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Objective To observe the value of apparent diffusion coefficient(ADC)for evaluating short-term efficacy of TACE for treating colorectal cancer liver metastases(CRLM).Methods Data of 60 liver metastases in 28 CRLM patients who underwent TACE were retrospectively analyzed.Based on MRI after the first TACE,according to the response evaluation criteria of solid tumors,the liver metastases were divided into response group(n=38)and non-response group(n=22).ADC parameters obtained with diffusion weighted imaging(DWI)before and after TACE,including ADC before TACE(ADCpre),after the first TACE(ADCpost1)and after the second TACE(ADCpost2)were compared between groups,while ADC change value(ΔADC)and the percentage of ΔADC were calculated.The maximum diameter of the target foci were measured,and the correlation between ΔADCpost1 and the change of the maximum diameter of target foci were analyzed.Receiver operating characteristic curve was drawn,the area under the curve(AUC)was calculated to observe the efficacy of ΔADCpost1 for evaluating short-term efficacy of TACE for CRLM.Results No significant difference of ADCpre was found between groups(P=0.484).After the first TACE,ADCpost1,ΔADCpost1 and percentage of ΔADCpost1 in response group were all higher than those in non-response group(all P＜0.05).After the second TACE,no significant difference of ADCpost2,ΔADCpost2 nor percentage of ΔADCpost2 was found between groups(all P＞0.05).The maximum diameter change of the target foci after the first TACE was(-0.48±0.93)cm,which was negatively correlated with ΔADCpost1(rs=-0.347,P=0.007).AUC of ΔADCpost1 for evaluating short-term efficacy of TACE for CRLM was 0.717.Conclusion ADC had good efficacy for evaluating short-term efficacy of TACE for treating CRLM.

Demyelination of the central nervous system often occurs in neurodegenerative diseases， such as multiple sclerosis （MS）. The myelin sheath， a layer of myelin membrane wrapping the axon， plays a role in the rapid conduction and metabolic coupling of impulses for neurons. The exposure of the axon will lead to axonal degeneratio， and further neuronal degeneration， which is the main cause of dysfunction and even disability in patients with demyelinating neurodegenerative diseases. In addition to the demyelination of mature myelin sheath， remyelination disorder is also one of the major reasons leading to the development of the diseases. The myelin sheath is composed of oligodendrocytes （OLs） derived from oligodendrocyte progenitor cells （OPCs） which are differentiated from neural stem cells （NSCs）. The process of myelin regeneration， i.e.， remyelination， is the differentiation of NSCs into OLs. Recent studies have shown that this process is regulated by a variety of genes. MicroRNAs， as important regulators of neurodegenerative diseases， form a complex regulatory network in the process of myelin regeneration. This review summarizes the main molecular pathways of myelin regeneration and microRNAs involved in this process and classifies the mechanisms and targets. This review is expected to provide a theoretical reference for the future research on the treatment of demyelinating diseases by targeting the regulation of microRNAs.

ObjectiveTo investigate the effects of Jiaohong pills （JHP） and its prescription， Pericarpium Zanthoxyli （PZ） and Rehmanniae Radix （RR） cognitive dysfunction in scopolamine-induced Alzheimer's disease （AD） mice and its mechanism through pharmacodynamic and metabolomics study. MethodThe animal model of AD induced by scopolamine was established and treated with PZ， RG and JHP， respectively. The effects of JHP and its formulations were investigated by open field test， water maze test， object recognition test， avoidance test， cholinergic system and oxidative stress related biochemical test. Untargeted metabolomics analysis of cerebral cortex was performed by ultra-performance liquid chromatography-Quadrupole/Orbitrap high resolution mass spectrometry （UPLC Q-Exactive Orbitrap MS）. ResultThe behavioral data showed that， compared with the model group， the discrimination indexes of the high dose of JHP， PZ and RR groups was significantly increased （P<0.05）. The staging rate of Morris water maze test in the PZ， RR， high and low dose groups of JHP was significantly increased （P<0.05， P<0.01）， the crossing numbers in the PZ， JHP high and low dose groups were significantly increased （P<0.05， P<0.01）； the number of errors in the avoidance test were significantly reduced in the PZ and high-dose JHP groups （P<0.01）， and the error latencies were significantly increased in the JHP and its prescription drug groups （P<0.01）. Compared with the model group， the activities of acetylcholinesterase in the cerebral cortex of the two doses of JHP group and the PZ group were significantly increased （P<0.05， P<0.01）， and the activity of acetylcholinesterase in the high-dose JHP group was significantly decreased （P<0.05）， and the level of acetylcholine was significantly increased （P<0.01）. At the same time， the contents of malondialdehyde in the serum of the two dose groups of JHP decreased significantly （P<0.05， P<0.01）. The results of metabolomics study of cerebral cortex showed that 149 differential metabolites were identified between the JHP group and the model group， which were involved in neurotransmitter metabolism， energy metabolism， oxidative stress and amino acid metabolism. ConclusionJHP and its prescription can antagonize scopolamine-induced cognitive dysfunction， regulate cholinergic system， and reduce oxidative stress damage. The mechanism of its therapeutic effect on AD is related to the regulation of neurotransmitter， energy， amino acid metabolism， and improvement of oxidative stress.

ObjectiveThis study explores the efficacy and pharmacological mechanism of Wujiwan in rats with inflammatory bowel disease （IBD） from the perspectives of the peroxisome proliferator-activated receptor γ （PPARγ） signaling pathway and T-cell immunity， providing reference for the treatment of IBD with traditional Chinese medicine. MethodThe study involved administering 2，4，6-trinitrobenzenesulfonic acid （TNBS） enemas to 35 rats to induce acute IBD. After 24 hours， the animals were divided into the following groups： normal group， model group， Wujiwan treatment group， and positive drug control group. Each group received gastric gavage for 8 consecutive days before the rats were dissected to compare the disease activity index （DAI） of the rat colon tissue， the colon mucosal damage index （CMDI）， and the spleen index. Enzyme-linked immunosorbent assay （ELISA） was used to measure the levels of interleukin-1β （IL-1β）， interleukin-10 （IL-10）， and tumor necrosis factor-α （TNF-α） in the serum. Quantitative real-time polymerase chain reaction （Real-time PCR） was used to determine the mRNA expression levels of T-bet （T-box expressed in T cells） and Gata3 （Gata-binding protein-3） in the colon tissue. Western blot analysis was conducted to detect the protein expression levels of PPARγ， T-bet， and nuclear factor-κB p65 （NF-κB p65） in the rat colon. ResultThe rat model of IBD was successfully established. Compared with the model group， the Wujiwan treatment group showed reduced DAI， CMDI， and spleen index， decreased content of TNF-α in the serum（P<0.01）， significantly increased content of IL-10（P<0.01）， and elevated mRNA content of T-bet and Gata3（P<0.05） in the colon tissue. The expression of PPARγ protein was augmented（P<0.05）， and the expression of T-bet and NF-κB p65 protein was decreased（P<0.05，P<0.01）. ConclusionWujiwan activates or upregulates PPARγ expression in IBD rats to inhibit the generation of pro-inflammatory factors， participates in the inflammatory immune process， and alleviates inflammatory reactions. Its mechanism may involve regulating the NF-κB pathway through PPARγ， enhancing Th2 cell transcription expression， and reducing Th1 cell transcription.

Traditional Chinese medicine （TCM） has a long history of application in China and has consistently played a vital role in treating diseases and saving lives. TCM prescriptions （compounds） constitute the primary form of clinical TCM treatment and significantly differ from western medicine （chemicals） due to the diverse composition and chemical constituents of TCM （compounds）. Nevertheless， the potential multi-component， multi-target， and multi-pathway action characteristics of TCM prescriptions also demonstrate their possible （complementary） therapeutic advantages when compared with single-component chemical drugs. Therefore， driven by the development of modern science and technology and the demands of the modernization and internationalization of TCM， modern theories regarding the complexity of TCM prescription effects have been continuously proposed： Different from the abstract language of traditional prescription theory， the modern TCM prescription theory is more inclined to illustrate the connotation of prescription compatibility concretely and vividly from an experimental and scientific perspective. In this paper， new theories on the complexity of TCM prescriptions proposed in recent years are summarized to provide research references and ideas for the greater role of TCM prescriptions and a better scientific understanding.

BACKGROUND:silencing information regulatory 1(SIRT1)regulates the function of related proteins in chondrocytes in a deacetylated manner and participates in chondrocyte proliferation and differentiation,thereby promoting cartilage defect repair. OBJECTIVE:To screen for signaling pathways with unclear action status after SIRT1 gene knockdown in chondrocytes,as well as diseases or functions that produce changes using high-throughput technology. METHODS:ATDC5 chondrocytes from mice in logarithmic growth phase were divided into two groups:the cells were transfected with SIRT1 gene knockdown negative control lentivirus in control group and SIRT1 gene knockdown lentivirus in experimental group.GeneChip? Mouse Genome 430 2.0 Array was used to detect the mRNA expression at 72 hours after transfection.Applied bioinformatics technology was also used to screen for unclear activation or inhibition signaling pathways and their related factors.Moreover,enrichment of disease or function modules was analyzed. RESULTS AND CONCLUSION:After knocking down the SIRT1 gene,there were 245 signaling pathways with unclear activation or inhibition status in the mouse ATDC5 chondrocytes.According to the ranking of-Log(P-value),we reported the factors in the top 20 signaling pathways with unclear activation or inhibition status,including IGFBP4,TGFBR1,CTGF,COL4A5,LHX2,IL1RL1,and KLF6.According to the ranking of-Log(P-value),there were significant changes in 14 disease or function modules,including cellular growth and proliferation,organism survival,cell death and survival.According to the number of differentially expressed genes,there were significant changes in three disease or function modules,including organismal injury and abnormalities,cancer,and cell death and survival.According to the comprehensive ranking of-Log(P-value)and the number of differentially expressed genes,the disease or function module related to intrinsic immune response was significantly activated.

Objective To explore whether 5/6 nephrectomy can establish a rat model of chronic renal failure-in-duced sarcopenia.Methods The rats were randomly divided into control group,sham operation group and 5/6 ne-phrectomy model group.Chronic renal failure and sarcopenia were further verified.Results Compared with the sham group:① In the model group,the qualitative analysis of urinary protein,serum creatinine,blood urea nitrogen and serum uric acid levels were increased(P＜0.05);② In the model group,the degree of renal fibrosis and the rate of apoptosis were high(P＜0.05);③ In the model group,the muscle strength and function declined(P＜0.05);④ In the model group,the degree of muscle fibrosis was obvious(P＜0.05).Conclusion Through the 5/6 nephrectomy method,an animal model of chronic renal failure-induced sarcopenia can be established,which provides an experimental basis for further prevention and treatment of this disease.

MiR-138-5p is a microRNA that plays an important regulatory role in the pathogenesis of osteoarthritis.MiR-138-5p regulates various biological processes,including inflammation,cell apoptosis and proliferation,and matrix degradation in osteoarthritis,by modulating signaling pathways including nuclear factor-κB,Wnt/β-catenin,and phosphoinositide 3-kinase/AKT.This review summarizes the research progress regarding the mechanism of miR-138-5p in osteoarthritis.

Objective To explore the value of deep learning(DL)models semi-automatic training system for automatic optimization of clinical image quality control of transthoracic echocardiography(TTE).Methods Totally 1 250 TTE videos from 402 patients were retrospectively collected,including 490 apical four chamber(A4C),310 parasternal long axis view of left ventricle(PLAX)and 450 parasternal short axis view of great vessel(PSAXGv).The videos were divided into development set(245 A4C,155 PLAX,225 PSAXGV),semi-automated training set(98 A4C,62 PLAX,90 PSAXGV)and test set(147 A4C,93 PLAX,135 PSAXGV)at the ratio of 5:2:3.Based on development set and semi-automatic training set,DL model of quality control was semi-automatically iteratively optimized,and a semi-automatic training system was constructed,then the efficacy of DL models for recognizing TTE views and assessing imaging quality of TTE were verified in test set.Results After optimization,the overall accuracy,precision,recall,and F1 score of DL models for recognizing TTE views in test set improved from 97.33％,97.26％,97.26％and 97.26％to 99.73％,99.65％,99.77％and 99.71％,respectively,while the overall accuracy for assessing A4C,PLAX and PSAXGV TTE as standard views in test set improved from 89.12％,83.87％and 90.37％to 93.20％,90.32％and 93.33％,respectively.Conclusion The developed DL models semi-automatic training system could improve the efficiency of clinical imaging quality control of TTE and increase iteration speed.