Neutrophil extracellular traps(NETs)are net-like complexes released by neutrophils and play a crucial role in antimicrobial defense. In addition, NETs can exacerbate inflammatory responses associated with various diseases, including diabetes, cardiovascular diseases, and autoimmune diseases. Currently, the role of NETs in ocular diseases has received extensive attention. This article systematically summarizes the formation mechanism of NETs and their role in maintaining intraocular homeostasis under physiological conditions. At the same time, it focuses on elaborating the pathogenic role of NETs in the field of ophthalmic diseases, such as dry eye, keratitis, uveitis, diabetic retinopathy, retinal vein occlusion, and age-related macular degeneration, emphasizing the importance of NETs as therapeutic targets for ocular diseases and the potential application value as new markers for ocular diseases. Future in-depth research on the mechanism of NETs in ocular diseases will provide a stronger theoretical basis for the treatment of related eye diseases.

Retinitis pigmentosa(RP)is an inherited retinal degenerative disease characterized by progressive photoreceptor cell degeneration, in which cataract—a common complication—significantly affects visual prognosis. Currently, phacoemulsification with intraocular lens implantation has become the main treatment for RP complicated with cataract. However, postoperative complications such as posterior capsular opacification, capsular contraction syndrome, intraocular lens dislocation, and macular edema occur at considerably higher rates in these patients, severely compromising the long-term outcomes of cataract surgery. Based on the latest clinical evidence, this review systematically elaborates on the clinical characteristics of RP with cataract, key perioperative surgical considerations, and recent advances in the prevention and management of complications, aiming to optimize the surgical approach, improve postoperative visual quality, and enhance long-term efficacy for RP patients, thereby providing an evidence-based medical reference.

Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, is a chronic inflammation of the gastrointestinal tract with unknown etiology. The cause of IBD is widely considered multifactorial, with prevailing hypotheses suggesting that the microbiome and various environmental factors contribute to inappropriate activation of the mucosal immune system in genetically susceptible individuals. Although the incidence of IBD has stabilized in Western countries, it is rapidly increasing in newly industrialized countries, particularly China, making IBD a global disease. Significant changes in multiple biomarkers before IBD diagnosis during the preclinical phase provide opportunities for earlier diagnosis and intervention. Advances in technology have driven the development of telemonitoring tools, such as home-testing kits for fecal calprotectin, serum cytokines, and therapeutic drug concentrations, as well as wearable devices for testing sweat cytokines and heart rate variability. These tools enable real-time disease activity assessment and timely treatment strategy adjustments. A wide range of novel drugs for IBD, including interleukin-23 inhibitors (mirikizumab, risankizumab, and guselkumab) and small-molecule drugs (etrasimod and upadacitinib), have been introduced in the past few years. Despite these advancements, approximately one-third of patients remain primary non-responders to the initial treatment, and half eventually lose response over time. Precision medicine integrating multi-omics data, advanced combination therapy, and complementary approaches, including stem cell transplantation, psychological therapies, neuromodulation, and gut microbiome modulation therapy, may offer solutions to break through the therapeutic ceiling.
Humans ; Inflammatory Bowel Diseases/therapy*

Radiochemotherapy-induced oral mucositis (OM) is a common oral complication in patients with tumors following head and neck radiotherapy or chemotherapy. Erosion and ulcers are the main features of OM that seriously affect the quality of life of patients and even the progress of tumor treatment. To date, differences in clinical prevention and treatment plans for OM have been noted among doctors of various specialties, which has increased the uncertainty of treatment effects. On the basis of current research evidence, this expert consensus outlines risk factors, clinical manifestations, clinical grading, ancillary examinations, diagnostic basis, prevention and treatment strategies and efficacy indicators for OM. In addition to strategies such as basic oral care, anti-inflammatory and analgesic agents, anti-infective agents, pro-healing agents, and photobiotherapy recommended in previous guidelines, we also emphasize the role of traditional Chinese medicine in OM prevention and treatment. This expert consensus aims to provide references and guidance for dental physicians and oncologists in formulating strategies for OM prevention, diagnosis, and treatment, standardizing clinical practice, reducing OM occurrence, promoting healing, and improving the quality of life of patients.
Humans ; Chemoradiotherapy/adverse effects* ; Consensus ; Risk Factors ; Stomatitis/etiology*

OBJECTIVE: Myocardial inflammation during myocardial infarction (MI) could be inhibited by regulating arachidonic acid (AA) metabolism. Recent studies demonstrated that Sini Decoction (SND) was identified to be an effective prescription for treating heart failure (HF) caused by MI. But the anti-inflammatory mechanism of SND remained unclear. The work was designed to investigate the anti-inflammatory mechanism of SND through the AA metabolism pathway in vitro and in vivo experiments. METHODS: An inflammatory injury model of H9c2 cells was established by lipopolysaccharide (LPS)-stimulated macrophage-conditioned medium (CM). The MI model was built by the ligation of left anterior descending (LAD) branch of coronary artery in rat. Meanwhile, the rats were divided into five groups: sham group, MI group, MI + Celecoxib group, MI + low-dose SND group (SND-L) and MI + high-dose SND group (SND-H). Cardiac function, histopathological changes and serum cytokines were examined four weeks later. Western blot analysis was conducted to verify the key enzymes levels in the AA metabolic pathway, including phospholipase A2 (PLA2), cyclooxygenases (COXs) and lipoxygenases (LOXs). RESULTS: These in vivo results demonstrated that SND could improve the cardiac function and pathological changes of rats with MI, and regulate the key inflammatory molecules in the AA metabolism pathway, including sPLA2, COX-1, COX-2, 5-LOX and 15-LOX. In vitro, SND could decrease the release of pro-inflammatory cytokines including TNF-α and IL-6 and inhibit cell apoptosis in CM-induced H9c2 cells. Moreover, SND could protect H9c2 cells from the damage of CM by regulating nuclear factor kappa-B (NF-κB) signal pathway and the expression of COX-2. CONCLUSION SND may be a drug candidate for anti-inflammatory treatment during MI by regulating the multiple targets in the AA metabolism pathway.

Liver failure is a common clinical syndrome of severe liver disease with rapid progression and high mortality. Therefore， early intervention in pre-liver failure or “golden window” is of great significance in improving the prognosis of patients. Hepatitis B virus-related acute-on-chronic liver failure and alcohol-related acute-on-chronic liver failure are the main topics of studies on pre-liver failure. This article discusses the pathogenesis of pre-liver failure and artificial liver support therapy， so as to guide the reasonable and affective applications of artificial liver technology in clinical practice， promote related studies， and thereby reduce the mortality rate of patients with liver failure.

Humans ; Gastrointestinal Microbiome ; Constipation/therapy* ; Probiotics/therapeutic use* ; Patients

Acute hypobaric hypoxic brain damage is a potentially fatal high-altitude sickness. Autophagy plays a critical role in ischemic brain injury, but its role in hypobaric hypoxia (HH) remains unknown. Here we used an HH chamber to demonstrate that acute HH exposure impairs autophagic activity in both the early and late stages of the mouse brain, and is partially responsible for HH-induced oxidative stress, neuronal loss, and brain damage. The autophagic agonist rapamycin only promotes the initiation of autophagy. By proteome analysis, a screen showed that protein dynamin2 (DNM2) potentially regulates autophagic flux. Overexpression of DNM2 significantly increased the formation of autolysosomes, thus maintaining autophagic flux in combination with rapamycin. Furthermore, the enhancement of autophagic activity attenuated oxidative stress and neurological deficits after HH exposure. These results contribute to evidence supporting the conclusion that DNM2-mediated autophagic flux represents a new therapeutic target in HH-induced brain damage.
Mice ; Animals ; Hypoxia ; Oxidative Stress ; Autophagy ; Cognition ; Sirolimus/therapeutic use*

AIM:To observe the clinical efficacy of 3% diquafosol sodium eye drops combined with sodium hyaluronate eye drops in the treatment of dry eyes after pterygium surgery with lacrimal insufficiency.METHODS: A total of 64 cases(64 eyes)of pterygium patients with lacrimal insufficiency were treated with pterygium resection combined with limbal stem cell transplantation, and they were given routine anti-inflammatory and infection prevention treatment postoperatively. In terms of postoperative dry eye treatment, all patients were randomly divided into two groups. The observation group was treated with 3% diquafosol sodium eye drops combined with sodium hyaluronate eye drops, and the control group was treated with sodium hyaluronate eye drops. The break-up time of tear film(BUT), fluorescein(FL), Schirmer's Ⅰ test(SⅠt), ocular surface disease index(OSDI)score, central corneal thickness(CCT)changes, adverse reactions and complications were observed and compared between the two groups at different times postoperatively.RESULTS: Both groups of pterygium patients were accompanied with mild to moderate dry eyes with insufficient tear secretion preoperatively. At 2 wk after operation, both groups showed shorter BUT and higher FL score compared with those preoperatively(P<0.05). There was no significant difference between the two groups(P>0.05). At 4 wk after operation, BUT in the observation group was prolonged, OSDI score was decreased(both P<0.05), and FL score in both groups was decreased compared with those at with 2 wk after operation(P<0.05). The observation group was better than the control group(P<0.05). At the first day after operation, the CCT of the two groups was thicker than that preoperatively(P<0.05), and there was no significant difference in SⅠt between the two groups before and after operation(P>0.05).CONCLUSION: In the treatment of dry eye after pterygium surgery with lacrimal insufficiency, 3% diquafosol sodium eye drops combined with sodium hyaluronate eye drops can effectively reduce the postoperative dry eye symptoms, and its clinical effect is better than that of sodium hyaluronate eye drops alone.