Liver cancer, one of the most common primary malignancies in humans, is a malignant tumor characterized by multifactorial induction, polygenic involvement, and intricate molecular mechanisms. This disease is characterized by its treatment challenges and poor prognosis, which are closely related to its unique tumor microenvironment composition. The tumor microenvironment of liver cancer is a dynamic ecosystem composed of heterogeneous cellular populations, soluble cytokines, and remodeled extracellular matrix. In recent years, significant progress has been made in the study of the tumor microenvironment of liver cancer, revealed an important role in the occurrence, development, and treatment of liver cancer. The key regulatory elements of the tumor microenvironment in liver cancer were systematically summarized, such as activation of hepatic stellate cells, dysfunction of immune cells, abnormalities of platelet, and remodeling of the extracellular matrix, which provided theoretical foundations for prevention and treatment strategies against liver cancer.

Objective:To investigate the mechanisms of baicalin in treating septic acute liver injury through a combination of network pharmacology and animal experiments.Methods:Thirty male C57BL/6 mice (6 weeks old) were divided into five groups ( n=6): control group (normal saline), model group [lipopolysaccharide (LPS) 10 mg/kg, intraperitoneal injection], low-dose baicalin group (10 mg/kg), high-dose baicalin group (20 mg/kg), and baicalin-only group (20 mg/kg, without LPS). Baicalin was administered orally for 14 consecutive days prior to modeling. Mice were sacrificed 24 h after LPS injection. Alanine transaminase, aspartate transaminase liver tissue histopathology were measured; neutrophil infiltration was visualized using immunofluorescence; mRNA expression levels of interleukin (IL)-1β, IL-17, IL-6, and tumor necrosis factor (TNF)-α were detected by RT-qPCR; and the expression of Toll-like receptor 4 (TLR4) and phosphorylated nuclear factor (NF)-κB proteins were analyzed by Western blotting. Results:In the LPS model group, the ALT, AST, and histopathological injury score were (148.60±22.02) U/L, (81.58±11.59) U/L, and 8.50(7.75, 9.25), respectively. These indicators were significantly reduced in the high-dose baicalin group with (77.90±16.79) U/L, (49.92±14.89) U/L, and 1.00(1.00, 2.25) (all P<0.05). Compared with the LPS group, neutrophil infiltration in the liver of high-dose baicalin group was also significantly reduced [1.18%(0.98%, 1.22%) vs. 6.13%(5.41%, 8.69%), P<0.05]. RT-qPCR results showed that the relative mRNA expression levels of inflammatory cytokines IL-1β [(1.03±0.06) vs. (2.60±0.34)], IL-17 [(1.21±0.12) vs. (2.94 ± 0.39)], IL-6 [(1.37±0.26) vs. (2.73±0.18)], and TNF-α [(1.18±0.10) vs. (3.30±0.92)] were significantly decreased in the high-dose baicalin group compared with the LPS group (all P<0.05). Western blot analysis revealed that the relative protein expression levels of TLR4 [(1.25±0.13) vs. (1.73±0.06)] and phosphorylated NF-κB [(1.25±0.25) vs. (1.79±0.12)] were also significantly lower in the high-dose baicalin group (both P<0.05). Conclusion:Baicalin reduces liver injury in septic mice by downregula-ting the expression of pro-inflammatory cytokines IL-1β, IL-6, TNF-α, and IL-17, potentially through the inhibition of the TLR4/NF-κB signaling pathway.

Objective:To investigate the mechanisms of baicalin in treating septic acute liver injury through a combination of network pharmacology and animal experiments.Methods:Thirty male C57BL/6 mice (6 weeks old) were divided into five groups ( n=6): control group (normal saline), model group [lipopolysaccharide (LPS) 10 mg/kg, intraperitoneal injection], low-dose baicalin group (10 mg/kg), high-dose baicalin group (20 mg/kg), and baicalin-only group (20 mg/kg, without LPS). Baicalin was administered orally for 14 consecutive days prior to modeling. Mice were sacrificed 24 h after LPS injection. Alanine transaminase, aspartate transaminase liver tissue histopathology were measured; neutrophil infiltration was visualized using immunofluorescence; mRNA expression levels of interleukin (IL)-1β, IL-17, IL-6, and tumor necrosis factor (TNF)-α were detected by RT-qPCR; and the expression of Toll-like receptor 4 (TLR4) and phosphorylated nuclear factor (NF)-κB proteins were analyzed by Western blotting. Results:In the LPS model group, the ALT, AST, and histopathological injury score were (148.60±22.02) U/L, (81.58±11.59) U/L, and 8.50(7.75, 9.25), respectively. These indicators were significantly reduced in the high-dose baicalin group with (77.90±16.79) U/L, (49.92±14.89) U/L, and 1.00(1.00, 2.25) (all P<0.05). Compared with the LPS group, neutrophil infiltration in the liver of high-dose baicalin group was also significantly reduced [1.18%(0.98%, 1.22%) vs. 6.13%(5.41%, 8.69%), P<0.05]. RT-qPCR results showed that the relative mRNA expression levels of inflammatory cytokines IL-1β [(1.03±0.06) vs. (2.60±0.34)], IL-17 [(1.21±0.12) vs. (2.94 ± 0.39)], IL-6 [(1.37±0.26) vs. (2.73±0.18)], and TNF-α [(1.18±0.10) vs. (3.30±0.92)] were significantly decreased in the high-dose baicalin group compared with the LPS group (all P<0.05). Western blot analysis revealed that the relative protein expression levels of TLR4 [(1.25±0.13) vs. (1.73±0.06)] and phosphorylated NF-κB [(1.25±0.25) vs. (1.79±0.12)] were also significantly lower in the high-dose baicalin group (both P<0.05). Conclusion:Baicalin reduces liver injury in septic mice by downregula-ting the expression of pro-inflammatory cytokines IL-1β, IL-6, TNF-α, and IL-17, potentially through the inhibition of the TLR4/NF-κB signaling pathway.

Speckle tracking echocardiography(STE)can be used to quantitatively evaluate cardiac function,detect abnormalities of the global and local cardiac wall motion,also help to understand the subtle changes of myocardial function,having high value for early diagnosis of cardiac remodeling after myocardial infarction(MI)and predicting risk and development of heart failure.The research progresses of STE for evaluating cardiac remodeling and heart failure after MI were reviewed in this article.

Objective To explore whether the effect of urine-derived stem cells(USCs)on chondro-cytes in osteoarthritis(OA)is related to the PI3K/AKT pathway.Methods Human urine was collected aseptically,and primary USCs were isolated and cultured through specific steps.Meanwhile,chondro-cytes were extracted from the knee joints of Sprague-Dawley rats to establish the OA model.USCs were co-cultured with OA chondrocytes by using Transwell co-culture system,and the transcriptome changes of chondrocytes before and after co-culture were analyzed by using the high-throughput RNA sequencing.Moreover,the phosphorylation levels of key proteins of the PI3K/AKT/mTOR pathway were detected using protein immunoblotting,and the PI3K agonist 740 Y-P was employed to further vali-date the relationship between the protective effect of USCs on OA chondrocytes,as well as its possi-ble relationship to the PI3K/AKT pathway and the possible mechanism.Results Transcriptomic analysis showed that the protective effect of USCs on OA chondrocytes might be related to the'PI3K-Akt sig-naling pathway'.Protein level analysis confirmed that USCs significantly inhibited the PI3K/AKT/mTOR pathway in OA chondrocytes.Moreover,protein immunoblotting and immunofluorescence showed that USCs improved the expression of OA-related proteins and autophagy-related proteins in OA chondro-cytes.What's more,the inhibitory effect of USCs on the PI3K/AKT/mTOR pathway was partially re-versed by using the PI3K agonist 740 Y-P,while the protective and autophagy-promoting effects of USCs on OA chondrocytes were down-regulated.Conclusion This study reveals the potential protective effect of USCs on OA chondrocytes through inhibition of the PI3K/AKT/mTOR signalling pathway and its close correlation with improved autophagy.Therefore,it provides a research basis and theoretical support for the future application of USCs in the treatment of OA.

Acute myocarditis(AM)may rapidly progress to fulminant myocarditis(FM),but lacks special clinical presentation.Multimodal echocardiography combined conventional transthoracic echocardiography,two-dimensional and three-dimensional speckle tracking imaging,myocardial contrast echocardiography and so on is helpful to detecting AM in early stage and assessing the severity,being of great value for clinical decision-making and prognostic evaluation.The research progresses of multimodal echocardiography in AM were reviewed in this article.

Objective:To explore the correlation between high cholinergic pathway signaling and cognitive function in patients with Parkinson disease(PD) accompanied with sleep disorder.Methods:PD patients admitted from 2017 to 2022 were divided into PD with sleep disorder group (PD-SD group) ( n=56) and PD without sleep disorder group (PD-NSD group) ( n=41) according to the Parkinson's disease sleep scale (PDSS) score. All participants underwent magnetic resonance imaging examination.All patients were evaluated by the PDSS, Hoehn-Yahr (H-Y), Montreal cognitive assessment scale (MoCA), and cholinergic pathways hyper intensities scale (CHIPS). The difference of cognitive function between the two groups and the correlation between CHIPS and cognitive function were analyzed.Independent sample t-test, Spearman correlation analysis, and binary Logistic regression analysis were performed on the data by SPSS 26.0 statistical software. Results:(1)The MoCA score of the PD-SD group (22.00 (5.00)) was lower than that of the PD-NSD group (26.00 (5.00)) ( Z=-3.830, P<0.05). The total and all aspects scores of CHIPS in PD-SD group were higher than those in PD-NSD group(the total score of the low external capsule: 12.00(8.00), 0(8.00), the total score of the high external capsule: 12.00(2.00), 6.00(9.00), the total score of the radial crown: 8.00(0), 4.00(4.00), the total score of the centrum semiovale: 3.00(4.00), 0(2.00), the total score of the right side: 16.00(9.00), 5.00(10.00), the total score of the left side: 17.00(6.00), 7.00(9.00), the total score of CHIPS: 32.00(14.00), 14.00(20.00))( Z=-5.081, -5.873, -4.933, -3.211, -5.562, -6.232, -5.995, all P<0.05). (2)The correlation analysis between the score of CHIPS and cognitive function in the PD-SD group showed that, the total score of the low external capsule ( r=-0.286), the total score of the centrum semiovale ( r=-0.307), the total score of the right side ( r=-0.376), the total score of the left side ( r=-0.284) and the total score of CHIPS ( r=-0.349) were negatively correlated with MoCA(all P<0.05). (3)Binary Logistic regression analysis showed that white matter lesions in centrum semiovale, low inner capsule, right and left leukodystrophy were not influence factors for cognitive impairment (all P>0.05). Conclusion:PD patients with sleep disorders have lower cognitive function scores, higher CHIPS scores, and significant changes in white matter lesions compared to those without sleep disorders. In PD patients with sleep disorders, the higher the CHIPS score, the lower the cognitive function score, and the more significant the rate of cognitive impairment occurrence and development.

Objective To explore whether the effect of urine-derived stem cells(USCs)on chondro-cytes in osteoarthritis(OA)is related to the PI3K/AKT pathway.Methods Human urine was collected aseptically,and primary USCs were isolated and cultured through specific steps.Meanwhile,chondro-cytes were extracted from the knee joints of Sprague-Dawley rats to establish the OA model.USCs were co-cultured with OA chondrocytes by using Transwell co-culture system,and the transcriptome changes of chondrocytes before and after co-culture were analyzed by using the high-throughput RNA sequencing.Moreover,the phosphorylation levels of key proteins of the PI3K/AKT/mTOR pathway were detected using protein immunoblotting,and the PI3K agonist 740 Y-P was employed to further vali-date the relationship between the protective effect of USCs on OA chondrocytes,as well as its possi-ble relationship to the PI3K/AKT pathway and the possible mechanism.Results Transcriptomic analysis showed that the protective effect of USCs on OA chondrocytes might be related to the'PI3K-Akt sig-naling pathway'.Protein level analysis confirmed that USCs significantly inhibited the PI3K/AKT/mTOR pathway in OA chondrocytes.Moreover,protein immunoblotting and immunofluorescence showed that USCs improved the expression of OA-related proteins and autophagy-related proteins in OA chondro-cytes.What's more,the inhibitory effect of USCs on the PI3K/AKT/mTOR pathway was partially re-versed by using the PI3K agonist 740 Y-P,while the protective and autophagy-promoting effects of USCs on OA chondrocytes were down-regulated.Conclusion This study reveals the potential protective effect of USCs on OA chondrocytes through inhibition of the PI3K/AKT/mTOR signalling pathway and its close correlation with improved autophagy.Therefore,it provides a research basis and theoretical support for the future application of USCs in the treatment of OA.

Speckle tracking echocardiography(STE)can be used to quantitatively evaluate cardiac function,detect abnormalities of the global and local cardiac wall motion,also help to understand the subtle changes of myocardial function,having high value for early diagnosis of cardiac remodeling after myocardial infarction(MI)and predicting risk and development of heart failure.The research progresses of STE for evaluating cardiac remodeling and heart failure after MI were reviewed in this article.