Research on Laser Cleaning Technology for Aircraft Skin Surface Paint Layer.

In this study, a pulsed laser operating at a wavelength of 1064 nm and with a pulse width of 100 ns was utilized for the removal of paint from the surface of a 2024 aluminum alloy. The experimental investigation was conducted to analyze the influence of laser parameters on the efficacy of paint layer removal from the aircraft skin's surface and the subsequent evolution in the microstructure of the laser-treated aluminum alloy substrate. The mechanism underlying laser cleaning was explored through simulation. The findings revealed that power density and scanning speed significantly affected the quality of cleaning. Notably, there were discernible damage thresholds and optimal cleaning parameters in repetitive frequency, with a power density of 178.25 MW/cm2, scanning speed of 500 mm/s, and repetitive frequency of 40 kHz identified as the primary optimal settings for achieving the desired cleaning effect. Thermal ablation and thermal vibration were identified as the principal mechanisms of cleaning. Moreover, laser processing induced surface dislocations and concentrated stress, accompanied by grain refinement, on the aluminum substrate.

Laparoscopic and open liver resection for hepatocellular carcinoma with type 2 diabetes mellitus: multicenter propensity score-matched study.

PURPOSE: This study aimed at analyzing and comparing the perioperative results and long-term oncological outcomes of hepatocellular carcinoma (HCC) patients with type 2 diabetes mellitus (T2DM) treated with laparoscopic (LLR) versus open liver resection (OLR). METHODS: Clinicopathological data of HCC patients with T2DM who underwent LLR or OLR as initial treatment from four medical centers were retrospectively reviewed. The survival outcomes of patients who underwent laparoscopic liver resection (LLR) were compared with those of patients who underwent open liver resection (OLR). Using the Kaplan-Meier method, survival curves for the two groups of patients were generated, and the log-rank test was used to compare survival differences. Propensity score matching (PSM) analysis was used to match patients of the LLR and OLR groups in a 1:1 ratio. RESULTS: 230 HCC patients with T2DM were enrolled, including 101 patients in the LLR group and 129 patients in the OLR group. After PSM, 90 patients were matched in each of the study group. Compared with the OLR group, the LLR group had less blood loss, a shorter hospitalization and fewer postoperative complications. The LLR group had a significantly better overall survival (OS) and recurrence-free survival (RFS) than the OLR group before and after PSM. Subgroup analysis demonstrated that HCC patients with T2DM had survival benefits from LLR regardless of the course of T2DM. CONCLUSIONS: Laparoscopic liver resection for HCC patients with T2DM can be safely performed with favorable perioperative and long-term oncological outcomes at high-volume liver cancer centers, regardless of the course of T2DM.

Regulatory T cells (Tregs) in liver fibrosis.

The ability of the human liver to both synthesize extracellular matrix(ECM), as well as regulate fibrogenesis, are integral functions to maintaining homoeostasis. Chronic liver injury stimulates fibrogenesis in response to the imbalance between ECM accumulation and fibrosis resolution. Liver disease that induces fibrogenesis is associated with multiple risk factors like hepatitis infection, schistosomiasis, alcohol, certain drugs, toxicants and emerging aetiology like diabetes and obesity. The activation of hepatic stellate cells (HSCs), whose function is to generate and accumulate ECM, is a pivotal event in liver fibrosis. Simultaneously, HSCs selectively promote regulatory T-cells (Tregs) in an interleukin-2-dependent pattern that displays a dual relationship. On the one hand, Tregs can protect HSCs from NK cell attack, while on the other hand, they demonstrate an inhibitory effect on HSCs. This paper reviews the dual role of Tregs in liver fibrogenesis which includes its promotion of immunosuppression, as well as its activation of fibrosis. In particular, the balance between Tregs and the Th17 cell population, which produce interleukin (IL)-17 and IL-22, is explored to demonstrate their key role in maintaining homoeostasis and immunoregulation. The contradictory roles of Tregs in liver fibrosis in different immune microenvironments and molecular pathways need to be better understood if they are to be deployed to manage this disease.

CD8+iTregs mediate the protective effect of rapamycin against graft versus host disease in a humanized murine model.

CD8+Tregs are important immunoregulatory cells that participate in immunopathological processes in many diseases. Rapamycin (Rapa) is a macrolide immunosuppressant that inhibits the mammalian target of rapamycin (mTOR) and has been shown to improve CD4+-induced Tregs (iTregs) generation. This study aimed to evaluate the role of Rapa in the generation and function of CD8+iTregs. Human CD8 + CD25-CD45RA + T cells were divided into two groups, one with Rapa and the other without Rapa, and both groups were cultured under Treg-induced conditions. Rapa significantly improved Foxp3 expression and the suppressive function of CD8+iTregs in vitro. Further studies showed that Rapa suppressed inflammatory cytokine expression and enhanced anti-inflammatory cytokine expression. Under inflammatory conditions in vitro, Rapa-CD8 + iTregs sustained Foxp3 and anti-inflammatory cytokine expression. An in-depth study showed that Rapa regulated CpG demethylation in the Foxp3 region and STAT1 and STAT3 phosphorylation in CD8+iTregs. Finally, we compared the regulatory ability of Rapa and all-trans retinoic acid, another reagent that stimulates CD4+ iTreg generation in vitro, which showed that Rapa, but not all-trans retinoic acid, improved CD8+ iTreg induction and suppressed CD4+T cell expansion in vitro and protected against graft-versus-host disease in a humanized murine model in vivo. These results strongly suggest that CD8+iTregs initiated by Rapa may represent a new therapeutic strategy for inflammatory and autoimmune diseases.

Resident Immune Cells of the Liver in the Tumor Microenvironment.

The liver is a central immunomodulator that ensures a homeostatic balance between protection and immunotolerance. A hallmark of hepatocellular carcinoma (HCC) is the deregulation of this tightly controlled immunological network. Immune response in the liver involves a complex interplay between resident innate, innate, and adaptive immune cells. The immune response in the liver is modulated by its continuous exposure to toxic molecules and microorganisms that requires a degree of immune tolerance to protect normal tissue from damage. In HCC pathogenesis, immune cells must balance a dual role that includes the elimination of malignant cells, as well as the repair of damaged liver tissue to maintain homeostasis. Immune response in the innate and adaptive immune systems extends to the cross-talk and interaction involving immune-regulating non-hematopoietic cells, myeloid immune cells, and lymphoid immune cells. In this review, we discuss the different immune responses of resident immune cells in the tumor microenvironment. Current FDA-approved targeted therapies, including immunotherapy options, have produced modest results to date for the treatment of advanced HCC. Although immunotherapy therapy to date has demonstrated its potential efficacy, immune cell pathways need to be better understood. In this review article, we summarize the roles of specific resident immune cell subsets and their cross-talk subversion in HCC pathogenesis, with a view to identifying potential new biomarkers and therapy options.

Perioperative and long-term survival outcomes of laparoscopic versus laparotomic hepatectomy for BCLC stages 0-A hepatocellular carcinoma patients associated with or without microvascular invasion: a multicenter, propensity score matching analysis.

PURPOSE: To analyze the long-term oncological outcomes of Barcelona Clinic Liver Cancer (BCLC) stages 0-A hepatocellular carcinoma (HCC) patients associated with or without microvascular invasion (MVI) treated with laparoscopic versus laparotomic liver resection. METHODS: Clinicopathological data of HCC patients with BCLC stages 0-A from four medical centers were retrospectively reviewed. The survival outcomes of patients who underwent laparoscopic hepatectomy were compared with those who underwent laparotomic hepatectomy. Subgroup analyses in terms of MVI were further performed to explore the effect of surgical approaches on the long-term survival outcomes. Propensity score matching (PSM) analysis was used to match patients between the laparoscopic and laparotomic resection groups in a 1:1 ratio. RESULTS: 495 HCC patients at BCLC stages 0-A were enrolled, including 243 in the laparoscopic resection group and 252 in the laparotomic resection group. Laparoscopic resection group had a shorter operation time, less blood loss, a lower frequency of blood transfusion and postoperative complication rates. The laparoscopic resection group had a significantly better overall survival (OS) and recurrence-free survival (RFS) than the laparotomic resection group before and after PSM. Subgroup analysis demonstrated that OS and RFS of patients without MVI were remarkably better in the laparoscopic resection group compared with the laparotomic resection group. However, no significant differences in OS and RFS between the two groups were found in patients with MVI after PSM. CONCLUSIONS: Pure laparoscopic hepatectomy for patients with BCLC stages 0-A HCC can be performed safely with favorable perioperative and long-term oncological outcomes at high-volume liver cancer centers, regardless of the presence of MVI.

Trans-activation of eotaxin-1 by Brg1 contributes to liver regeneration.

Infiltration of eosinophils is associated with and contributes to liver regeneration. Chemotaxis of eosinophils is orchestrated by the eotaxin family of chemoattractants. We report here that expression of eotaxin-1 (referred to as eotaxin hereafter), but not that of either eotaxin-2 or eotaxin-3, were elevated, as measured by quantitative PCR and ELISA, in the proliferating murine livers compared to the quiescent livers. Similarly, exposure of primary murine hepatocytes to hepatocyte growth factor (HGF) stimulated eotaxin expression. Liver specific deletion of Brahma-related gene 1 (Brg1), a chromatin remodeling protein, attenuated eosinophil infiltration and down-regulated eotaxin expression in mice. Brg1 deficiency also blocked HGF-induced eotaxin expression in cultured hepatocytes. Further analysis revealed that Brg1 could directly bind to the proximal eotaxin promoter to activate its transcription. Mechanistically, Brg1 interacted with nuclear factor kappa B (NF-κB)/RelA to activate eotaxin transcription. NF-κB knockdown or pharmaceutical inhibition disrupted Brg1 recruitment to the eotaxin promoter and blocked eotaxin induction in hepatocytes. Adenoviral mediated over-expression of eotaxin overcame Brg1 deficiency caused delay in liver regeneration in mice. On the contrary, eotaxin depletion with RNAi or neutralizing antibodies retarded liver regeneration in mice. More important, Brg1 expression was detected to be correlated with eotaxin expression and eosinophil infiltration in human liver specimens. In conclusion, our data unveil a novel role of Brg1 as a regulator of eosinophil trafficking by activating eotaxin transcription.

Clinical effect of laparoscopic partial splenectomy for both benign tumours and trauma-10 years of experience at a single institution.

BACKGROUND: This retrospective study aimed to present our surgical experience in patients with benign tumour or trauma in spleen who underwent laparoscopic partial splenectomy (LPS) and to compare the results with those of patients who underwent an open partial splenectomy (OPS). METHODS: We analysed the medical data of patients who underwent LPS or OPS between January 2010 and January 2020. RESULTS: In total, 41 patients were enrolled. Nine patients underwent open surgery, 32 patients underwent laparoscopic surgery. The proportion of patients with tumours in the upper pole in LPS group was more than patients in OPS group. No difference was observed in estimated blood loss, allogeneic transfusion, postoperative stay, pathology and complications between LPS and OPS groups. The operation time in the LPS group (137.5 ± 30.8 min) was longer than that in the OPS group (88.3 ± 30.1 min) for patients with splenic traumatic rupture (P = 0.019). CONCLUSIONS: LPS is an effective and safe spleen-preserving surgery as OPS. The advantages are small trauma, light pain and quick recovery. It is suitable for patients with benign tumours or trauma confined to one side of the spleen.

Caspase-3/Treg and PI3K/AKT/mTOR pathway is involved in Liver Ischemia Reperfusion Injury (IRI) protection by everolimus.

Ischemia-reperfusion injury (IRI) of the liver is a severe complication that can follow hemorrhagic shock and liver surgery. Regulatory T cells (Treg) show the potential of improving outcomes of IRI. Everolimus is an mTOR inhibitor used in liver transplantation and the treatment of tumor patients through PI3K/AKT/mTOR pathway. The present study was designed to investigate the efficacy and mechanism of everolimus on Treg for the treatment of IRI. Hepatocytes were exposed to H2O2 and hypoxic conditions to investigate the effects of everolimus on reactive oxygen species ROS-induced and H/R-induced injury in vitro. The effects of everolimus on liver IRI were investigated in a warm ischemia liver model in vivo. Our results indicate that everolimus markedly protected liver IRI in vivo and vitro. Furthermore, everolimus increased the levels of phospho- (p-)AKT, p-mTOR but not p-GSK following IRI. Taken together, our data showed that everolimus protected against IRI via regulation of caspase-3/Treg and the PI3K/AKT/mTOR signalling pathway, which provides new insight into the treatment of liver IRI.

Treatment of hepatic venous system hemorrhage and carbon dioxide gas embolization during laparoscopic hepatectomy via hepatic vein approach.

With the improvement of laparoscopic surgery, the feasibility and safety of laparoscopic hepatectomy have been affirmed, but intraoperative hepatic venous system hemorrhage and carbon dioxide gas embolism are the difficulties in laparoscopic hepatectomy. The incidence of preoperative hemorrhage and carbon dioxide gas embolism could be reduced through preoperative imaging evaluation, reasonable liver blood flow blocking method, appropriate liver-breaking device, controlled low-center venous pressure technology, and fine-precision precision operation. In the case of blood vessel rupture bleeding in the liver vein system, after controlling and reducing bleeding, confirm the type and severity of vascular damage in the liver and venous system, take appropriate measures to stop the bleeding quickly and effectively, and, if necessary, transfer the abdominal treatment in time. In addition, to strengthen the understanding, prevention and emergency treatment of severe CO2 gas embolism in laparoscopic hepatectomy is also the key to the success of surgery. This study aims to investigate the methods to deal with hepatic venous system hemorrhage and carbon dioxide gas embolization based on author's institutional experience and relevant literature. We retrospectively analyzed the data of 60 patients who received laparoscopic anatomical hepatectomy of hepatic vein approach for HCC. For patients with intraoperative complications, corresponding treatments were given to cope with different complications. After the operation, combined with clinical experience and literature, we summarized and discussed the good treatment methods in the face of such situations so that minimize the harm to patients as much as possible.

Impact of type 2 diabetes mellitus on the prognosis of patients with hepatocellular carcinoma after laparoscopic liver resection: A multicenter retrospective study.

Background: The effect of type 2 diabetes mellitus (T2DM) on survival of patients with hepatocellular carcinoma (HCC) after laparoscopic liver resection (LLR) has not been reported. This study aimed to explore the relationship between preoperative T2DM and long-term prognosis in HCC patients undergoing LLR. Methods: HCC patients receiving LLR as initial treatment at four cancer centers were retrospectively included in this study. Clinicopathological factors associated with the prognosis of HCC patients were identified using univariate and multivariate Cox regression analysis. Recurrence-free survival (RFS) and overall survival (OS) curves between different cohorts of patients were generated using the Kaplan-Meier method and compared using the log-rank test. Results: Of 402 HCC patients included, 62 patients had T2DM and 340 patients did not have T2DM. The OS and RFS of patients with T2DM were significantly worse compared to those without T2DM (P = 0.001 and 0.032, respectively). In Cox multivariate analysis, T2DM was identified as an independent risk factors for OS (HR = 2.31, 95% CI = 1.38-3.85, P = 0.001) and RFS (HR = 1.66, 95% CI = 1.08-2.55, P = 0.020). Conclusions: Following laparoscopic surgical approach, HCC patients with T2DM had poorer prognoses than those without T2DM. Preoperative T2DM was an independent risk factor for HCC patients. Thus, patients with concurrent HCC and T2DM should be closely monitored after LLR.

Hsa_circ_0011385 knockdown represses cell proliferation in hepatocellular carcinoma.

Circular RNAs (circRNAs), continuous loops of single-stranded RNA, regulate gene expression during the development of various cancers. However, the function of circRNAs in hepatocellular carcinoma (HCC) is rarely discussed. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the mRNA levels of circ_0011385, miR-361-3p, and STC2 in 96 pairs of HCC tissues (tumor tissues and adjacent normal tissues), HCC cell lines, and L02 (human normal liver cell line) cells. The relationships between circ_0011385 expression and clinical features of HCC were evaluated. Functional experiments in vitro or in vivo were used to evaluate the biological function of circ_0011385. Bioinformatics analysis was performed to predict miRNAs and mRNAs sponged by circ_0011385. RNA immunoprecipitation (RIP) and dual-luciferase reporter gene assays were used to elucidate the interactions among circ_0011385, miR-361-3p, and STC2 (stanniocalcin 2). ChIP and dual-luciferase reporter gene assays were used to identify the upstream regulator of circ_0011385. High expression of circ_0011385 was observed in HCC tissues and cell lines and was significantly associated with tumor size, TNM stage, and prognosis. In addition, inhibition of circ_0011385 expression prevented the proliferation of HCC cells in vitro and in vivo. Circ_0011385 sponged miR-361-3p, thereby regulating the mRNA expression of STC2. In addition, the transcription of circ_0011385 was regulated by SP3. Circ_0011385 knockdown suppressed cell proliferation and tumor activity in HCC. Circ_0011385 may therefore serve as a new biomarker in the diagnosis and treatment of HCC.

Redox-sensitive activation of CCL7 by BRG1 in hepatocytes during liver injury.

Liver injuries induced by various stimuli share in common an acute inflammatory response, in which circulating macrophages home to the liver parenchyma to participate in the regulation of repair, regeneration, and fibrosis. In the present study we investigated the role of hepatocyte-derived C-C motif ligand 7 (CCL7) in macrophage migration during liver injury focusing on its transcriptional regulation. We report that CCL7 expression was up-regulated in the liver by lipopolysaccharide (LPS) injection (acute liver injury) or methionine-and-choline-deficient (MCD) diet feeding (chronic liver injury) paralleling increased macrophage infiltration. CCL7 expression was also inducible in hepatocytes, but not in hepatic stellate cells or in Kupffer cells, by LPS treatment or exposure to palmitate in vitro. Hepatocyte-specific deletion of Brahma-related gene 1 (BRG1), a chromatin remodeling protein, resulted in a concomitant loss of CCL7 induction and macrophage infiltration in the murine livers. Of interest, BRG1-induced CCL7 transcription and macrophage migration was completely blocked by the antioxidant N-acetylcystine. Further analyses revealed that BRG1 interacted with activator protein 1 (AP-1) to regulate CCL7 transcription in hepatocytes in a redox-sensitive manner mediated in part by casein kinase 2 (CK2)-catalyzed phosphorylation of BRG1. Importantly, a positive correlation between BRG1/CCL7 expression and macrophage infiltration was identified in human liver biopsy specimens. In conclusion, our data unveil a novel role for BRG1 as a redox-sensitive activator of CCL7 transcription.

Acidic Microenvironment Aggravates the Severity of Hepatic Ischemia/Reperfusion Injury by Modulating M1-Polarization Through Regulating PPAR-γ Signal.

Hepatic injury induced by ischemia and reperfusion (HIRI) is a major clinical problem after liver resection or transplantation. The polarization of macrophages plays an important role in regulating the severity of hepatic ischemia/reperfusion injury. Recent evidence had indicated that the ischemia induces an acidic microenvironment by causing increased anaerobic glycolysis and accumulation of lactic acid. We hypothesize that the acidic microenvironment might cause the imbalance of intrahepatic immunity which aggravated HIRI. The hepatic ischemia/reperfusion injury model was established to investigate the effect of the acidic microenvironment to liver injury. Liposomes were used to deplete macrophages in vivo. Macrophages were cultured under low pH conditions to analyze the polarization of macrophages in vitro. Activation of the PPAR-γ signal was determined by Western blot. PPAR-γ agonist GW1929 was administrated to functionally test the role of PPAR-γ in regulating macrophage-mediated effects in the acidic microenvironment during HIRI. We demonstrate that acidic microenvironment aggravated HIRI while NaHCO3 reduced liver injury through neutralizing the acid, besides, liposome abolished the protective ability of NaHCO3 through depleting the macrophages. In vivo and vitro experiment showed that acidic microenvironment markedly promoted M1 polarization but inhibited M2 polarization of macrophage. Furthermore, the mechanistic study proved that the PPAR-γ signal was suppressed during the polarization of macrophages under pH = 6.5 culture media. The addition of PPAR-γ agonist GW1929 inhibited M1 polarization under acidic environment and reduced HIRI. Our results indicate that acidic microenvironment is a key regulator in HIRI which promoted M1 polarization of macrophages through regulating PPAR-γ. Conversely, PPAR-γ activation reduced liver injury, which provides a novel therapeutic concept to prevent HIRI.

DDIT4 S-Nitrosylation Aids p38-MAPK Signaling Complex Assembly to Promote Hepatic Reactive Oxygen Species Production.

Mitogen-activated protein kinase (MAPK) signaling plays a significant role in reactive oxygen species (ROS) production. The authors have previously shown that Brahma-related gene 1 (BRG1), a chromatin remodeling protein, contributes to hepatic ROS accumulation in multiple animal and cellular models of liver injury. Here it is reported that DNA damage-induced transcript 4 (DDIT4) is identified as a direct transcriptional target for BRG1. DDIT4 overexpression overcomes BRG1 deficiency to restore ROS production whereas DDIT4 knockdown phenocopies BRG1 deficiency in suppressing ROS production in vitro and in vivo. Mechanistically, DDIT4 coordinates the assembly of the p38-MAPK signaling complex to drive ROS production in an S-nitrosylation dependent manner. Molecular docking identifies several bioactive DDIT4-inteacting compounds including imatinib, nilotinib, and nateglinide, all of which are confirmed to attenuate hepatic ROS production, dampen p38-MAPK signaling, and ameliorate liver injury by influencing DDIT4 S-nitrosylation. Importantly, positive correlation between ROS levels and BRG1/DDIT4/S-nitrosylated DDIT4 levels is detected in human liver biopsy specimens. In conclusion, the data reveal a transcription-based signaling cascade that contributes to ROS production in liver injury.

The comparation of short-term outcome between laparoscopic and open pancreaticoduodenectomy: a propensity score matching analysis.

Pancreaticoduodenectomy (PD) is one of the most complex and delicate operations in abdominal surgery. With the development of laparoscopic techniques, more and more pancreatic experts have become skilled in laparoscopic pancreaticoduodenectomy (LPD). However, the short-term efficacy of LPD compared to open pancreaticoduodenectomy (OPD) remains unclear. Here, we performed a propensity score matching study aiming to compare the short outcomes of patients who underwent LPD or OPD after the learning curve and established a risk model of pancreatic fistula. The data of 346 patients who had OPD or LPD from July 2015 to January 2020 were retrieved. After a 1:1 matching, 224 patients remained. The operation time was significantly longer (P = 0.001) but the amount of bleeding was significantly lower (P = 0.001) in the LPD group than in the OPD group. Patients in LPD group had fewer blood transfusions (P = 0.002) than those in OPD group. More lymph nodes (P < 0.001) were dissected in LPD group. The rate of grade B/C pancreatic fistula was significantly higher in the LPD group than in the OPD group (16.1% vs. 6.3%, P = 0.002). By multi variate Logistic regression analysis, we identified pancreatic tumor, malignancy and low body mass index were risk factors of Grade B/C pancreatic fistula after PD operation. Then, we developed a Grade B/C pancreatic fistula nomogram with the risk factors. The C-index of the nomogram was 0.836 (95% CI 0.762-0.910). In conclusion, LPD could be technically feasible, get less trauma and achieve similar short-term outcome as compared with OPD.

Minimally Invasive Surgery of Primary Retroperitoneal Tumors from the Perspective of General Surgeons: 6 Years of Experience at a Single Institution.

Objective: This retrospective study aimed to present our surgical experience in patients with primary retroperitoneal tumors (PRTs) who underwent laparoscopic surgery and to compare the results with those of patients who underwent an open operation. Materials and Methods: We analyzed the medical data of patients who underwent retroperitoneal tumor resection through laparoscopic surgery or open operation between February 2014 and November 2019. Results: In total, 77 patients were enrolled. In total, 37 patients underwent open surgery and 40 patients underwent laparoscopic surgery. The tumor size in the open surgery group (10.2 ± 5.4 cm) was more significant than that in the laparoscopic surgery group (6.5 ± 3.1 cm) (P < .001). No difference was observed in operative time, blood loss, and transfusion between the two groups. Postoperative hospitalization in the open group (8.43 ± 2.77 days) was longer than that in the laparoscopic group (5.63 ± 2.16 days) (P < .001). The patients with PRTs in the IV area had minimal bleeding (16.67 ± 40.82 mL) and minimum postoperative hospitalization (3.83 ± 1.60 days). Conclusions: Laparoscopic resection of PRT is feasible in the selection of appropriate cases. The advantages are small trauma, light pain, quick recovery, and short hospital stay. It is especially suitable for benign PRTs with small size and cystic or small adhesion with vital organs or great vessels.

Preoperative Prognostic Nutritional Index and Neutrophil-to-Lymphocyte Ratio Predict Survival Outcomes of Patients With Hepatocellular Carcinoma After Curative Resection.

Increasing evidence indicates that preoperative prognostic indices can serve as independent predictors of survival in patients with cancer. However, the applicability of these indices in patients with hepatocellular carcinoma (HCC) is controversial. This study aims to investigate the prognostic value of these indices in patients with HCC after curative hepatectomy. We retrospectively analyzed the data of 215 patients who underwent curative resection for HCC. Prognostic indices including prognostic nutritional index (PNI) and neutrophil-to-lymphocyte ratio (NLR) were evaluated by comparing by the area under the curve (AUC). Univariate analysis and multivariate analysis were performed to identify independent prognostic factors. Additionally, risk factors were combined to predict the survival of patients. We found that serum albumin concentration, tumor diameter, tumor stage, degree of differentiation, PNI, and NLR were independent prognostic factors for overall survival (OS). Vascular invasion, tumor stage, degree of differentiation, and PNI were independent prognostic factors for recurrence-free survival (RFS). The cutoff value of the PNI and NLR was 43.75 and 3.29, respectively. Patients with low NLR and high PNI had the best outcomes, potentially indicative of the intensive antitumor effects of the immune system. Moreover, patients with at least three risk factors had a significantly lower OS and RFS compared with those with two or fewer risk factors. This new nomogram based on PNI and NLR may provide an accessible and individualized prediction of survival and recurrence for HCC patients.

The C-reactive protein to albumin ratio is an excellent prognostic predictor for gallbladder cancer.

A number of inflammation indicators based on C-reactive protein (CRP) and albumin have been widely used to predict the prognosis in several types of tumors, but their functions in gallbladder cancer (GBC) have rarely been explored. The aim of our study is to evaluate and compare the prognostic values of the C-reactive protein to albumin ratio (CAR), Glasgow prognostic score (GPS), modified Glasgow prognostic score (mGPS) and high-sensitivity modified Glasgow prognostic score (HS-mGPS) in patients with GBC. 144 GBC patients who received curative surgery in our hospital from January 2010 to May 2017 were enrolled in this research. The Kaplan-Meier analysis showed that the median OS of the patients in the high CAR group was significantly shorter than the patients in the low group (p < 0.001), and higher scores of GPS, mGPS and HS-mGPS were also associated with decreased OS, respectively. However, according to the Receiver Operating Characteristic (ROC) curve, the CAR was superior to the other prognostic scores in determining the prognosis for the GBC patients. In the multivariate analysis, CAR was verified as an independent risk factor for poor prognosis, together with tumor differentiation, T stage and postoperative complications. All in all, compared to the other three CRP-albumin-related prognostic predictors, CRA is a better indicator in predicting poor long-term outcomes in GBC patients after radical surgery.

Nomogram Based on Systemic Immune Inflammation Index and Prognostic Nutrition Index Predicts Recurrence of Hepatocellular Carcinoma After Surgery.

BACKGROUND: Surgery is a potential cure for hepatocellular carcinoma (HCC), but its postoperative recurrence rate is high, its prognosis is poor, and reliable predictive indicators are lacking. This study was conducted to develop a simple, practical, and effective predictive model. MATERIALS AND METHODS: Preoperative clinical and postoperative pathological data on patients with HCC undergoing partial hepatectomies at the Third Affiliated Hospital of Soochow University from January 2010 to December 2015 were retrospectively analyzed, and a nomogram was constructed. The model performance was evaluated using C-indexes, receiver operating characteristic curves, and calibration curves. The results were verified from validation cohort data collected at the same center from January 2016 to January 2017 and compared with the traditional staging systems. RESULTS: Three hundred three patients were enrolled in this study: 238 in the training cohort and 65 in the validation cohort. From the univariate and multivariate Cox regression analyses in the training cohort, six independent risk factors, i.e., age, alpha-fetoprotein (AFP), tumor size, satellite nodules, systemic immune inflammation index (SII), and prognostic nutritional index (PNI), were filtered and included in the nomogram. The C-index was 0.701 [95% confidence interval (CI): 0.654-0.748] in the training cohort and 0.705 (95% CI: 0.619-0.791) in the validation cohort. The areas under the curve for the 1- and 3-year recurrence-free survival were 0.706 and 0.716 in the training cohort and 0.686 and 0.743 in the validation cohort, respectively. The calibration curves showed good agreement. Compared with traditional American Joint Committee on Cancer 8th edition (AJCC8th) and Barcelona Clinic Liver Cancer (BCLC) staging systems, our nomogram showed better predictive ability. CONCLUSION: Our nomogram is simple, practical, and reliable. According to our nomogram, predicting the risk of recurrence and stratifying HCC patient management will yield the greatest survival benefit for patients.