PANoptosis is a newly defined type of programmed cell death (PCD), which is triggered by a variety of stimuli and covers three known forms of PCD: apoptosis, pyroptosis and necroptosis. In physiological state, cell death plays an important protective role against pathogen invasion, but its over-activation may aggravate inflammatory response and cause tissue damage. Studies have shown that the occurrence and progression of acute lung injury/acute respiratory distress syndrome (ALI/ARDS), asthma, chronic obstructive pulmonary disease (COPD) and other lung diseases are closely related to PANoptosis. The purpose of this review is to deeply explore the molecular mechanism of PANoptosis and its regulatory factors in lung diseases, in order to discover potential therapeutic targets and provide new targets and innovative ideas for clinical treatment for lung diseases.
Humans ; Lung Diseases ; Apoptosis ; Pyroptosis ; Pulmonary Disease, Chronic Obstructive ; Necroptosis ; Acute Lung Injury

Bone Transplantation/adverse effects* ; Transplantation, Autologous/adverse effects*

Objective:To evaluate the effect of hydrogen on lipopolysaccharide (LPS) and nigericin-induced pyroptosis in macrophages and the role of long non-coding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1).Methods:Human monocyte-derived macrophages THP-1 cells were cultured in vitro and divided into 4 groups ( n=25 each) using a random number table method: control group (group C), LPS and nigericin group (group LN), hydrogen-rich medium+ LPS and nigericin group (group H+ LN), and lentiviral transfection+ hydrogen-rich medium+ LPS-nigericin group (group LV+ H+ LN). THP-1 cells were cultured in the common culture medium for 24 h in group C. LPS at a final concentration of 100 ng/ml and nigericin 10 μmol/L were added to the culture medium, and the cells were incubated for 24 h in group LN. In group H+ LN, the culture medium was replaced with 0.6 mmol/L hydrogen-rich medium, then LPS at a final concentration of 100 ng/ml and nigericin 10 μmol/L were immediately added, and the cells were incubated for 24 h. In group LV+ H+ LN, THP-1 cells over-expressing NEAT1 stably after being transfected with lentivirus were used, then LPS at a final concentration of 100 ng/ml and nigericin 10 μmol/L were immediately added, and the cells were incubated for 24 h. Cell viability was detected by CCK-8 assay. Lactic dehydrogenase (LDH) release was assessed by colorimetric method. The amount of LDH released was measured by colorimetry. The concentrations of interleukin-1beta (IL-1β) and IL-18 in culture medium were measured by enzyme-linked immunosorbent assay. The pyroptotic rate was detected by flow cytometry. The expression of nucleotide-binding oligomerization domain-like receptor-containing pyrin domain 3 (NLRP3), apoptosis-associated speck-like protein (ASC), caspase-1 and gasdermin D (GSDMD) was detected by Western blot. The expression of NEAT1 gene was determined by quantitative real-time polymerase chain reaction. Results:Compared with group C, the cell viability was significantly decreased, the amount of LDH released, concentrations of IL-1β and IL-18, and pyroptotic rate were increased, and the expression of NEAT1 gene, NLRP3, ASC, caspase-1 and GSDMD was up-regulated in group LN ( P<0.05). Compared with group LN, the cell viability was significantly increased, the amount of LDH released, concentrations of IL-1β and IL-18, and pyroptotic rate were decreased, and the expression of NEAT1 gene, NLRP3, ASC, caspase-1 and GSDMD was down-regulated in group H+ LN ( P<0.05). Compared with group H+ LN, the cell viability was significantly decreased, the amount of LDH released, concentrations of IL-1β and IL-18, and pyroptotic rate were increased, and the expression of NEAT1 gene, NLRP3, ASC, caspase-1 and GSDMD was up-regulated in group LV+ H+ LN ( P<0.05). Conclusions:Hydrogen can ameliorate LPS and nigericin-induced pyroptosis in macrophages, and the mechanism may be associated with down-regulating the expression of lncRNA NEAT1.

Objective To analyze the research status,hot directions and frontier trends of traditional Chinese medicine in the prevention and treatment of diseases by regulating Wnt signaling pathway based on bibliometrics.Methods Based on Citespace and Vosviewer bibliometric software,the literature on the regulation of Wnt signaling pathway by traditional Chinese medicine in CNKI and WoSCC was visually analyzed.Results As of April 2023,607 and 257 related literatures were published in Chinese and English respectively.Since 2008,the number of literatures published in this field has shown a fluctuating increasing trend.China is the country with the most publications;guangzhou University of Traditional Chinese Medicine and Hunan University of Traditional Chinese Medicine were the institutions with the most publications in the Chinese database,and Shanghai University of Traditional Chinese Medicine was the institution with the most publications in the English literature database.Combined with the research direction of each research team and keyword clustering and burst analysis,the research hotspots of traditional Chinese medicine regulating Wnt signaling pathway are focused on osteoporosis,osteoarthritis and renal fibrosis.Diseases such as gastric cancer and breast cancer have become emerging research directions in recent years.Electroacupuncture therapy to promote stem cell proliferation and treat neurological diseases is one of the frontier research trends in this field.The mechanism of traditional Chinese medicine regulating the interaction between Wnt and NF-kappaB signaling pathway to prevent and treat diseases has great research potential.Conclusion In recent years,the prevention and treatment of diseases by traditional Chinese medicine targeting Wnt signaling pathway has developed rapidly.Various expert teams have obtained rich research results,and the research hotspots show a diversified trend.In-depth exploration of this can provide strong evidence for the molecular mechanism of traditional Chinese medicine in the treatment of various diseases.

The hypoxic microenvironment and inflammatory state of residual tumors caused by insufficient radio-frequency ablation(iRFA)are major reasons for rapid tumor progression and pose challenges for immu-notherapy.We retrospectively analyzed the clinical data of patients with hepatocellular carcinoma(HCC)treated with RFA and observed that iRFA was associated with poor survival outcomes and progression-free survival.Using an orthotopic HCC mouse model and a colorectal liver metastasis model,we observed that treatment with melatonin after iRFA reduced tumor growth and metastasis and achieved the best out-comes when combined with anti-programmed death-ligand 1(anti-PD-L1)therapy.In mechanism,melatonin inhibited the expression of epithelial-mesenchymal transitions,hypoxia-inducible factor(HIF)-1 α,and PD-L1 in tumor cells after iRFA.Flow cytometry revealed that melatonin reduced the proportion of myeloid-derived suppressor cells and increased the proportion of CD8+T cells.Transcriptomic analysis revealed an upregulation of immune-activated function-related genes in residual tumors.These findings demonstrated that melatonin can reverse hypoxia and iRFA-induced inflammation,thereby overcoming the immunosuppressive tumor microenvironment(TME)and enhancing the efficacy of immunotherapy.

The current linear economy model relies on fossil energy and increases CO₂ emissions, which contributes to global warming and environmental pollution. Therefore, there is an urgent need to develop and deploy technologies for carbon capture and utilization to establish a circular economy. The use of acetogens for C1-gas (CO and CO₂) conversion is a promising technology due to high metabolic flexibility, product selectivity, and diversity of the products including chemicals and fuels. This review focuses on the physiological and metabolic mechanisms, genetic and metabolic engineering modifications, fermentation process optimization, and carbon atom economy in the process of C1-gas conversion by acetogens, with the aim to facilitate the industrial scale-up and carbon negative production through acetogen gas fermentation.
Fermentation ; Gases/metabolism* ; Carbon Dioxide/metabolism* ; Metabolic Engineering ; Carbon/metabolism*

Through the development of the guidance for case handling of radiological health law enforcement, health supervisors are instructed to accurately grasp the key points of law enforcement and case handling and standardize the process of collecting evidence and law application to ensure the correct implementation of administrative penalty. This article explains the structure and content of the guidance for case handling of radiological health law enforcement by taking the case of arranging radiation workers who have not undergone an occupational health examination to engage in the radiological occupational-disease-inductive operation in medical institutions as an example.

Purpose To synthetically evaluate MR diffusion kurtosis imaging (DKI) using Meta-analysis to differentiate diagnostic value of benign and malignant breast lesions and quantitatively analyze mean kurtosis (MK) values of benign and malignant breast lesions in an attempt to provide evidence-based facts for clinical decision making. Materials and Methods Computer-based retrieval of Chinese and English literatures concerning differential diagnosis of benign and malignant breast lesions with application of DKI publicly published at home and abroad in PubMed, Ebsco, Embase, CNKI, Cochrane Library, CBM, VIP Data database from January. 1, 2006 to September. 30, 2017. Two valuators independently screened and extracted data according to inclusion and exclusion criteria, and drew on QUADAS for quality assessment, Stata 12.0 and Meta-Disc 1.4 software for Meta analysis and extraction of relevant parameters. Results Totally 8 up-to-standard literatures were included, including 3 in English and 5 in Chinese. The total number of focus was 689. Corresponding effect model analysis revealed that MK value in malignant breast lesion group was higher than that in benign lesion group, the difference of which was statistically significant. The optimal diagnostic threshold was determined by the maximum Youden index, which was approximately 0.71 in size,with combined sensitivity of 0.907(95% CI 0.860-0.939),specificity of 0.910(95% CI 0.856-0.945),positive likelihood ratio of 10.053(95% CI 6.293-16.059),negative likelihood ratio of 0.102(95% CI 0.068-0.154),and diagnostic test odds ratio of 98.203(95% CI 55.014-175.296).The area under receiver operating characteristic curve was 0.96.MK value suggested 94% posterior malignant rate of malignant breast lesions, and 13% malignant rate of benign breast lesions. Conclusion MK value has high diagnostic value for benign and malignant breast lesions with good sensitivity and specificity.

Objective To evaluate the effect of oxycodone on intestinal ischemia-reperfusion injury in rats and the role of autophagy.Methods Twenty-four healthy adult male Sprague-Dawley rats,aged 6-9 weeks,weighing 180-220 g,were divided into 4 groups (n =6 each) using a random number table method:sham group (group S),intestinal I/R group (group I/R),oxycodone group (group O) and oxycodone plus autophagy inhibitor 3-methyladenine (3-MA) group (group O+3-MA).Intestinal I/R was induced via clamping the superior mesenteric artery for 1 h,followed by 2-h reperfusion in all the groups except for group S.Oxycodone 0.5 mg/kg was injected via caudal vein at 15 min before ischemia in group O and group O+3-MA.3-MA 30 mg/kg was intraperitoneally injected at 10 min before ischemia in group O+3-MA.Rats were gavaged with fluorescein-isothiocyanate-conjugated dextran (FITC-dextran) immediately before ischemia.Blood samples were collected from the cardiac apex at 2 h of reperfusion to detect the level of serum FITC-dextran.Blood samples were collected from the cardiac apex at 2 h of reperfusion to measure the concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) in serum by enzyme-linked immunosorbent assay.Small intestinal tissues were obtained at 2 h of reperfusion for examination of the pathological changes and for determination of the expression of occludin,Beclin-1 and microtubule-associated protein 1 light chain 3 (LC3) (by Western blot).Intestinal damage was assessed and scored according to Chiu.The ratio of LC3 Ⅱ expression to LC3 Ⅰ expression (LC3 Ⅱ / Ⅰ) was calculated.Results Compared with group S,the Chiu's score,levels of serum FITC-dextran,TNF-α and IL-1β and LC3 Ⅱ/Ⅰ ratio were significantly increased,the expression of Beclin-1 was up-regulated,and the expression of occludin was down-regulated in group I/R (P＜0.05).Compared with group I/R,the Chiu's score and levels of serum FITC-dextran,TNF-α and IL-1β were significantly decreased,LC3 Ⅱ / Ⅰ ratio was increased,and the expression of occludin and Beclin-1 was up-regulated in group O (P＜0.05),and no significant change was found in the parameters mentioned above in group O+ 3-MA (P＞0.05).Compared with group O,the Chiu's score and levels of serum FITC-dextran,TNF-α and IL-1β were significantly increased,LC3 Ⅱ / Ⅰ ratio was decreased,and the expression of occludin and Beclin-1 was down-regulated in group O + 3-MA (P＜ 0.05).Conclusion Oxycodone can ameliorate intestinal I/R injury,and the mechanism may be related to enhancing autophagy in intestinal tissues of rats.

Objective To evaluate the effect of oxycodone pretreatment on oxygen-glucose deprivation and restoration (OGD/R)-induced injury to small intestinal epithelial cells of rats and the role of different opioid receptors.Methods IEC-6 cells were divided into 5 groups (n=15 each) using a random number table:control group (group C),group OGD/R,oxycodone group (group O),μ opioid receptor antagonist CTOP plus oxycodone group (group CTOP+O) and κ opioid receptor antagonist BNI plus oxycodone group (group BNI+O).Cells were cultured for 8 h in normal culture atmosphere in group C.Cells were subjected to OGD for 4 h followed by restoration of oxygen-glucose supply in normal culture medium for 4 h in OGD/R,O,CTOP+O and BNI+O groups.Oxycodone at a final concentration of 1 μg/ml was added at 5 min before OGD/R in O,CTOP+O and BNI+O groups.CTOP and BNI at a final concentration of 5 μmol/L were added at 10 min before OGD/R in group CTOP+O and group BNI+O,respectively.Five holes in each group were selected at 8 h of OGD/R for determination of the cell viability (by MTT assay),lactic dehydrogenase (LDH) release rate (by colorimetry) and levels of tumor necrosis factor-alpha (TNF-α),interleukin-1beta (IL-1β) and high-mobility group box 1 protein (HMGB1) in supernatant (by enzyme-linked immunosorbent assay).Results Compared with group C,the cell viability was significantly decreased,and the LDH release rate and levels of TNF-α,IL-1β and HMGB1 were increased in OGD/R,O,CTOP+Oand BNI+ O groups (P＜ 0.05).Compared with group OGD/R,the cell viability was significantly increased,and the LDH release rate and levels of TNF-o,IL-1β and HMGB1 were decreased in group O (P＜0.05).Compared with group O,the cell viability was significantly decreased,and the LDH release rate and levels of TNF-α,IL-1β and HMGB1 were increased in CTOP+O and BNI+O groups (P＜0.05).Conclusion Oxycodone pretreatment can mitigate OGD/R-induced injury to small intestinal epithelial cells of rats and the mechanism is related to activating μ and κ opioid receptors.