Patients with alcoholic cirrhosis often experience varying degrees of malnutrition， and the patients with malnutrition are more susceptible to complications such as infections and ascites， which may lead to a poor prognosis. Therefore， it is particularly important to conduct nutritional risk screening for patients in clinical practice， and appropriate nutritional assessment tools should be used to evaluate the nutritional status of patients and develop individualized nutritional supplementation regimens， thereby promoting disease recovery and improving prognosis and quality of life. This article elaborates on the specific methods for nutritional screening， assessment， and management in patients with alcoholic cirrhosis and points out that systematic nutritional screening and assessment can help to identify the patients with malnutrition in the early stage and provide timely intervention. Individualized nutritional supplementation regimens should be adjusted based on the conditions of patients， so as to meet their nutritional needs， promote the recovery of liver function， improve overall health status， and enhance long-term quality of life.

Objective: To investigate the role and mechanism of the heat-clearing and detoxifying drug Laggerae Herba in regulating the nuclear factor-erythroid 2-related factor-2(Nrf2)/solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4) signaling pathway to inhibit ferroptosis and improve chronic heart failure induced by transverse aortic arch constriction in mice. Methods: Twenty-four male ICR mice were divided into the sham (n=6) and transverse aortic arch constriction groups (n=18) according to the random number table method. The transverse aortic arch constriction group underwent transverse aortic constriction surgery to establish models. After modeling, the transverse aortic arch constriction group was further divided into the model, captopril, and Laggerae Herba groups according to the random number table method, with six mice per group. The captopril (15 mg/kg) and Laggerae Herba groups (1.95 g/kg) received the corresponding drugs by gavage, whereas the sham operation and model groups were administered the same volume of ultrapure water by gavage once a day for four consecutive weeks. After treatment, the cardiac function indexes of mice in each group were detected using ultrasound. The heart mass and tibia length were measured to calculate the ratio of heart weight to tibia length. Hematoxylin and eosin staining were used to observe the pathological changes in myocardial tissue. Masson staining was used to observe the degree of myocardial fibrosis. Wheat germ agglutinin staining was used to observe the degree of myocardial cell hypertrophy. Prussian blue staining was used to observe the iron deposition in myocardial tissue. An enzyme-linked immunosorbent assay was used to detect the amino-terminal pro-brain natriuretic peptide (NT-proBNP) and glutathione (GSH) contents in mice serum. Colorimetry was used to detect the malondialdehyde (MDA) content in mice serum. Western blotting was used to detect the Nrf2, GPX4, SLC7A11, and ferritin heavy chain 1 (FTH1) protein expressions in mice cardiac tissue. Results: Compared with the sham group, in the model group, the ejection fraction (EF) and fractional shortening (FS) of mice decreased, the left ventricular end-systolic volume (LVESV) and left ventricular end-systolic diameter (LVESD) increased, the left ventricular anterior wall end-systolic thickness (LVAWs) and left ventricular posterior wall end-systolic thickness (LVPWs) decreased, the ratio of heart weight to tibia length increased, the myocardial tissue morphology changed, myocardial fibrosis increased, the cross-sectional area of myocardial cells increased, iron deposition appeared in myocardial tissue, the serum NT-proBNP and MDA levels increased, the GSH level decreased, and Nrf2, GPX4, SLC7A11, and FTH1 protein expressions in cardiac tissue decreased (P<0.05). Compared with the model group, in the captopril and Laggerae Herba groups, the EF, FS, and LVAWs increased, the LVESV and LVESD decreased, the ratio of heart weight to tibia length decreased, the myocardial cells were arranged neatly, the degree of myocardial fibrosis decreased, the cross-sectional area of myocardial cells decreased, the serum NT-proBNP level decreased, and the GSH level increased. Compared with the model group, the LVPWs increased, the iron deposition in myocardial tissue decreased, the serum MDA level decreased, and Nrf2, GPX4, SLC7A11, and FTH1 protein expressions in cardiac tissue increased (P<0.05) in the Laggerae Herba group. Conclusion Laggerae Herba improves the cardiac function of mice with chronic heart failure caused by transverse aortic arch constriction, reduces the pathological remodeling of the heart, and reduces fibrosis. Its mechanism may be related to Nrf2/SLC7A11/GPX4 pathway-mediated ferroptosis.

Chronic refractory wound （CRW） presents significant clinical treatment challenges due to pathological characteristics such as persistent inflammation， bacterial infection， oxidative stress and inadequate angiogenesis. Astragali Radix， a traditional Chinese medicinal herb， exerts multi-target pharmacological effects on CRW through its active components， including Astragalus polysaccharides， flavonoids， and astragaloside Ⅳ， etc. Fundamental studies indicate that these components promote CRW healing by modulating inflammatory responses， inhibiting pathogen growth， improving antioxidant capacity and stimulating neovascularization. Network pharmacology and bioinformatics studies have revealed that active components of Astragali Radix target and modulate key signaling nodes such as nuclear factor-κB， phosphatidylinositol 3-kinase/Akt， AMP-activated protein kinase， and vascular endothelial growth factor receptor， as well as inflammation-angiogenesis-related pathways， thereby synergistically exerting anti-inflammatory and pro-angiogenic effect. Clinical applications have demonstrated that oral formulations （e.g.， Huangqi guizhi decoction， Danggui huangqi decoction， etc.） reduce healing time of CRW and lower inflammatory marker levels， while topical preparations （e.g.， Zizhu ointment， Huangqi shengji ointment， electrostatically spun Astragalus polysaccharide composite nanofibre dressings， etc.） significantly improve healing rates of CRW and minimize complications.

Objective: This study aimed to construct an animal model of heart failure with preserved ejection fraction (HFpEF) that integrates disease and syndrome based on the "deficiency-blood stasis-toxin" pathogenesis and to evaluate it comprehensively. Methods: The HFpEF mouse model was constructed using a combination of Nω-nitro-L-arginine methyl ester (L-NAME) and a high-fat diet. According to the random number table method, SPF-grade male C57BL/6J mice were randomly assigned to the control, L-NAME, high-fat diet, and model groups, 10 in each group. Comprehensive observations and data collection on macroscopic signs (e.g., fur condition, mental state, stool and urine, oral and nasal condition, paw and body condition, etc.) and cardiac function were performed after 10 and 16 weeks of model induction. Additionally, the syndrome evolution was elucidated based on diagnostic criteria for clinical syndromes of heart failure. Furthermore, pathological and molecular biological examinations of myocardial tissue were performed to assess the stability and reliability of the model. Results: Mice in the model group showed typical characteristics of syndrome of qi deficiency and blood stasis, as well as syndrome of internal heat accumulation, including lethargy, slow response, dull paw color and oral/nasal color, exercise intolerance, abnormal platelet activation, dry feces, and dark yellow urine. The time window for these syndromes was between 10 and 16 weeks post-modeling. Cardiac function assessments revealed severe diastolic dysfunction, concentric myocardial hypertrophy, and myocardial fibrosis in the model group. Pathological examinations showed a significantly increased collagen deposition in the myocardial interstitium, enlarged cross-sectional area of cardiomyocytes, and sparse coronary microvasculature in the model group. Molecular biological analyses indicated marked activation of the inducible nitric oxide synthase/nuclear factor kappa-light-chain-enhancer of activated B cells/NOD-like receptor family pyrin domain containing 3 inflammatory pathway and significantly elevated inflammation levels in the myocardial tissue of the model group. Although mice in the L-NAME and high-fat diet groups also showed certain manifestations of qi deficiency syndrome, the substantial cardiac damage was relatively limited compared to the control group. Conclusion This study has constructed an animal model of HFpEF that integrates disease and syndrome based on the "deficiency-blood stasis-toxin" pathogenesis. The macroscopic and microscopic characteristics of this model are consistent with the manifestations of syndrome of qi deficiency and blood stasis, toxin syndrome, and syndrome of internal heat accumulation. Moreover, it can stably simulate the HFpEF state and reflect phenotypic changes in human disease. This model provides a suitable experimental platform to explore the pathogenesis of HFpEF, evaluate the effectiveness of traditional Chinese medicine (TCM) treatment regimens, and promote in-depth research on TCM syndromes of heart failure.

OBJECTIVE To investigate the intervention effect of kushenol F （KSC-F） on ulcerative colitis （UC） mice. METHODS Totally 30 male C57BL/6J mice were randomly divided into the normal group， model group， positive drug group （sulfasalazine， 703 mg/kg）， KSC-F 50 mg/kg group （KSC-F50 group）， and KSC-F 100 mg/kg group （KSC-F100 group）， with 6 mice in each group. Except for the normal group， the mice in the remaining groups were given 3% dextran sulfate sodium solution continuously for 7 days to induce UC model. Concurrently， administration groups received corresponding drug solution intragastrically， once a day， for 10 consecutive days. During the experiment， the changes in body weight and bowel movements of the mice were observed. Disease activity index scoring was performed after the last administration. The histopathological morphology of colonic tissue was examined. The levels of inflammatory factors in the serum and colon tissue were measured. Additionally， the mRNA expression of inflammatory factors， and the protein expressions of inflammation-related proteins [interleukin-1β （IL-1β）， forkhead box O1（FOXO1）， phosphoinositide 3-kinase（PI3K）， phosphorylated PI3K（p-PI3K）， p38 mitogen-activated protein kinase（p38 MAPK）， phosphorylated p38 MAPK（p-p38 MPAK） and phosphorylated protein kinase B（p- Akt）] were determined in colonic tissue. RESULTS KSC-F could alleviate weight loss and colonic tissue damage in UC mice. KSC- F reduced the levels of IL-1β， IL-6， IL-8 and tumor necrosis factor-α （TNF-α） in serum， as well as IL-1β， IL-6， IL-17 and TNF- α in colonic tissue to varying degrees and increased the levels of IL-10 in both serum and colonic tissue （P＜0.05 or P＜0.01）. Moreover， KSC-F decreased the expression levels of IL-1β， IL-17 and TNF-α mRNA， as well as p-PI3K， p-p38 MAPK， and p- Akt proteins in colonic tissue to varying degrees， and increased the expression levels of IL-10 mRNA and FOXO1 protein in colonic tissue （P＜0.05 or P＜0.01）. CONCLUSIONS KSC-F effectively alleviates UC symptoms in mice by inhibiting PI3K， Akt and p38 MAPK activation， mitigating the release of pro-inflammatory factors such as IL-1β， IL-6， TNF- α，promoting the anti-inflammatory factor IL-10 secretion， and reducing inflammation-induced colonic tissue damage.

Objective To investigate the effect and possible mechanism of Qili Qiangxin Capsule on the en-dothelial mesenchymal transition of myocardial cells in mice with heart failure after myocardial infarction.Methods A total of 21 male C57BL/6 mice aged 6-8 weeks were divided into a normal control group,a drug control group(normal mice were treated with high-dose Qili Qiangxin Capsule),and a heart failure model group.The heart failure model group was divided into a positive drug control group[microRNA21(miR-21)inhibitor intervention],high,medium,and low dose Qili Qiangxin Capsule intervention groups,a total of seven groups.The heart failure model group underwent ligation of the left anterior descending coronary artery,while the normal control group and the drug control group underwent the same surgical procedure as the model group,but left anterior descending coronary artery ligation was not performed.A small animal ultrasound ima-ging system was used to detect hemodynamic parameters in mice.HE staining was used to observe pathologi-cal changes in mouse myocardium.Sirius red staining was used to detect myocardial tissue fibrosis in mice.Wheat-germ agglutinin staining was used to evaluate the degree of myocardial cell enlargement.Enzyme linked immunosorbent assay(ELISA)was used to detect the expression of N-terminal pro brain natriuretic peptide(NT-proBNP)and cardiac troponin I(cTnⅠ)in mouse serum heart failure markers,as well as the expression levels of activator protein-1(AP-1)and transforming growth factor-β1(TGF-β1)in mouse myocardial tissue.Real time fluorescence quantitative PCR(qRT-PCR)was used to detect the expression level of miR-21 in pe-ripheral blood of mice.Western blot was used to detect CD31 and VE-cadherin in mouse myocardial tissue,and immunohistochemistry was used to detect the expression levels of a-smooth muscle actin(a-SMA),iron death inhibitory protein 1(FSP1),bone morphogenetic protein 7(BMP7),TGF-β1,Smad2/3,and p-Smad2/3 pro-teins.Results Qili Qiangxin Capsule significantly improved heart function and myocardial tissue pathological damage in heart failure mice,reduced myocardial tissue fibrosis levels,alleviated compensatory hypertrophy of non infarcted myocardial cells,inhibited endothelial mesenchymal transition in myocardial tissue,decreased the expression of miR-21,TGFβ1,a-SMA,FSP1 and Smad2/3,and increased the expression of BMP7,VE-cadher-in,and CD31.Conclusion Qili Qiangxin Capsule may improve myocardial injury in mice with heart failure caused by myocardial infarction by regulating the expression of miR-21 and affecting the downstream TGF-β1/Smad2/3 signaling pathway.

Objective To observe the changes in the subfoveal choroidal thickness(SFCT)of children and adoles-cents with different refractive states using optical coherence tomography angiography.Methods A total of 171 children and adolescents were followed.They were divided into the lower primary school group(6-8 years old),upper primary school group(9-11 years old),and junior high school group(12-14 years old)according to their age at the time of en-rollment.Dioptric examinations(including best corrected visual acuity,diopter,intraocular pressure,corneal curvature,axial length and SFCT)were performed,data collection was conducted twice in half a year(initial examination and review after half a year),and the eyeball parameters and changes in eyeball parameters after half a year among all groups were compared.Results The axial length and SFCT of subjects had significant differences among all groups(both P＜0.05).In children and adolescents,the axial length gradually lengthened and SFCT gradually thickened with age,while intraocular pressure and corneal curvature were not associated with age(both P＞0.05).In the initial examination and review after half a year,there was no significant difference in intraocular pressure,corneal curvature and SFCT of subjects with differ-ent refractive states in all groups(all P＞0.05),while the axial length of myopic subjects was greater than that of non-my-opic subjects in all groups(all P＜0.05).In the review after half a year,the SFCT of non-myopic subjects in the lower pri-mary school group and upper primary school group was significantly thickened(P＜0.001,P=0.003),while there was no significant difference in SFCT of myopic subjects in all groups compared with the value half a year ago(all P＞0.05).The axial length of all subjects showed a positive correlation with the SFCT in the initial examination and review after half a year(r=0.354,0.228,P＜0.05).Conclusion Myopia affects the increase in SFCT in children and adolescents.

Acute－on－chronic liver failure （ACLF） refers to acute liver function decompensation on the basis of chronic liver diseases and is a complex clinical syndrome characterized by organ failure and high short－term mortality. ACLF is reversible and has diverse long－term outcomes and prognoses. The clinical classification of ACLF based on disease characteristics is of great significance for optimizing the management pathways for ACLF. With reference to the definition and clinical features of ACLF in the East and the West， this article redefines ACLF from the new perspective of onset manifestations and dynamic outcomes and proposes a new clinical classification of ACLF. The first classification of ACLF is based on the clinical features of intrahepatic and extrahepatic organ failure at disease onset， i.e.， type Ⅰ ACLF （liver failure on the basis of chronic liver diseases） and type Ⅱ ACLF （acute decompensation on the basis of chronic liver diseases comorbid with multiple organ failure）. The second classification is the dynamic clinical classification of ACLF based on clinical outcome， i.e.， type A （rapid progression）， type B （rapid recovery）， type C （slow progression）， type D （slow recovery）， and type E （slow persistence）. The proposed clinical classification of ACLF from the new perspective expects Eastern and Western scholars to have a more inclusive understanding of ACLF， narrow differences， optimize disease management paths， and rationally use medical resources， thereby providing a reference for clinicians.

ObjectiveTo investigate the characteristics of intrahepatic and extrahepatic organ failure at the onset of acute－on－chronic liver failure（ACLF）， to explore the features of a new clinical classification system of ACLF， and to provide a basis for the diagnosis， treatment， prognostic analysis of the disease. MethodsA retrospective analysis was performed for the clinical data of the patients who were hospitalized Beijing YouAn Hospital， Capital Medical University， from January 2015 to October 2022 and were diagnosed with ACLF for the first time. According to the conditions of intrahepatic and extrahepatic organ failure at disease onset， they were classified into type Ⅰ ACLF and type Ⅱ ACLF. Type Ⅰ ACLF referred to liver failure on the basis of chronic liver diseases， and type Ⅱ ACLF referred to acute decompensation of chronic liver diseases combined with multiple organ failure. The clinical features of patients with type Ⅰ or type Ⅱ ACLF were analyzed， and the receiver operating characteristic （ROC） curve was used to assess the value of MELD， MELD－Na， and CLIF－C ACLF scoring system in predicting the 90－day prognosis of ACLF patients with type Ⅰ or type Ⅱ ACLF. The independent－samples t test was used for comparison of normally distributed continuous data between two groups， and the Wilcoxon rank－sum test was used for comparison of non－normally distributed continuous data between two groups； the chi－square test or the Fisher’s exact test was used for comparison of categorical data between two groups. ResultsA total of 582 patients with ACLF were enrolled， among whom there were 535 patients with type Ⅰ ACLF and 47 patients with type Ⅱ ACLF. Hepatitis B and alcoholic liver disease were the main causes in both groups， with no significant difference between the two groups （P>0.05）. Chronic non－cirrhotic liver disease （28.2%） and compensated liver cirrhosis （56.8%） were the main underlying liver diseases in type Ⅰ ACLF， while compensated liver cirrhosis （34.0%） and decompensated liver cirrhosis （61.7%） were the main underlying liver diseases in type Ⅱ ACLF， and there was no significant difference in underlying liver diseases between the patients with type Ⅰ ACLF and those with type Ⅱ ACLF （P<0.001）. The patients with type Ⅱ ACLF had significantly higher median MELD score， MELD－Na score， and CLIF－C ACLF score than those with type Ⅰ ACLF （all P<0.001）. The patients with type Ⅱ ACLF had significantly higher 28－ and 90－day mortality rates than those with type Ⅰ ACLF （38.3%/53.2% vs 15.5%/27.5%， P<0.001）. For the patients with type Ⅰ ACLF who did not progress to multiple organ failure， the patients with an increase in MELD score accounted for 63.7% in the death group and 10.1% in the survival group （P<0.001）， while for the patients with type Ⅰ ACLF who progressed to multiple organ failure， there was no significant difference in the change in MELD score between the survival group and the death group （P>0.05）. In the patients with type Ⅰ ACLF， MELD score， MELD－Na score， and CLIF－C ACLF score had an area under the ROC curve （AUC） of 0.735， 0.737， and 0.740， respectively， with no significant difference between any two scores （all P>0.05）. In the patients with type Ⅱ ACLF， CLIF－C ACLF score had a significantly higher AUC than MELD score （0.880 vs 0.560， P<0.01） and MELD－Na score （0.880 vs 0.513， P<0.01）. ConclusionThere are differences in underlying liver diseases， clinical features， and prognosis between type Ⅰ and type Ⅱ ACLF， and different prognosis scoring systems have different emphases， which provide a basis for the new clinical classification system of ACLF from the perspective of evidence－based medicine.

BACKGROUND: Pneumonia-like primary pulmonary lymphoma (PPL) was commonly misdiagnosed as infectious pneumonia, leading to delayed treatment. The purpose of this study was to establish a computed tomography (CT)-based radiomics model to differentiate pneumonia-like PPL from infectious pneumonia. METHODS: In this retrospective study, 79 patients with pneumonia-like PPL and 176 patients with infectious pneumonia from 12 medical centers were enrolled. Patients from center 1 to center 7 were assigned to the training or validation cohort, and the remaining patients from other centers were used as the external test cohort. Radiomics features were extracted from CT images. A three-step procedure was applied for radiomics feature selection and radiomics signature building, including the inter- and intra-class correlation coefficients (ICCs), a one-way analysis of variance (ANOVA), and least absolute shrinkage and selection operator (LASSO). Univariate and multivariate analyses were used to identify the significant clinicoradiological variables and construct a clinical factor model. Two radiologists reviewed the CT images for the external test set. Performance of the radiomics model, clinical factor model, and each radiologist were assessed by receiver operating characteristic, and area under the curve (AUC) was compared. RESULTS: A total of 144 patients (44 with pneumonia-like PPL and 100 infectious pneumonia) were in the training cohort, 38 patients (12 with pneumonia-like PPL and 26 infectious pneumonia) were in the validation cohort, and 73 patients (23 with pneumonia-like PPL and 50 infectious pneumonia) were in the external test cohort. Twenty-three radiomics features were selected to build the radiomics model, which yielded AUCs of 0.95 (95% confidence interval [CI]: 0.94-0.99), 0.93 (95% CI: 0.85-0.98), and 0.94 (95% CI: 0.87-0.99) in the training, validation, and external test cohort, respectively. The AUCs for the two readers and clinical factor model were 0.74 (95% CI: 0.63-0.83), 0.72 (95% CI: 0.62-0.82), and 0.73 (95% CI: 0.62-0.84) in the external test cohort, respectively. The radiomics model outperformed both the readers' interpretation and clinical factor model ( P <0.05). CONCLUSIONS The CT-based radiomics model may provide an effective and non-invasive tool to differentiate pneumonia-like PPL from infectious pneumonia, which might provide assistance for clinicians in tailoring precise therapy.
Humans ; Retrospective Studies ; Pneumonia/diagnostic imaging* ; Analysis of Variance ; Tomography, X-Ray Computed ; Lymphoma/diagnostic imaging*