The prevalence of acute pancreatitis (AP) is increasing, but current treatments remain inadequate. Photobiomodulation (PBM) therapy has demonstrated anti-inflammatory effects under various conditions; however, its role in AP has not been explored. Evaluating this could introduce a noninvasive treatment option for AP. This study aimed to assess PBM’s potential of PBM in reducing cerulein-induced AP inflammation and elucidate the underlying mechanisms. Animal Experiment: Mice were categorized into control, model, and experimental groups. AP was induced with cerulein injections in depilated mice, followed by seven PBM irradiation sessions in the experimental group. Blood samples collected 24 h post-injection were analyzed for TNF-α, IL-6, amylase, and lipase levels. The pancreatic tissue was histologically examined and scored. Cell Experiment: AR42J cells, grouped similarly, were subjected to cerulein exposure and PBM irradiation. An NF-κB inhibitor has been introduced into some groups. Measurements included amylase, NF-κB p65, phosphorylated NF-κB p65, and (Robot Operating System) ROS levels in the supernatant. Animal Experiment: PBM treatment reduced pancreatic tissue edema and serum amylase, lipase, TNF-α, and IL-6 levels. Cell Experiment: ROS levels increased, NF-κB p65 expression decreased, and TNF-α, IL-6, amylase, and lipase in the cell supernatant decreased post-PBM treatment. The addition of the NF-κB inhibitor BAY 11-7082 to the PBM-treated group did not increase ROS levels. PBM therapy shows potential as a noninvasive AP treatment by modulating ROS-mediated NF-κB signaling. Clinical studies are needed to confirm the efficacy and explore the applications of AP treatment.

Combinational photo-and chemodynamic therapy (PDT/CDT) is a promising approach for oncotherapy, leveraging multiple reactive oxygen species (ROS) to induce tumor cell death. In the tumor microenvironment, severe hypoxia and overexpressed antioxidant glutathione (GSH) together significantly weaken ROS-mediated cytotoxicity. To this end, a multifunctional nanoplatform consisting of flake-like manganese oxide (MnO2) shell and ZnPc-loaded photosensitizer core was elaborately constructed. The MnO2 shell consumes GSH while generating Mn2+ ions, which in turn act as Fenton-like catalysts to convert endogenous H2O2 into highly toxic hydroxyl radicals for enhanced CDT as well as O2 for hypoxia alleviation. More importantly, the heavy-doped ZnPc molecules in the particle core are prevented from aggregating via Zn-pyridine coordination to attain a high singlet oxygen quantum yield of 0.36, thereby reinforcing PDT efficacy with an adequate supply of O2. In vitro and in vivo studies demonstrate significantly enhanced antitumor efficacy compared to PDT or CDT alone while maintaining negligible systemic toxicity. The integration of GSH depletion, O2 generation, and efficient ROS production within a single nanoplatform overcomes multiple barriers in PDT/CDT, offering a robust strategy for effective cancer treatment.

AIMS:Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of the oral cavity. Although the molecular mechanisms of OSCC have been explored, they remain incompletely understood. This study aimed to comprehensively analyze key molecular pathways involved in the occurrence and progression of OSCC, with the goal of identifying novel biomarkers for early diagnosis and potential therapeutic targets to improve patient prognosis. METHODS:OSCC datasets (GSE31056 and GSE51010) were obtained from the Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) were identified and subjected to functional enrichment analysis, weighted gene co-expression network analysis (WGCNA), and protein-protein interaction (PPI) network analysis to predict core genes. Immune infiltration analysis was performed to estimate immune cell proportions. The Comparative Toxicogenomics Database (CTD) was used to identify diseases associated with the core genes. Real-time quantitative polymerase chain reaction (RT-qPCR) was conducted to validate the expression levels of core genes and related proteins. RESULTS:A total of 1017 DEGs were identified, which were mainly enriched in metabolic pathways, as well as the p53 and PPAR signaling pathways. Integration of three algorithms identified four central genes: BUB1, CCNB2, KIF23, and NEK2. Among them, BUB1 and CCNB2 were significantly overexpressed in OSCC compared with normal tissue samples. CTD analysis linked these genes to oral tumors, inflammation, and immune system diseases. Immune infiltration analysis revealed a higher proportion of neutrophils in OSCC samples. RT-qPCR confirmed elevated expression of BUB1, CCNB2, KIF23, NEK2, BAX, and Caspase-3 in OSCC. CONCLUSION:Overexpression of BUB1 and CCNB2 may enhance cell cycle activity and inflammatory responses, thereby promoting OSCC cell proliferation.

INTRODUCTION:Pyroptosis, a form of inflammatory programmed cell death, is implicated in acute pancreatitis (AP). Acinar cell pyroptosis plays a pivotal role in the pathogenesis of AP. Circular RNA has emerged as an important regulatory molecule in AP; however, its specific function and mechanism in modulating acinar cell pyroptosis during AP are unknown. METHODS:Healthy male C57BL/6 mice were divided into control group and acute pancreatitis group. Cell experiments are also divided into two groups: control group and drug-treated (caerulein and lipopolysaccharide) group. Tissue detection was used hematoxylin-eosin staining. Serum analysis was assessed by Enzyme-linked immunosorbent assay (ELISA). Differential expression of circRNA in pancreatic head tissue was screened using RNA-sequencing and circ0001415 was validated by real-time PCR. immunofluorescence, Western blot assay, ELISA, and real-time PCR were performed to detect cell pyroptosis in the mice and caerulein and lipopolysaccharide-induced pancreatic acinar cell line MPC-83 cell models. Gene knockdown and Luciferase reporter assay was used to confirm the regulatory role of circRNA0001415 in acinar cell pyroptosis. RESULTS:We found that circ0001415 is significantly upregulated in the pancreatic head tissue of these mice. Subsequent experiments indicated that circ0001415 likely serves as a molecular sponge for microRNA-1946a, thereby potentially enhancing the expression levels of the pyroptosis-associated protein caspase 1. Consequently, circ0001415 upregulation appears to counteract the decrease in acinar cell pyroptosis observed in AP. In vitro studies revealed that the knockdown of circ0001415 intensified the pyroptosis of acinar cells induced by lipopolysaccharide and caerulein. CONCLUSION:These findings provide novel insights suggesting that the upregulation of circ0001415 may serve as a protective mechanism against the dampening effects on acinar cell pyroptosis following AP. Overall, circ0001415 is a potential molecular target for AP treatment.

This study investigates the impact of Photobiomodulation (PBM) at different wavelengths on non-superficial cancer cells. Utilizing three laser protocols (650 nm, 810 nm, and 915 nm), the research explores cytotoxic effects, ROS generation, and cell migration. Results reveal varied responses across cell lines, with 810 nm PBM inducing significant ROS levels and inhibiting PAN-1 cell migration. The study suggests potential therapeutic applications for PBM in non-superficial cancers, emphasizing the need for further exploration in clinical settings.

Pancreatic cancer is one of the most aggressive malignant tumors of the digestive system.Lymph node metastasis(LNM),as the main way of invasion and metastasis,can occur in the early stage of pancreatic cancer and be considered the most important factor affecting the clinical treatment and prognosis of patients with pancreatic can-cer.Previous studies have found that the incidence of lymphatic invasion of cancer cells is 3-5 times higher than that of vascular invasion.1 Although LNM of pancreatic cancer has obvious clinical importance,the specific mo-lecular mechanism is still unclear.

Non-invasive laser irradiation can induce photobiomodulation (PBM) effects in cells and tissues, which can help reduce inflammation and pain in several clinical scenarios. The purpose of this study is to review the current literature to verify whether PBM can produce dose effects in anti-inflammatory experiments by summarizing the clinical and experimental effects of different laser parameters of several diseases. The so-called Arndt-Schulz curve is often used to describe two-phase dose reactions, assuming small doses of therapeutic stimulation, medium doses of inhibition, and large doses of killing. In the past decade, more and more attention has been paid to the clinical application of PBM, especially in the field of anti-inflammation, because it represents a non-invasive strategy with few contraindications. Although there are different types of lasers available, their use is adjusted by different parameters. In general, the parameters involved are wavelength, energy density, power output, and radiation time. However, due to the biphasic effect, the scientific and medical communities remain puzzled by the ways in which the application of PBM must be modified depending on its clinical application. This article will discuss these parameter adjustments and will then also briefly introduce two controversial theories of the molecular and cellular mechanisms of PBM. A better understanding of the extent of dualistic dose response in low-intensity laser therapy is necessary to optimize clinical treatment. It also allows us to explore the most dependable mechanism for PBM use and, ultimately, standardize treatment for patients with various diseases.

Pancreatic cancer is a malignant tumor of the digestive system that is highly malignant, difficult to treat, and confers a poor prognosis for patients. BRAF-activated noncoding RNA (BANCR) has been proven to play an important role in the invasion and metastasis of pancreatic cancer. In this study, we focused on BANCR as a potential therapeutic target for human pancreatic cancer. The BANCR level in pancreatic cancer tissues and cells is affected by m6A methylation. Based on this, the aim of our study was to investigate the effect of a highly potent and selective first-in-class catalytic inhibitor of METTL3 (STM2457) on BANCR m6A methylation and its malignant biological behaviors in pancreatic cancer. The relationship between BANCR expression and BANCR m6A modification was detected with RT-qPCR and MeRIP-PCR. The expression of methyltransferase-like 3 (METTL3), the key enzyme involved in m6A methylation, in pancreatic cancer tissues was detected using a Western blot. STM2457 was used in vitro to investigate its resistance to the proliferation, invasion, and metastasis of pancreatic cancer cells. BANCR was overexpressed in pancreatic cancer tissues and cells, which was associated with poor clinical outcomes and validated in pancreatic cancer cell lines. m6A modification was highly enriched within BANCR and enhanced its expression. Remarkably, STM2457 inhibited the proliferation, invasion, and metastasis of pancreatic cancer cells by down-regulating BANCR m6A modifications. This study demonstrates the promise of BANCR as a new diagnostic and therapeutic target for pancreatic cancer and reveals the therapeutic effect that STM2457 exerts on pancreatic cancer by down-regulating BANCR m6A modifications.

Neuroendocrine neoplasms (NENs) are rare heterogeneous tumors that can develop in almost any organ, with the digestive organs, including the gastrointestinal tract and pancreas being the most commonly affected sites. Despite the fact that advances in initial therapies have progressed, there is presently no recognized effective treatment for advanced NEN. Immune checkpoint inhibitors (ICIs) have shown superior efficacy in treating several types of solid tumors. Despite their successful role in the treatment of partial NENs, such as small cell lung cancer, and Merkel cell carcinoma, the role of ICIs in most of the NENs remains limited. Nevertheless, due to their specific anti-tumor mechanisms and acceptable safety profile, ICIs are a promising avenue for further study in NENs therapy. Recent clinical trials have illustrated that combination therapy with ICI is more efficient than monotherapy, and multiple clinical trials are constantly ongoing to evaluate the efficacy and safety of these combination therapies. Therefore, the purpose of this review is to provide a comprehensive summary of the clinical progress of immunotherapy in NENs affecting the digestive system, with a specific emphasis on the application of programmed cell death protein 1/programmed death receptor ligand 1 inhibitor. Furthermore, this review has an exploration of the potential beneficiary population and the inherent value of utilizing immunotherapy in the management of NENs.

Background Long noncoding RNAs ( lncRNAs) have proved to play important roles in the tumorigenesis and development of pancreatic carcinoma (PC). The aim of our study is to investigate the expression of long noncoding BRAF-activated noncoding RNA (BANCR) and its role in PC lymph node metastasis. Methods BANCR expression was detected in PC tissues by using Real-time quantitative PCR (RT-qPCR). The correlation between BANCR expression and lymph node metastasis was analyzed. Immunofluorescence staining was used to determine microlymphatic vessel density (MLVD) of peritumoral tissues. The correlation between MLVD and lymph node metastasis and the association between BANCR expression and MLVD were also analyzed. VEGF-C and VEGFR-3 expressions in PC cells were detected by western blot in vitro , and the regulatory role of BANCR on VEGF-C/VEGFR-3 was identified by cell transfection techniques. The transfected PC cells were co-cultured with human lymphatic endothelial cells (HLECs) and the MLVD was detected by the magnification inverted fluorescence microscope. Results BANCR expression was remarkably increased in PC tissues, especially in the lymph node metastasis group (P < 0.0001). MLVD of the PC tissues in the lymph node metastasis group was significantly higher than the group without lymph node metastasis (P < 0.0001). The BANCR expression level significantly correlated with MLVD (P < 0.05). The result was further verified in PC cell lines. Depletion of BANCR inhibits lymphangiogenesis and down regulates VEGF-C/VEGFR-3 (P < 0.05). However, Overexpression of VEGF-C could counteract the inhibitory effect of siBANCR on lymphangiogenesis. Conclusions BANCR promotes lymphangiogenesis and lymph node metastasis of PC by regulating the VEGF-C /VEGFR-3 signaling pathway.

The aim of the present study was to explore the effects of BRAF-activated non-protein coding RNA (BANCR) on pancreatic microlymphangiogenesis in pancreatic cancer (PC) and its molecular mechanism under hypoxic conditions. Reverse transcription-quantitative PCR (RT-qPCR) was used to detect the expression of BANCR in SW1990 and PANC-1 PC cell lines under normoxic and hypoxic conditions. Subsequently, the expression of BANCR in the PC cells was knocked down using small interfering RNAs (siRNAs). Western blotting and RT-qPCR analyses were performed to detect the expression of hypoxia-inducible factor (HIF-1α), VEGF-C and VEGFR-3 in the transfected cells. In addition, the transfected PC cells were co-cultured with human lymphatic endothelial cells and the lymphatic microvessel density (MLVD) was detected under normal and hypoxic conditions. Furthermore, HIF-1α expression in the PC cells was knocked down using siRNAs, and VEGF-C and VEGFR-3 mRNA expression in the HIF-1α knockdown cells was detected using RT-qPCR. The results showed that the expression of BANCR in the SW1990 and PANC-1 PC cell lines was significantly higher than that in human pancreatic duct endothelial cells. Additionally, the expression of BANCR was significantly increased in PC cells under hypoxic conditions compared with normoxic conditions. The MLVD of PC cells under hypoxic conditions was significantly higher compared with that under normoxic conditions, and the MLVD in the si-BANCR group was lower than that in the si-NC group, indicating that si-BANCR downregulated MLVD. These results indicate that BANCR positively regulated the expression of HIF-1α in PC cells at the transcriptional and translational levels. Finally, the expression levels of VEGF-C and VEGFR-3 in PC cells were significantly reduced when BANCR or HIF-1α expression was knocked down. In conclusion, the results demonstrate that the expression of BANCR in PC cells was significantly increased under hypoxic conditions and suggest that BANCR promoted tumor cell lymphangiogenesis by upregulating the HIF-1α/VEGF-C/VEGFR-3 pathway, which plays an important role in the process of PC lymph node metastasis.

Spinal cord injury(SCI),either from trauma or degenerative changes,can res ult in severe disability and impaired quality of life.Understanding the cellular processes and molecular mechanisms that underlie SCI is imperative to identifying molecular targets for potential therapy.Recent studies have shown that non-coding RNAs,including both long non-coding RNAs(lncRNAs) and circular RNAs(circRNAs),regulate various cellular processes in SCI.In this review,we will describe the changes in lncRNA and circRNA expression that occur after SCI and how these changes may be related to SCI progression.Current evidence for the roles of lncRNAs and circRNAs in neuronal cell death and glial cell activation will also be reviewed.Finally,the possibility that lncRNAs and circRNAs are novel modulato rs of SCI pathogenesis will be discussed.

Objective: To further systematically understand the molecular mechanisms that aspirin prevents colon carcinogenesis. Methods: We detected the global protein expression profiles of colorectal cancer along with the treatment of aspirin by a quantitative proteomic approach. We analyzed the proteomic results using bioinformatics（including differential proteins, protein annotation, Kegg Pathways and protein-protein interaction network ）. Cell viability of HT29 cells treated with aspirin was determined by CCK8 assay. The expression of differential proteins p53 and CDK1 were quantified by real-time PCR and Western blot. We measured cell cycle distribution and cell apoptosis of H1299 cells exposed to aspirin by flow cytometric analysis. Results: We found 552 proteins that were significantly dysregulated after10mM aspirin treatment of colon cancer cells. Further enrichment analysis of the dysregulated proteins suggested that cell cycle-related proteins are the most differential proteins such as p53, CDK1, CyclinB, Chk1, Chk2 and CyclinD. The results of real-time PCR and Western blot showed that p53 and CDK1 obvious upregulation after aspirin exposed to colon cancer cells. We also detected that aspirin promoted the G1/S arrest of cell cycle in HT29 cells. We confirmed aspirin induced cell apoptosis in human HT29 colon cancer cells with concentration-dependent increase. Conclusions: The result indicated that aspirin induced colorectal cancer cells G1 arrest and cell apoptosis by p53-CDK1 pathway. Accordingly, aspirin may represent a promising preventive candidate for colon cancer.

BACKGROUND:As the base of hepatitis B patients has been increasing annually, it has developed into a high incidence source of primary liver cancer worldwide. The fatality rate of liver cancer is still relatively high. Among the many treatment methods, liver resection is the first-line treatment of primary liver cancer. Although precision hepatectomy has achieved rapid development in recent years, the understanding of its efficacy is still not completely clear. This study aimed to analyze and compare the safety and effectiveness of precision hepatectomy and traditional hepatectomy in the treatment of primary liver cancer.METHODS:We performed a literature search of the CNKI, Wanfang, Weipu.com, PubMed, Cochrane Library, Web of Science databases for studies on precision liver resection (precision group) and traditional liver resection (traditional group) for the treatment of primary liver cancer. Data including the operation time, intraoperative blood loss, hospital stay, postoperative complications, liver function, and survival rate were analyzed using RevMan 5.3 software to compare the differences in the effects of the two surgical procedures.RESULTS:Ten articles were included in the study, involving a total of 1,969 patients, including 1,045 cases in the precision group and 924 cases in the traditional group. Meta-analysis results showed that compared with the traditional group, the precision group had a longer operation time [mean difference (MD) =8.01, P=0.004], and total bilirubin (TBiL; MD =-2.78, P=0.055) was similar. Meanwhile, the precision group exhibited advantages in terms of intraoperative blood loss (MD =-149.37, P=0.000), hospital stay (MD =-5.59, P=0.000), postoperative liver function indexes [aspartate aminotransferase (AST; MD =-11.61, P=0.000) and alanine aminotransferase (ALT; MD =-18.53, P=0.000)], postoperative complication rate [relative risk (RR) =0.51, P=0.000], and 1-year survival rate (RR =1.11, P=0.000).DISCUSSION:The application of precision surgery in the treatment of primary liver cancer can be a safe and effective method. It can minimize intraoperative blood loss, mitigate surgical risk, reduce postoperative complications, improve patient prognosis and quality of life, and provide better short-term curative effect and patient benefits.

Objective To analyze the function of miR-10b-5p in suppressing the invasion and proliferation of primary hepatic carcinoma cells by downregulating erythropoietin-producing hepatocellular receptor A2 (EphA2). Material and Methods. Eighty-six hepatic carcinoma (HCC) tissue specimens and 86 corresponding adjacent tissue specimens were collected, and the mRNA expression of miR-10b-5p and Ephrin type-A receptor 2 (EphA2) in the specimens was determined using a reverse transcription-polymerase chain reaction (RT-PCR) assay. Western blot was employed to quantify EphA2, B-cell chronic lymphocytic leukemia/lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), and Caspase-3 in the cells, and CCK8, Transwell assay, and flow cytometry were applied to evaluate the proliferation, invasion, and apoptosis of cells, respectively. Moreover, the dual luciferase reporter assay was utilized for correlation analysis between miR-10b-5p and EphA2. Results miR-10b-5p was lowly expressed in HCC, while EphA2 was highly expressed. Cell experiments revealed that miR-10b-5p overexpression or EphA2 knockdown could reduce cell proliferation, accelerate apoptosis, strongly upregulate Bax and Caspase-3, and downregulate Bcl-2. In contrast, miR-10b-5p knockdown or EphA2 overexpression gave rise to reverse biological phenotypes. Furthermore, dual luciferase reporter assay verified that miR-10b-5p was a target of EphA2, and the rescue experiment implied that transfection of pCMV-EphA2 or Si-EphA2 could reverse EphA2 expression and cell biological functions caused by miR-10b-5p overexpression or knockdown. Conclusions miR-10b-5p reduced HCC cell proliferation but accelerate apoptosis by regulating EphA2, suggesting it has the potential to be a clinical target for HCC.

BACKGROUND:Colorectal cancer (CRC) is a malignant tumor of the digestive tract, with high incidence and mortality. This study aims to investigate the expression of plasma omentin-1 level in patients with CRC and its correlation with the prognosis of patients. METHODS:Clinical data of 319 patients (case group) who underwent radical resection of CRC in our hospital from June 2015 to March 2018 were collected, simultaneously, 300 people without the apparent physical disease who underwent physical examination in our hospital during the same period were randomly selected as the control group, plasma omentin-1 levels in the two groups were compared by T-test. Cancer patients were followed up, and multi-factor COX regression analysis was used to analyze the factors affecting patients' recurrence and survival. RESULTS:The level of plasma omentin-1 in patients with colorectal cancer is closely related to TNM staging and lymph node metastasis. The CRC case group was significantly reduced after surgery, but it was still higher than that in the control group (P<0.05). At the end of the follow-up, 28 cases were lost to follow-up, and 291 cases (91.22%) were effectively followed up. During the follow-up period, the recurrence and metastasis rate was 30.58% (89/291), and the mortality rate was 19.26% (56/291). According to the multi-factor analysis, the risk factors for the recurrence of CRC patients were TNM stage III-IV (OR =1.978, 95% CI: 1.088-3.596), lymph node metastasis (OR =2.073, 95% CI: 1.179-3.645) and omentin-1 level ≥50 ng/mL (OR =3.347, 95% CI: 1.416-7.912). The risk factors for the survival of patients with CRC were poorly differentiated (OR =1.960, 95% CI: 0.985-3.900), lymph node metastasis (OR =2.452, 95% CI: 1.213-4.956), vascular carcinoma thrombus (OR =2.026, 95% CI: 1.036-3.960) and omentin-1 level ≥50 ng/mL (OR =2.067, 95% CI: 1.013-4.218). CONCLUSIONS:The level of plasma omentin-1 is highly expressed in patients with CRC, an independent risk factor for the recurrence and survival of patients.

Objective According investigate the expression of NLRP3 in liver tissues of mice with hepatic ischemia-reperfusion injury (HIRI),to determin the role of NLRP3 in the process of HIRI.Methods Established mice model of partial HIRI.Forty-two male C57BL/6 mice (aged 7 to 8 weeks,weight 20 to 25 g) were respectively divided into 7 groups:no-treatment control group,sham operation group,HIRI groups (2、6、12、24 h) and CY-09 group,6 mice in each group.The injury of the hepatic tissues in the 7 groups was analyzed based on detecting the levels of alanine transaminase (ALT),aspartate transaminase (AST),interleukin-1β (IL-1β),interleukin-18 (IL-18),tumor necrosis factor-α (TNF-α) by ELISA.HE and TUNEL staining were used to observe the pathological changes of liver tissues after HIRI.Western blotting assay were carried out to detect the expressions of NLRP3 and Caspase-1.Measurement data were expressed as mean ± standard deviation (Mean ± SD),and one-way variance analysis was used for comparison between groups.If the variance was not uniform,Dunnett C test was used.Results Serum ALT,AST,IL-1 β,IL-18 and TNF-α of mice detected in HIRI groups were higher than no-treatment control group and sham operation group at all endpoints (P ＜ 0.05).The relative expression of NLRP3 and Caspase-1 in the liver tissues of mice in the HIRI groups were significantly higher than that in the no-treatment control group and sham operation group.Serum ALT,AST,IL-1β,IL-18 and TNF-α of mice detected in CY-09 group were lower than HIRI groups at all endpoints (P ＜ 0.05).Less hepatocellular necrosis were exhibited in CY-09 group,comparing to HIRI groups.The hepatocyte apoptosis rate of mice in the CY-09 group was significantly lower than that in the 12 h HIRI group (P ＜ 0.05).The relative expression of NLRP3 in the liver tissues of mice in the CY-09 group was significantly lower than that in other groups.The relative expression of Caspase-1 in the liver tissues of mice in the CY-09 group was significantly lower than that in other groups except the no-treatment control group and sham operation group.Conclusions HIRI cause an increase in NLRP3 expression.The inhibition of NLRP3 can reduce HIRI.

Bi-plane robots have been widely applied in clinical use to place cannulated screws for internal fixation surgery of femur neck fractures, which is performed precisely and automatically using two online fluoroscopic images. However, the setup procedure of the bi-plane robot is empirical, and physicians usually have to re-run the setup procedure, exposing the patient to high doses of radiation in clinical applications. In this article, a motion compensation method is proposed by a novel use of the binocular vision principle to improve the bi-plane robot setup using two doses of radiation within 2 min. The entry point, exit point, and angle errors of the three-dimensional trajectory reconstruction are 1.23 ± 0.39 mm, 1.49 ± 0.49 mm, and 0.33° ± 0.23°, respectively. The motion compensation method significantly reduces the dose of radiation and the operation time of the setup procedure and has acceptable accuracy.

Objective To analyze the relationship between the clinical features of hepatoblastoma and serum alpha-fetoprotein level.Methods We did a retrospective study in 74 cases into the relationship of clinical stages,treatment,prognosis,and AFP value in hepatoblastoma.Results In Stage Ⅰ and Ⅱ patients,the average AFP was (36 333 ± 13 782) ng/ml and in Stage Ⅲ and Ⅳ,the average AFP was (78 346 ± 27 956) ng/ml,P ＜ 0.05.68 patients received preoperative chemotherapy with alpha-fetoprotein determinations before and after chemotherapy respectively.In 44 cases AFP decreased ＞ 50％ after chemotherapy,and in 20 cases AFP declined ＞90％,while in 13 cases AFP increased after chemotherapy.15 cases had serum AFP measured on the first postoperative day,among them 10 cases had a ＞ 50％ AFP decline,3 cases had a ＜ 50％ AFP decline,while in 2 cases AFP value increased.52 cases were postoperatively followed-up,with overall 3 year-survival rate of 86.5％ ; 7 cases recurred,4 died.The average preop AFP level in 7 recurred cases was (27 060 ± 3 569) ng/ml,while the average preop AFP level in those of 3-year recurrence-free was (29 865 ± 5 867) ng/ml,P ＞ 0.05.Only 57％ tumor recurred cases had back to normal AFP level within one month postop,while 89％ long term survivals reported normal range of AFP during that period,P ＜ 0.05.Conclusions Serum AFP level in patients with hepatoblastoma is related to the course of disease.It can be used to estimate the effect of clinical chemotherapy.The speed of alpha-fetoprotein decline postop can be used as an indicator of prognosis.The postoperative normal AFP level within 4 weeks predicts a favorable prognosis.