Objective To investigate the relationship between CT lung volume parameters(CT-LVP)and pulmonary function grade in patients with idiopathic pulmonary fibrosis(IPF)and its prediction of acute exacerbation.Methods A total of 204 patients with IPF were selected and divided into mild group(67 cases),moderate group(72 cases)and severe group(65 cases)according to the semi-quantitative scoring method of high-resolution computed tomography(HRCT).The correlation between CT-LVP and pul-monary function parameters(PFP)were analyzed.The predictive value of CT-LVP for acute exacerbation in severe IPF was ana-lyzed.Results The whole lung volume(WLV),normal lung volume(NLV)and normal lung volume percentage(NLV%)in severe group were lower than those in mild and moderate groups,whereas interstitial lung disease volume(ILDV)and interstitial lung disease volume percentage(ILDV%)were higher than those in mild and moderate groups,with statistical significance(P<0.05).WLV,NLV,ILDV,NLV%,ILDV%showed strong correlations with forced expiratory volume in 1 second percentage(FEV1%),forced expiratory volume in 1 second to forced vital capacity ratio(FEV1/FVC),diffusing capacity of the lung for carbon monoxide percent-age(DLCO%),and residual volume to total lung capacity ratio(RV/TLC).Receiver operating characteristic(ROC)curve analysis showed that the combination of WLV,NLV,ILDV,NLV%and ILDV%had higher accuracy in predicting acute exacerbation,area under the curve(AUC)>0.75(P<0.05).Conclusion CT-LVP is closely related to PFP,and the accuracy of CT-LVP combination in predicting acute exacerbation is high,which provides a theoretical basis for preventing acute exacerbation of IPF.

Objective To investigate the relationship between CT lung volume parameters(CT-LVP)and pulmonary function grade in patients with idiopathic pulmonary fibrosis(IPF)and its prediction of acute exacerbation.Methods A total of 204 patients with IPF were selected and divided into mild group(67 cases),moderate group(72 cases)and severe group(65 cases)according to the semi-quantitative scoring method of high-resolution computed tomography(HRCT).The correlation between CT-LVP and pul-monary function parameters(PFP)were analyzed.The predictive value of CT-LVP for acute exacerbation in severe IPF was ana-lyzed.Results The whole lung volume(WLV),normal lung volume(NLV)and normal lung volume percentage(NLV%)in severe group were lower than those in mild and moderate groups,whereas interstitial lung disease volume(ILDV)and interstitial lung disease volume percentage(ILDV%)were higher than those in mild and moderate groups,with statistical significance(P<0.05).WLV,NLV,ILDV,NLV%,ILDV%showed strong correlations with forced expiratory volume in 1 second percentage(FEV1%),forced expiratory volume in 1 second to forced vital capacity ratio(FEV1/FVC),diffusing capacity of the lung for carbon monoxide percent-age(DLCO%),and residual volume to total lung capacity ratio(RV/TLC).Receiver operating characteristic(ROC)curve analysis showed that the combination of WLV,NLV,ILDV,NLV%and ILDV%had higher accuracy in predicting acute exacerbation,area under the curve(AUC)>0.75(P<0.05).Conclusion CT-LVP is closely related to PFP,and the accuracy of CT-LVP combination in predicting acute exacerbation is high,which provides a theoretical basis for preventing acute exacerbation of IPF.

Objective: To investigate whether zerumbone ( ZER) has the effect of preventing cisplatin ( Cis) -induced acute kidney injury (Cis-AKI) . Methods: The MTT method was used to detect the effect of different concentrations of ZER on the cell viability of Cis-AKI. The in vivo and in vitro models of Cis-AKI mice were estab- lished by dividing into control group , separate administration group , model group , and dose group. Western blot and immunofluorescence experiments were used to detect the expression changes of kidney injury marker-1 ( KIM- 1) , phosphorylated NF-κB p65 ( P-p65 ) , Cleaved casepase3 , receptor interacting protein kinase 1 ( RIPK1) , RIPK3 , and tumor necrosis factor-α (TNF-α) . Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect the mRNA expression of KIM-1 , TNF-α , interleukin-6 ( IL-6) , and monocyte chemoattractant protein-1(MCP-1) . Periodic acid-Schiff (PAS) staining confirmed the therapeutic effect of ZER on Cis-AKI. RNA-seq and cell thermal shift (CETSA) were used to explore possible target proteins. Results : MTT results showed that ZER could alleviate the decrease in cell viability of Cis-AKI ; in vivo and in vitro studies showed that compared with the model group , after treatment with ZER , its KIM-1 , P-p65 , Cleaved casepased3 , RIPK1 , RIPK3 , TNF -α expres- sion decreased significantly , and the mRNA expression of KIM-1 , TNF-α , IL-6 mRNA , and MCP-1 decreased. PAS staining showed that ZER had a therapeutic effect on Cis-AKI. RNA-seq and CETSA analysis showed that ZER might prevent and treat Cis-AKI by targeting the PIM1 protein. Conclusion ZER may alleviate Cis-AKI and im- prove inflammatory response and necroptosis by regulating PIM1 protein. ZER is expected to be a potential drug for the prevention and treatment of Cis-AKI.

The pathogenesis of immune-mediated liver injury is related to immune regulation disorders. In recent years, researchers have focused on the unique role of invariant natural killer T cells (iNKT cells) in immune-mediated liver injury. iNKT cells, a special subset of lymphocytes, are crucial for immune regulation by bridging innate and adaptive immunity. iNKT cells interact with various immune cells and possess strong immune regulatory capabilities, but their role is complex, potentially promoting liver injury or protecting the liver from damage. This article reviews the latest research progress on iNKT cells in immune-mediated liver injury and describes some factors that regulate immune liver injury by altering the expression of glycosphingolipids, such as liver X receptor and tumor progression site2. In addition, the research results are explored to assist in deepening the understanding of the mechanism of immune-mediated liver injury so as to provide new directions for the development of related treatment strategies.

BACKGROUND: The role of inflammation in the development of gestational diabetes mellitus (GDM) has recently become a focus of research. The systemic immune-inflammation index (SII) and systemic inflammation response index (SIRI), novel indices, reflect the body's chronic immune-inflammatory state. This study aimed to investigate the associations between the SII or SIRI and GDM. METHODS: A prospective birth cohort study was conducted at Beijing Obstetrics and Gynecology Hospital from February 2018 to December 2020, recruiting participants in their first trimester of pregnancy. Baseline SII and SIRI values were derived from routine clinical blood results, calculated as follows: SII = neutrophil (Neut) count × platelet (PLT) count/lymphocyte (Lymph) count, SIRI = Neut count × monocyte (Mono) count/Lymph count, with participants being grouped by quartiles of their SII or SIRI values. Participants were followed up for GDM with a 75-g, 2-h oral glucose tolerance test (OGTT) at 24-28 weeks of gestation using the glucose thresholds of the International Association of Diabetes and Pregnancy Study Groups (IADPSG). Logistic regression was used to analyze the odds ratios (ORs) (95% confidence intervals [CIs]) for the the associations between SII, SIRI, and the risk of GDM. RESULTS: Among the 28,124 women included in the study, the average age was 31.8 ± 3.8 years, and 15.76% (4432/28,124) developed GDM. Higher SII and SIRI quartiles were correlated with increased GDM rates, with rates ranging from 12.26% (862/7031) in the lowest quartile to 20.10% (1413/7031) in the highest quartile for the SII ( Ptrend <0.001) and 11.92-19.31% for the SIRI ( Ptrend <0.001). The ORs (95% CIs) of the second, third, and fourth SII quartiles were 1.09 (0.98-1.21), 1.21 (1.09-1.34), and 1.39 (1.26-1.54), respectively. The SIRI findings paralleled the SII outcomes. For the second through fourth quartiles, the ORs (95% CIs) were 1.24 (1.12-1.38), 1.41 (1.27-1.57), and 1.64 (1.48-1.82), respectively. These associations were maintained in subgroup and sensitivity analyses. CONCLUSION The SII and SIRI are potential independent risk factors contributing to the onset of GDM.
Humans ; Female ; Pregnancy ; Diabetes, Gestational/immunology* ; Prospective Studies ; Adult ; Inflammation/immunology* ; Glucose Tolerance Test ; Birth Cohort

Objective Mendelian randomization was used to analyze the causal association between 20 serum metabolites and the risk of ovarian cancer.Methods The gene variations of 20 serum metabolites were obtained from the MRC IEU database as tool variables reflecting exposure levels,while gene variations of ovarian cancer patients were used as instrumental variables reflecting outcome levels.The ovarian cancer dataset ieu-a-1120 included 66,450 European women samples(of which 25,509 were ovarian cancer),and the dataset ieu-a-1228 included 54,990 European women samples(of which 14,049 were ovarian cancer).Two-sample two-way Mendelian randomization analysis was performed on both datasets.This study used inverse variance-weighted(IVW),weigh-ted median method,MR-Egger regression,and combined various analysis methods such as simple mode,and weighted mode.The caus-al effects of 20 metabolites and the risk of ovarian cancer were analyzed.Cochran's Q test was used to perform sensitivity analysis and to verify the reliability of the results.MR Egger intercept test was used to assess the horizontal pleiotropy of tool variables,and use the leave-one-out method to assess whether there were single nucleotide polymorphisms(SNPs)in the results that might have a potential impact on the incidence of ovarian cancer.Finally,the effects of uridine on ovarian cancer cells were verified through cell proliferation and apoptosis experiments.Results The results showed a negative correlation between uridine and the occurrence of ovarian cancer,with statistically significance(ieu-a-1228:P=0.025;ieu-a-1120:P=0.017).MR-Egger regression analysis confirmed the sensitiv-ity and robustness of the analysis results.The CCK8 assay confirmed that uridine inhibited the proliferation of ovarian cancer cells in a concentration-dependent manner,and uridine at a concentration of 10 mM significantly promoted apoptosis in SKOV3 cells(P<0.001)and A2780 cells(P<0.001).Flow cytometry analysis showed that after treatment for 24 hours,uridine at a concentration of 10 mM had the strongest pro-apoptotic effect on ovarian cancer cells,which was significant in SKOV3 and A2780 cells(P<0.05 and P<0.001,respectively).Conclusion Uridine is negatively correlated with the risk of ovarian cancer,which lays a theoretical founda-tion for further understanding the pathogenesis of ovarian cancer and optimizing clinical treatment strategies.

Objective Mendelian randomization was used to analyze the causal association between 20 serum metabolites and the risk of ovarian cancer.Methods The gene variations of 20 serum metabolites were obtained from the MRC IEU database as tool variables reflecting exposure levels,while gene variations of ovarian cancer patients were used as instrumental variables reflecting outcome levels.The ovarian cancer dataset ieu-a-1120 included 66,450 European women samples(of which 25,509 were ovarian cancer),and the dataset ieu-a-1228 included 54,990 European women samples(of which 14,049 were ovarian cancer).Two-sample two-way Mendelian randomization analysis was performed on both datasets.This study used inverse variance-weighted(IVW),weigh-ted median method,MR-Egger regression,and combined various analysis methods such as simple mode,and weighted mode.The caus-al effects of 20 metabolites and the risk of ovarian cancer were analyzed.Cochran's Q test was used to perform sensitivity analysis and to verify the reliability of the results.MR Egger intercept test was used to assess the horizontal pleiotropy of tool variables,and use the leave-one-out method to assess whether there were single nucleotide polymorphisms(SNPs)in the results that might have a potential impact on the incidence of ovarian cancer.Finally,the effects of uridine on ovarian cancer cells were verified through cell proliferation and apoptosis experiments.Results The results showed a negative correlation between uridine and the occurrence of ovarian cancer,with statistically significance(ieu-a-1228:P=0.025;ieu-a-1120:P=0.017).MR-Egger regression analysis confirmed the sensitiv-ity and robustness of the analysis results.The CCK8 assay confirmed that uridine inhibited the proliferation of ovarian cancer cells in a concentration-dependent manner,and uridine at a concentration of 10 mM significantly promoted apoptosis in SKOV3 cells(P<0.001)and A2780 cells(P<0.001).Flow cytometry analysis showed that after treatment for 24 hours,uridine at a concentration of 10 mM had the strongest pro-apoptotic effect on ovarian cancer cells,which was significant in SKOV3 and A2780 cells(P<0.05 and P<0.001,respectively).Conclusion Uridine is negatively correlated with the risk of ovarian cancer,which lays a theoretical founda-tion for further understanding the pathogenesis of ovarian cancer and optimizing clinical treatment strategies.

The pathogenesis of immune-mediated liver injury is related to immune regulation disorders. In recent years, researchers have focused on the unique role of invariant natural killer T cells (iNKT cells) in immune-mediated liver injury. iNKT cells, a special subset of lymphocytes, are crucial for immune regulation by bridging innate and adaptive immunity. iNKT cells interact with various immune cells and possess strong immune regulatory capabilities, but their role is complex, potentially promoting liver injury or protecting the liver from damage. This article reviews the latest research progress on iNKT cells in immune-mediated liver injury and describes some factors that regulate immune liver injury by altering the expression of glycosphingolipids, such as liver X receptor and tumor progression site2. In addition, the research results are explored to assist in deepening the understanding of the mechanism of immune-mediated liver injury so as to provide new directions for the development of related treatment strategies.

A 36-year-old healthy male served as an allogeneic hematopoietic stem cell donor was given recombinant human granulocyte colony-stimulating factor injection (rhG-CSF) 300 μg by subcutaneous injection once daily for 5 consecutive days. On day 4 of stem cell mobilization, peripheral stem cell collection was performed and rhG-CSF 250 μg was given in addition. The donor experienced dry cough, dyspnea, and difficulty breathing on the next day. Chest CT scan showed diffuse patchy and nodular shadows in both lungs, and relevant tests excluded bacterial/viral infection of the lungs and heart failure. It was considered to be acute lung injury caused by rhG-CSF. After giving glucocorticoids and symptomatic treatments, the symptoms gradually subsided, and the peripheral blood stem cell collection was successful. In the continuing treatment of glucocorticoids, the symptoms of the donor were further improved, and chest CT scan showed marked improvement. At a 3 years of follow-up, the donor' work and life were normal, and no lung discomfort symptoms recurred.

Objective To explore the prognostic impact of Qili Qiangxin capsules(QLQX)in patients with ST-segment elevation myocardial infarction(STEMI).Methods Retrospective collecting the clinical data of STEMI patients treated at PingAn Hospital affiliated to Hebei Medical University from January 2020 to January 2022,divided into QLQX group and non-QLQX group according to treatment plan.Follow-up patients for 1 year,with the main endpoint being major adverse cardiovascular and cerebrovascular events(MACCEs)at 30 d and 1 year;The secondary endpoints were cardiogenic death,myocardial reinfarction,emergency coronary revascularization,stroke,and major bleeding at 30 d and 1 year,as well as severe STEMI complications(30 d),re-admission due to heart failure(1 year),and all-cause mortality(1 year).Results A total of 210 STEMI patients were included(125 in the QLQX group and 85 in the non QLQX group).Univariate or Kaplan Meier analysis showed that the MACCE,cardiogenic death,malignant arrhythmia at 30 d,myocardial reinfarction,re-admission due to heart failure,and all-cause mortality rates in the QLQX group were significantly lower than those in the non QLQX group at 30 d and 1 year(P＜0.05),while there were no significant differences in the incidence of other observed endpoint events between the two groups(P＞0.05).In addition,QLQX may be a protective factor for MACCEs in STEMI patients(30 d:HR=0.157,95％CI 0.032 to 0.756,P=0.021;1 year:HR=0.208,95％CI 0.087 to 0.497,P=0.014).Conclusion QLQX adjuvant therapy may improve MACCEs in STEMI patients.