Background: Influenza A viruses (IAVs) are the major pathogens associated with respiratory infections which can result in extensive pathological damage in lungs and serious complications. Isorhamnetin, an abundant natural flavonoid in fruits and medicinal plants, has recently been shown to have strong antioxidative, anti-inflammatory, and antiviral effects. Objective: This study investigated the pharmacological effects of isorhamnetin on viral pneumonia and explored the underlying mechanisms by in vivo and in vitro experiments. Materials and methods: In the present study, the protective effect of isorhamnetin against IAV was evaluated by the cytopathogenic effect assay, cell counting kit-8 assay, real-time polymerase chain reaction, and immunofluorescence assay in vitro. Then the pathological damage associated with pneumonia was examined by calculating the pulmonary index and performing micro-CT and hematoxylin-eosin staining in vivo. Thereafter, the related protein or gene levels of factors in the mitogen-activated protein kinase (MAPK) and nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathways were determined by Western blot and immunofluorescence staining. Results: Isorhamnetin exerted significant anti-influenza effects and inhibited the expression of viral RNA in A549 cells, counteracting oxidative stress and apoptosis by suppressing the production of reactive oxygen species and caspase-3. The in vivo experiment results showed that isorhamnetin (20 and 40 mg/kg) caused a significant decrease in the pulmonary index, ameliorated pathological damage in the lung tissue, decreased viral load and NA activity, and reduced cytokines and nuclear factors. Furthermore, isorhamnetin could counteract the B cell lymphoma-2/B cell lymphoma-2–associated X protein (Bax) imbalance induced by PR8, suppress activation of the MAPK pathway, and upregulate the expression of Nrf2 and HO-1. Conclusions: Isorhamnetin can protect against viral pneumonia by activating the Nrf2/HO-1 pathway and suppressing the MAPK path-way. This study deciphers the pharmacological mechanism of isorhamnetin in alleviating pathological damage in viral pneumonia and provides rationale for the application of isorhamnetin in influenza treatment.

Background: Influenza A viruses (IAVs) are the major pathogens associated with respiratory infections which can result in extensive pathological damage in lungs and serious complications. Isorhamnetin, an abundant natural flavonoid in fruits and medicinal plants, has recently been shown to have strong antioxidative, anti-inflammatory, and antiviral effects. Objective: This study investigated the pharmacological effects of isorhamnetin on viral pneumonia and explored the underlying mechanisms by in vivo and in vitro experiments. Materials and methods: In the present study, the protective effect of isorhamnetin against IAV was evaluated by the cytopathogenic effect assay, cell counting kit-8 assay, real-time polymerase chain reaction, and immunofluorescence assay in vitro. Then the pathological damage associated with pneumonia was examined by calculating the pulmonary index and performing micro-CT and hematoxylin-eosin staining in vivo. Thereafter, the related protein or gene levels of factors in the mitogen-activated protein kinase (MAPK) and nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathways were determined by Western blot and immunofluorescence staining. Results: Isorhamnetin exerted significant anti-influenza effects and inhibited the expression of viral RNA in A549 cells, counteracting oxidative stress and apoptosis by suppressing the production of reactive oxygen species and caspase-3. The in vivo experiment results showed that isorhamnetin (20 and 40 mg/kg) caused a significant decrease in the pulmonary index, ameliorated pathological damage in the lung tissue, decreased viral load and NA activity, and reduced cytokines and nuclear factors. Furthermore, isorhamnetin could counteract the B cell lymphoma-2/B cell lymphoma-2–associated X protein (Bax) imbalance induced by PR8, suppress activation of the MAPK pathway, and upregulate the expression of Nrf2 and HO-1. Conclusions: Isorhamnetin can protect against viral pneumonia by activating the Nrf2/HO-1 pathway and suppressing the MAPK path-way. This study deciphers the pharmacological mechanism of isorhamnetin in alleviating pathological damage in viral pneumonia and provides rationale for the application of isorhamnetin in influenza treatment.

Background: Influenza A viruses (IAVs) are the major pathogens associated with respiratory infections which can result in extensive pathological damage in lungs and serious complications. Isorhamnetin, an abundant natural flavonoid in fruits and medicinal plants, has recently been shown to have strong antioxidative, anti-inflammatory, and antiviral effects. Objective: This study investigated the pharmacological effects of isorhamnetin on viral pneumonia and explored the underlying mechanisms by in vivo and in vitro experiments. Materials and methods: In the present study, the protective effect of isorhamnetin against IAV was evaluated by the cytopathogenic effect assay, cell counting kit-8 assay, real-time polymerase chain reaction, and immunofluorescence assay in vitro. Then the pathological damage associated with pneumonia was examined by calculating the pulmonary index and performing micro-CT and hematoxylin-eosin staining in vivo. Thereafter, the related protein or gene levels of factors in the mitogen-activated protein kinase (MAPK) and nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathways were determined by Western blot and immunofluorescence staining. Results: Isorhamnetin exerted significant anti-influenza effects and inhibited the expression of viral RNA in A549 cells, counteracting oxidative stress and apoptosis by suppressing the production of reactive oxygen species and caspase-3. The in vivo experiment results showed that isorhamnetin (20 and 40 mg/kg) caused a significant decrease in the pulmonary index, ameliorated pathological damage in the lung tissue, decreased viral load and NA activity, and reduced cytokines and nuclear factors. Furthermore, isorhamnetin could counteract the B cell lymphoma-2/B cell lymphoma-2–associated X protein (Bax) imbalance induced by PR8, suppress activation of the MAPK pathway, and upregulate the expression of Nrf2 and HO-1. Conclusions: Isorhamnetin can protect against viral pneumonia by activating the Nrf2/HO-1 pathway and suppressing the MAPK path-way. This study deciphers the pharmacological mechanism of isorhamnetin in alleviating pathological damage in viral pneumonia and provides rationale for the application of isorhamnetin in influenza treatment.

Objective: This study aims to investigate the therapeutic effects and underlying mechanisms of Xuanfei Baidu Decoction (XFBD) in a mouse model of dampness-heat toxin pneumonia. By exploring how XFBD exerts its effects, we seek to deepen our understanding of its role in treating pulmonary diseases and to address the current knowledge gap regarding its mechanisms of action, thereby supporting its clinical application. Methods: Ultra-high-performance liquid chromatography and high-resolution mass spectrometry (HRMS) were employed to analyze the chemical constituents of XFBD. The protective effects of XFBD were evaluated using a dampness-heat toxin-induced mouse model, established through dampness-heat exposure and HCoV-229E infection. XFBD was administered orally, followed by assessments including lung index measurement, micro-CT imaging, viral load quantification, cytokine analysis, and histological evaluation via hematoxylin-eosin staining. Proteomics and single-cell transcriptomic analyses were conducted to explore the potential mechanisms underlying XFBD’s pharmacological effects. A cellular model of HCoV-229E infection was developed to investigate changes in the cAMP/PKA signaling pathway. Molecular docking and surface plasmon resonance (SPR) experiments confirmed the strong binding affinity between key XFBD components and PKA. Finally, PKA activators and inhibitors were applied in vitro to validate these mechanistic findings. Results: In vivo studies demonstrated that XFBD significantly reduced the lung index, improved the structural integrity of lung and tongue tissues, and decreased levels of proinflammatory mediators, including IL-6, IL-8, and TNF-α. Proteomic and single-cell transcriptomic analyses showed that the differentially expressed proteins after XFBD treatment were primarily associated with inflammatory responses and immune regulation. The cAMP/PKA signaling pathway was identified as a key mechanism underlying these therapeutic effects. Notably, Western blot, ELISA, molecular docking, and SPR analyses confirmed that XFBD elevated cAMP levels and p-PKA expression, thereby activating the cAMP/PKA signaling pathway in vitro. Conclusion: This study demonstrated that XFBD significantly alleviates symptoms in mice with dampness-heat toxin pneumonia. Its therapeutic effects are mediated, at least in part, through activation of the cAMP/PKA signaling pathway. These findings provide compelling evidence that XFBD is an effective herbal remedy against HCoV-229E infection.

The European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS) have recently updated and published the 2024 ESC guidelines for the management of atrial fibrillation. Based on the latest evidences, the guidelines have been updated in many aspects, such as diagnostic criteria for atrial fibrillation, AF-CARE treatment principles, comorbidities and risk factor management. In particular, there are significant changes in the recommendations for surgical management of atrial fibrillation in the guidelines. Therefore, this paper aims to interpret the content updates of the guidelines in AF-CARE treatment principles, diagnostic criteria and surgical treatment of atrial fibrillation, especially highlighting the updates and new suggestions about surgical treatment of atrial fibrillation.

Objective To observe the clinical efficacy and safety of Kangyan Jingfang in the treatment of post-operative cancer-related fatigue in Stage ⅡB-Ⅲ colorectal cancer.Methods A total of 66 patients with stage ⅡB-Ⅲ colorectal cancer who were diagnosed as cancer-related fatigue(CRF)based on TCM syndrome differentiation as spleen vacuity and essence depletion were divided into treatment group and control group randomly,with 33 cases in each group.The treatment group was treated with conventional symptomatic treatment combined with Kangyan Jingfang,and the control group was treated with conventional symptomatic treatment,the course of treatment was 60 days.The scores of cancer-related Fatigue(CFS),TCM syndrome accumulation scale,the revised Piper fatigue scale,Karnofsky performance status,hospital anxiety and depression scale(HAD),tumor markers(CEA,CA19-9,CA72-4,CA12-5,CA15-3,CA242,CA50,Septin9 gene methylation,etc.),immune function(CD3+T lymphocyte level,CD4+T lymphocyte level,CD8+T lymphocyte level and CD4+/CD8+ratio)and safety indexes(blood routine,liver and kidney function)were compared between the two groups in order to evaluate the clinical efficacy of Kangyan Jingfang on CRF.Results 60 cases were included in the observation finally,including 30 cases in each group.After treatment,the scores CFS,TCM syndrome accumulation scale,the revised Piper fatigue scale and HAD of two groups were decreased,but the treatment group before treatment showed a significant decrease in all indicators compared to the control group(P<0.05).The KPS score in the treatment group improved after treatment compared to the control group significantly(P<0.05).CEA,CA19-9 and the methylation of Septin9 gene were significantly decreased in the treatment group after treatment(P<0.05).CD3 and CD4 in treatment groups were higher than control group after treatment significantly(P<0.05).There were no significant abnormal changes in safety indexes before and after treatment(P>0.05).Conclusion Kangyan Jingfang can effectively improve the clinical symptoms of cancer-related fatigue in patients with stage ⅡB-Ⅲ colorectal cancer after surgery,reduce the physical and emotional suffering of patients,improve the quality of life,and enhance the immune function of the body.The efficacy is safe and reliable,and it has certain clinical application value.

Objective To observe the clinical efficacy and safety of Kangyan Jingfang in the treatment of post-operative cancer-related fatigue in Stage ⅡB-Ⅲ colorectal cancer.Methods A total of 66 patients with stage ⅡB-Ⅲ colorectal cancer who were diagnosed as cancer-related fatigue(CRF)based on TCM syndrome differentiation as spleen vacuity and essence depletion were divided into treatment group and control group randomly,with 33 cases in each group.The treatment group was treated with conventional symptomatic treatment combined with Kangyan Jingfang,and the control group was treated with conventional symptomatic treatment,the course of treatment was 60 days.The scores of cancer-related Fatigue(CFS),TCM syndrome accumulation scale,the revised Piper fatigue scale,Karnofsky performance status,hospital anxiety and depression scale(HAD),tumor markers(CEA,CA19-9,CA72-4,CA12-5,CA15-3,CA242,CA50,Septin9 gene methylation,etc.),immune function(CD3+T lymphocyte level,CD4+T lymphocyte level,CD8+T lymphocyte level and CD4+/CD8+ratio)and safety indexes(blood routine,liver and kidney function)were compared between the two groups in order to evaluate the clinical efficacy of Kangyan Jingfang on CRF.Results 60 cases were included in the observation finally,including 30 cases in each group.After treatment,the scores CFS,TCM syndrome accumulation scale,the revised Piper fatigue scale and HAD of two groups were decreased,but the treatment group before treatment showed a significant decrease in all indicators compared to the control group(P<0.05).The KPS score in the treatment group improved after treatment compared to the control group significantly(P<0.05).CEA,CA19-9 and the methylation of Septin9 gene were significantly decreased in the treatment group after treatment(P<0.05).CD3 and CD4 in treatment groups were higher than control group after treatment significantly(P<0.05).There were no significant abnormal changes in safety indexes before and after treatment(P>0.05).Conclusion Kangyan Jingfang can effectively improve the clinical symptoms of cancer-related fatigue in patients with stage ⅡB-Ⅲ colorectal cancer after surgery,reduce the physical and emotional suffering of patients,improve the quality of life,and enhance the immune function of the body.The efficacy is safe and reliable,and it has certain clinical application value.

ObjectiveTo evaluate the effectiveness of Lutongning granules in the treatment of trigeminal neuralgia in animal models and study its mechanism of action， so as to provide laboratory data support for the clinical application of Lutongning granules and precise treatment. MethodMale SD rats were randomly divided into normal group， model group， carbamazepine group （0.06 g·kg^-1·d^-1）， high-dose Lutongning group （2.70 g·kg^-1·d^-1）， and low-dose Lutongning group （1.35 g·kg^-1·d^-1） according to the stratified basic mechanical pain thresholds， with 10 rats in each group. A trigeminal neuralgia model of rats was prepared by injecting 30% talc suspension into the infraorbital foramen area of the rat. The drug groups were administered 10 mL·kg^-1 of drugs by gavage after 2 h of modeling. The normal group and the model group were administered distilled water by gavage under the same conditions once a day for 10 consecutive days. Von Frey brushes were used to determine the mechanical pain threshold of rats. A fully automated blood and body fluid analyzer was employed to detect the blood routine of rats. Hematoxylin and eosin （HE） staining was utilized to detect the pathological changes in the trigeminal ganglion and medulla oblongata tissue. Transmission electron microscopy was used to scan the ultrastructure of the medulla oblongata tissue. Enzyme-linked immunosorbent assay （ELISA） was used to detect the levels of inflammatory factors interleukin （IL）-1， IL-6， IL-8， tumor necrosis factor （TNF）-α， neuropeptide substance P， and β-endorphins （β-EP） in the serum of rats， and Western blot was used to detect the protein expression levels of IL-1β， purinergic receptor P2X7 （P2X7R）， and phosphorylated p38 mitogen-activated protein kinase （p-p38 MAPK）. ResultCompared with that in the normal group， the pain threshold of rats in the model group was significantly lower （P<0.01）. The absolute value of neutrophils （NEUT#） and the percentage of neutrophils （NEUT） were significantly improved， and the percentage of lymphocytes （LYMPH） was significantly reduced （P<0.01）. The serum levels of IL-1， IL-6， IL-8， and TNF-α were significantly increased （P<0.01）. SP content in brain tissue was significantly increased， and β-EP content was significantly decreased （P<0.01）. The relative protein expression of IL-1β， P2X7R， and p-p38 MAPK was significantly increased （P<0.05）. HE staining and transmission electron microscopy results of medulla oblongata tissue revealed neuronal degeneration， mild proliferation of microglial cells， reduction in the number of myelinated nerves， and obvious demyelination. The trigeminal nerve fibers of rats were disarranged， and some nerve fibers showed vacuolization. Axons were swollen， and Schwann cells proliferated. Demyelination was observed. Compared with the model group， each administration group significantly increased the pain threshold of rats （P<0.05， P<0.01）， reduced NEUT# and NEUT， and elevated LYMPH （P<0.05， P<0.01）. The administration group significantly decreased the levels of IL-1， IL-6， IL-8， and TNF-α in serum and SP in brain tissue （P<0.01） and increased the level of β-EP （P<0.01）. They significantly down-regulated the protein expression of IL-1β， P2X7R， and p-p38 MAPK（P<0.05， P<0.01） and significantly ameliorated the pathological changes in medulla oblongata tissue and trigeminal nerves of rats. ConclusionLutongning Granules had significant therapeutic effects on trigeminal neuralgia induced by injection of talc into the infraorbital foramen of model rats， and the mechanism may be related to amelioration of P2X7R-mediated neuroinflammation and inhibition of demyelination of myelinated nerves.

Gastric cancer is one of the most common malignant tumors in the world, and its incidence and mortality are among the top of malignant tumors in China. Since Kitano et al com-plete the first laparoscopic radical gastrectomy for gastric cancer in the world in 1992, the laparos-copic technology has developed rapidly. After more than 30 years of exploration and practice, the clinical diagnosis and treatment of gastric cancer in China has also made considerable progress. A large number of clinical studies at home and abroad have confirmed that laparoscopic radical gas-trectomy is no less effective than traditional open surgery in the short and long term. Laparoscopic radical gastrectomy has the characteristics of less trauma, faster recovery of gastrointestinal func-tion, less postoperative pain, and shorter average hospital stay. It has gradually replaced open surgery as the mainstream surgical method for gastric cancer. As the concept of surgical treatment for gastric cancer continues to update, emerging minimally invasive technologies continue to emerge, including robotic surgery systems and indocyanine green tracing technology, which are increasingly used in gastric cancer surgery, making gastric cancer surgery more minimally invasive and accurate, the quality of perigastric lymph node dissection and the domestic gastric cancer surgery technology further improving. Based on the relevant research at home and abroad, the authors review and summarize the latest progress in recent years with the topic of minimally invasive surgery for gastric cancer, aiming to systematically describe the current situation and future prospects of gastric cancer surgery. It is believed that in the future, the clinical diagnosis and treatment of gastric cancer in China will be more standardized, minimally invasive and accurate, more high-quality multicenter clinical research will be carry out and the diagnosis and treatment of gastric cancer will be further improved in China.

Currently, in precision cardiac surgery, there are still some pressing issues that need to be addressed. For example, cardiopulmonary bypass remains a critical factor in precise surgical treatment, and many core aspects still rely on the experience and subjective judgment of cardiopulmonary bypass specialists and surgeons, lacking precise data feedback. With the increasing elderly population and rising surgical complexity, precise feedback during cardiopulmonary bypass becomes crucial for improving surgical success rates and facilitating high-complexity procedures. Overcoming these key challenges requires not only a solid medical background but also close collaboration among multiple interdisciplinary fields. Establishing a multidisciplinary team encompassing professionals from the medical, information, software, and related industries can provide high-quality solutions to these challenges. This article shows several patents from a collaborative medical and electronic information team, illustrating how to identify unresolved technical issues and find corresponding solutions in the field of precision cardiac surgery while sharing experiences in applying for invention patents.