host cell gene expression and various signaling pathways by the virus. The type I interferon signaling pathway, as the first line of defense against viral infections, is an important component of the host’s antiviral innate immunity. Meanwhile, type Ⅱ and type Ⅲ interferon systems also influence viral replication through different mechanisms. Literature reports that influenza virus can induce degradation of related cellular proteins to evade the host’s antiviral immune response. This article focuses on the regulation of the interferon system by influenza virus, discussing the molecular mechanisms and biological significance of how the virus promotes ubiquitination and degradation of proteins related to typeⅠ , Ⅱ , and Ⅲ interferon pathways. Understanding how influenza virus antagonizes interferon-mediated antiviral responses is conducive to the development of new anti-influenza therapies by targeting host factors.