Objective To investigate the value of real-time virtual navigation system (RVS) combined with CEUS in guiding radiofrequency ablation (RFA) therapy of neonatal or recurrent lesions of hepatocellular carcinoma (HCC).Methods Totally 111 patients with neonatal or recurrent lesions of HCC after RFA therapy were enrolled.Seventy-eight patients with 86 lesions (77 neonatal lesions and 9 recurrent lesions) underwent RFA guided by RVS combined with CEUS (RVS combined with CEUS group),and 33 patients with 38 lesions (26 neonatal lesions and 12 recurrent lesions) underwent RFA guided by CEUS alone (control group).The precise localization,inactivation rate and local recurrence rate between the two groups were compared.Results Eighty-four lesions (84/86,97.67％) in RVS combined with CEUS group and 25 lesions (25/38,65.79％) in control group were clearly showed and localized (P＜0.001).One month after RFA therapy,the tumor inactivation rate in RVS combined with CEUS group and control group was 95.35 ％ (82/86) and 76.31％ (29/38),respectively (P=0.003).The local recurrence rate in RVS combined with CEUS group was 8.14％ (7/86),while was 36.84％ (14/38) in control group (x2 =15.434,P＜0.001).Conclusion RVS combined with CEUS guidance can improve the accurate position rate and early inactivation rate of RFA therapy for neonatal or recurrent lesions of HCC.

Fanconi anemia (FA) is an inheritable disorder that presents with bone marrow failure, developmental anomalies, and an increased susceptibility to cancer. The etiology of this condition stems from a genetic mutation that disrupts the proper repair of interstrand DNA cross-links (ICLs). The resultant dysregulation of the DNA damage response mechanism can induce genomic instability, thereby elevating the mutation rates and the likelihood of developing cancer. The FA pathway assumes a pivotal role in safeguarding genome stability through its involvement in the repair of DNA cross-links and the maintenance of overall genomic integrity. A mutation in the germ line of any of the genes responsible for encoding the FA protein results in the development of FA. The prevalence of aberrant FA gene expression in somatic cancer, coupled with the identification of a connection between FA pathway activation and resistance to chemotherapy, has solidified the correlation between the FA pathway and cancer. Consequently, targeted therapies that exploit FA pathway gene abnormalities are being progressively developed and implemented. This review critically examines the involvement of the FA protein in the repair of ICLs, the regulation of the FA signaling network, and its implications in cancer pathogenesis and prognosis. Additionally, it explores the potential utility of small-molecule inhibitors that target the FA pathway.

Objective To explore the changes in serum energy metabolites in patients with peripheral T-cell lymphoma,and investigate serum biomarkers for monitoring peripheral T-cell lymphoma from the perspective of energy metabolism.Methods Multiple/selected reaction monitoring(MRM/SRM)was used to detect the energy-related metabolites in the sera of 16 patients with newly diagnosed peripheral T-cell lymphoma admitted in the Hematology Medical Center of the Second Affiliated Hospital of Army Medical University from November 2020 to December 2021,as well as 10 recruited healthy volunteers.The corresponding clinical data including medical history,laboratory results and image data were collected and retrospectively analyzed.Results Significant differences were seen in the contents and expression profiles of serum energy metabolism-related products between the patients and the healthy volunteers.The patients had significantly reduced serum contents of cyclic AMP,succinate,citrate and cis-aconitate(P＜0.05),and elevated D-glucose 6-phosphate content(P＜0.05).The serum contents of citrate and succinate were negatively correlated with the risk stratification(low-,moderate-and high-risk)and clinical stage of the disease(P＜0.05).Meanwhile,there was a negative correlation between the contents of L-malic acid and citrate and the mid-term efficacy evaluation results,such as complete/partial response(CR/PR)or stable disease(SD)(P＜0.05).For patients with extranodal NK/T cell lymphoma(n=10),there were also significant reductions in the contents of cyclic AMP,succinate,citrate,isocitrate and cis-aconitate in the sera of patients compared with healthy volunteers(P＜0.05),and the contents of citrate and succinate were negatively correlated with the clinical stage(P＜0.05)and were rather correlated with mid-term efficacy evaluation results(CR/PR or SD)(P＜0.05).For patients with angioimmunoblastic T-cell lymphoma(n=6),the serum contents of cyclic AMP,citrate and succinate were significantly lower,while the content of D-glucose 6-phosphate was higher when compared with the healthy volunteers(P＜0.05),and the content of succinate was negatively correlated with both clinical stage and risk grade of the patients(P＜0.05).Conclusion There are 5 serum differential metabolites identified between patients with peripheral T-cell lymphoma and healthy controls,and succinate and citrate are expected to be serum biomarkers of peripheral T-cell lymphoma.

OBJECTIVE： To screen the best proportion of Astragalus membranaceus injection combined with Erigeron breviscapus injection against cerebral ischemia-reperfusion injury in rats. METHODS： Male SD rats were randomly divided into sham operation group， model group and administration group [different A. membranaceus injection-E. breviscapus injection proportion groups， being A（0 ∶ 10）， B（2 ∶ 8）， C（4 ∶ 6）， D（6 ∶ 4）， E（8 ∶ 2）， F（10 ∶ 0）groups， set by baseline geometric proportion increasing and decreasing design]， with 8 rats in each group. Except for sham operation group， reperfusion injury model of middle cerebral artery occlusion were induced by modified suture method in rats. The each administration group was given relevant medicine intraperitoneally once immediately after inducing model， and then given again after 24 hours （medication interval between the two injections of 30 min）. Constant volume of normal saline was given to rats in sham operation group and model group. Forty-eight hours after reperfusion， Longa scoring method was used to evaluate neurological impairment of rats， and neurological impairment score was recorded. Serum content of MDA and activity of SOD were measured by colorimetry assay. TTC assay was used to detect cerebral infraction， and cerebral infarction rate was calculated. Kim’s formula was used to calculate the synergistic index （q） of rats in administration groups. RESULTS： Compared with sham operation group， neurological impairment score and serum content of MDA were increased significantly in model group， while activity of SOD was decreased significantly （P＜0.01）. The area of cerebral infarction increased significantly， and the rate of cerebral infarction increased significantly （P＜0.01）. Compared with model group， neurological impairment scores and serum contents of MDA were decreased significantly in group A， B， C， D and E； neurological impairment score of group C was significantly lower than those of group A and F； serum contents of MDA in group B， C， D and E were significantly lower than that of group F （P＜0.05 or P＜0.01）. Activities of SOD in group A， B， C， D and E were increased significantly， and group C was significantly higher than group F （P＜0.05 or P＜0.01）. The cerebral infarction area of rats in each administration group was reduced to varying degrees. The cerebral infarction rates of rats in group B， C， D and E were significantly reduced， and group C and D were significantly lower than group F， while group C was significantly lower than group A （P＜0.05 or P＜0.01）. The q values of group B， C， D and E were 0.90， 1.30， 1.00， 0.70 （neurological impairment score） and 0.79， 1.27， 0.98， 0.82 （cerebral infarction rate）. CONCLUSIONS： Different ratios of A. membranaceus injection and E. breviscapus injection have certain protective effects on cerebral ischemia-reperfusion injury model rats， can relieve their neurological deficits， alleviate their oxidative stress and reduce their cerebral infarction areas. The effect of the combination of the two drugs is better than that of single use， and the optimum ratio is 4 ∶ 6.

Lipid homeostasis is considered to be related to intestinal metabolic balance, while its role in the pathogenesis and treatment of ulcerative colitis (UC) remains largely unexplored. The present study aimed to identify the target lipids related to the occurrence, development and treatment of UC by comparing the lipidomics of UC patients, mice and colonic organoids with the corresponding healthy controls. Here, multi-dimensional lipidomics based on LC-QTOF/MS, LC-MS/MS and iMScope systems were constructed and used to decipher the alteration of lipidomic profiles. The results indicated that UC patients and mice were often accompanied by dysregulation of lipid homeostasis, in which triglycerides and phosphatidylcholines were significantly reduced. Notably, phosphatidylcholine 34:1 (PC34:1) was characterized by high abundance and closely correlation with UC disease. Our results also revealed that down-regulation of PC synthase PCYT1α and Pemt caused by UC modeling was the main factor leading to the reduction of PC34:1, and exogenous PC34:1 could greatly enhance the fumarate level via inhibiting the transformation of glutamate to N-acetylglutamate, thus exerting an anti-UC effect. Collectively, our study not only supplies common technologies and strategies for exploring lipid metabolism in mammals, but also provides opportunities for the discovery of therapeutic agents and biomarkers of UC.

Stroke is considered a leading cause of mortality and neurological disability, which puts a huge burden on individuals and the community. To date, effective therapy for stroke has been limited by its complex pathological mechanisms. Autophagy refers to an intracellular degrading process with the involvement of lysosomes. Autophagy plays a critical role in maintaining the homeostasis and survival of cells by eliminating damaged or non-essential cellular constituents. Increasing evidence support that autophagy protects neuronal cells from ischemic injury. However, under certain circumstances, autophagy activation induces cell death and aggravates ischemic brain injury. Diverse naturally derived compounds have been found to modulate autophagy and exert neuroprotection against stroke. In the present work, we have reviewed recent advances in naturally derived compounds that regulate autophagy and discussed their potential application in stroke treatment.