PHF12 regulates HDAC1 to promote tumorigenesis via EGFR/AKT signaling pathway in non-small cell lung cancer.

BACKGROUND: Lung cancer stands as the second most prevalent malignant neoplasm worldwide. Addressing the underlying mechanisms propelling the progression of non-small cell lung cancer is of paramount importance. In this study, we have elucidated the pivotal role of PHF12 in this context. MATERIALS AND METHODS: We harnessed clinical lung cancer tissue samples and non-small cell lung cancer cell lines to discern the expression pattern of PHF12. In vitro assays probing cell proliferation were conducted to substantiate the functional impact of PHF12. Furthermore, an in vivo Xenograft model was employed to dissect the role of PHF12. Employing ChIP assays and qRT-PCR, we delved into the intricate binding dynamics between PHF12 and HDAC1. Mechanistic insights into the PHF12-HDAC1 axis in lung cancer progression were pursued via RNA-seq and GSEA analyses. RESULTS: Notably, PHF12 exhibited a substantial upregulation within tumor tissue, concomitant with its correlation to HDAC1. The trilogy of cell proliferation assays, transwell assays, and the Xenograft model collectively underscored the promoting influence of PHF12 on lung cancer proliferation, both in vitro and in vivo. The ChIP assay unveiled the transcriptional regulatory role of PHF12 in governing HDAC1 expression. This correlation extended to both mRNA and protein levels. PHF12 promotes NSCLC progression through regulating HDCA1 expression. Intriguingly, the rescue of function within NSCLC cell lines post PHF12 knockdown was achievable through HDAC1 overexpression. Additionally, our findings unveiled the capacity of the PHF12-HDAC1 axis to activate the EGFR/AKT signaling pathway, thereby further corroborating its significance in lung cancer progression. CONCLUSION: Our study identified PHF12 as an oncogenic role in lung cancer proliferation and migration for the first time. PHF12 transcriptionally regulate HDAC1 and activate EGFR/AKT signaling pathway in NSCLC progression. PHF12 may serve as an important target in lung cancer therapy.

Spinal interleukin-16 mediates inflammatory pain via promoting glial activation.

Proinflammatory cytokines are crucial contributors to neuroinflammation in the development of chronic pain. Here, we identified il16, which encodes interleukin-16 (IL-16), as a differentially expressed gene in spinal dorsal horn of a complete Freund's Adjuvant (CFA) inflammatory pain model in mice by RNA sequencing. We further investigated whether and how IL-16 regulates pain transmission in the spinal cord and contributes to the development of inflammatory pain hypersensitivity. RNA sequencing and bioinformatics analysis revealed elevated IL-16 transcript levels in the spinal dorsal horn after CFA injection. This increase was further confirmed by qPCR, immunofluorescence, and western blotting. Knockdown of IL-16 by intrathecal injection of IL-16 siRNA not only attenuated CFA-induced mechanical and thermal pain hypersensitivity, but also inhibited enhanced c-fos expression and glial activation in the spinal dorsal horn in male mice injected with CFA. Moreover, exogenous IL-16 induced nociceptive responses and increased c-fos expression and glial activation in spinal dorsal horn. This effect was largely impaired when CD4, the binding receptor for IL-16, was inhibited. In addition, CD4 expression was upregulated in the spinal dorsal horn after CFA injection and CD4 was present in microglia and in contact with astrocytes and activated spinal neurons. Taken together, these results suggest that enhanced IL-16-CD4 signaling triggers pain and activates microglia and astrocytes in the spinal dorsal horn, thus contributing to inflammatory pain. IL-16 may serve as a promising target for the treatment of inflammatory pain.

Effects of Insulin Combined with Traditional Chinese Medicine Assisted Comprehensive Nursing Intervention on Oxidative Stress State, Cell Adhesion Factor, and Pregnancy Outcome of Patients with Gestational Diabetes Mellitus.

Objectives: The changes of oxidative stress state, cell adhesion factor (sICAM-1) level, blood glucose, and blood lipid of patients with gestational diabetes mellitus (GDM) assisted by insulin combined with traditional Chinese medicine (TCM) prescription were detected to explore the effect of TCM treatment on maternal and infant outcomes of GDM. Methods: A total of 60 patients diagnosed with GDM from January 2019 to December 2019 were selected. Among them, 30 patients were treated with insulin combined with TCM prescription (control group), and 30 patients were treated with nursing intervention based on control group (study group). Serum of maternal vein and fetal umbilical vein was collected. The contents of superoxide dismutase (SOD) and lipid oxide (MDA) were determined. The content of intercellular adhesion factor (ICAM-1) was measured, and the differences of fasting blood glucose (FPG), glycosylated hemoglobin (HbA1c), triglyceride (TG), cholesterol (CHO) and low density lipoprotein (LDL-C) between 2 groups were compared. The incidence of maternal and infant adverse outcomes was assessed. Results: After treatment, blood glucose indexes in 2 groups were decreased, and the study group was lower than the control group. After treatment, LDL-C, TC and TG in 2 groups were lower than before, and the study group was lower than the control group. HDL-C was higher than before treatment, and the study group was higher than the control group. After treatment, oxidation-related substances SOD and GSH-Px in 2 groups were higher than before, and those in study group were higher than those in control group. ROS and MDA were lower than before treatment, and the level of sICAM-1 in the study group was significantly higher than that in the control group. Clinical application of insulin combined with TCM prescription assisted comprehensive nursing intervention in the treatment of gestational diabetes, pregnancy outcome is improved. Conclusions: Oxidative stress imbalance exists in GDM and the causes of adverse pregnancy outcomes are closely related to oxidative stress and vascular endothelial injury. TCM can improve the oxidative stress imbalance and the pregnancy outcome of patients with GDM from the perspective of reducing vascular endothelial injury. Comprehensive nursing intervention for pregnant women with GDM can optimize the outcome of pregnancy and is worthy of clinical application.

miR­486­5p suppresses gastric cancer cell growth and migration through downregulation of fibroblast growth factor 9.

Non­coding RNAs serve essential roles in regulating mRNA and protein expression and dysregulation of non­coding RNAs participates in a variety of types of cancer. microRNAs (miRNAs/miRs), which are 21­24 nucleotides non­coding RNAs, have been shown to be important for the development of gastric cancer (GC). However, the role of miR­486­5p in GC remains to be elucidated. The present study found that miR­486­5p was downregulated in GC tissues. Comparing with gastric normal cells GES­1, GC cells, including MKN­45, AGS, HGC27 and MKN74, had reduced abundance of miR­486­5p transcript. CCK8 and colony formation assays demonstrated that GC cell growth and proliferation were enhanced by miR­486­5p inhibitors and were suppressed by miR­486­5p mimics. miR­486­5p also suppressed cell cycle process and migration and promoted apoptosis in GC cells, as verified by propidium iodide (PI) staining, Transwell assay and PI/Annexin V staining. miR­486­5p downregulated fibroblast growth factor 9 (FGF9) through combining to its 3'untranslated region. Overexpression of FGF9 accelerated the growth and proliferation of GC cells. The expression of miR­486­5p was negatively associated with FGF9 mRNA expression in GC samples. These results revealed that miR­486­5p was a tumor suppressor in GC. Downregulation of FGF9 contributed to the role of miR­486­5p in GC.

Humanistic care and psychological counseling on psychological disorders in medical students after COVID-19 outbreak: A protocol of systematic review.

BACKGROUND: The objective of this study is to investigate the effects of humanistic care and psychological counseling (HCPC) on psychological disorders (PD) in medical students after coronavirus disease 2019 (COVID-19) outbreak. METHODS: We will search randomized controlled trials or case-controlled studies of HCPC on PD in medical students after COVID-19 outbreak in the following electronic databases: PUBMED/MEDLINE, EMBASE, Cochrane Library, CINAHL, AMED, WANGFANG, and CNKI. The time is restricted from the construction of each database to the present. All process of study selection, data collection, and study quality evaluation will be carried out by two independent authors. Any different opinions will be solved by a third author through discussion. We will employ RevMan 5.3 software to conduct statistical analysis. RESULTS: This study will provide a better understanding of HCPC on PD in medical students after COVID-19 outbreak. CONCLUSIONS: This study may offer strong evidence for clinical practice to treat PD in medical students after COVID-19 outbreak. STUDY REGISTRATION: CRD42020193199.

Low-dose CT combined mammography in diagnosis of overflow breast disease: A protocol of systematic review.

BACKGROUND: Overflow breast disease (OBD), also known as breast nipple discharge, refers fluid or liquid that comes out of nipple. Many patients with breast cancer experience such condition. However, it is not easy to detect it at early stage, especially for pathological OBD. Previous study found low-dose CT combined mammography (LDCTMG) could help in diagnosis of OBD. However, there is no systematic review investigating this issue. Therefore, this study will examine the accuracy of LDCTMG in diagnosis of OBD. METHODS: This study protocol will search literature sources in electronic databases and other sources. The electronic databases will be retrieved in The Cochrane Library, the Cochrane Register of Diagnostic Test Accuracy Studies, PUBMED, EMBASE, Web of Science, CINAHL, CNKI, and WANGFANG from inception to the present. We will also search other sources. All literature sources will be sought without restrictions to the language and publication status. Two researchers will independently carry out study selection, data extraction, and study quality assessment. Statistical analysis will be performed using RevMan 5.3. RESULTS: This study will exert a high-quality synthesis of eligible studies on the analysis of LDCTMG in diagnosis of OBD. CONCLUSIONS: The results of this study may provide evidence to help judge whether LDCTMG is accurate in diagnosis of OBD. STUDY REGISTRATION: INPLASY202050116.

Effect of roux-en Y gastric bypass surgery on patients with type 2 diabetes mellitus: A protocol of systematic review and meta-analysis.

BACKGROUND: Previous studies have reported that roux-en Y gastric bypass surgery (RYGBS) can benefit patients with type 2 diabetes mellitus (T2DM). However, their conclusions are still inconsistent. Thus, this study will aim to assess the effect of RYGBS for patients with T2DM. METHODS: In this study, the electronic databases of MEDLINE, EMBASE, CENTRAL, CINAHL, AMED, and CNKI from inceptions to the present without any limitations to language and publication status. All randomized controlled trials on assessing the effect of RYGBS for patients with T2DM will be included in this study. Two independent authors will carry out study search and selection according to the previous designed inclusion and exclusion criteria. At the same time, 2 authors will independently evaluate the risk of bias assessment by Cochrane risk of bias tool. Any disagreements between 2 authors will be solved by a third author through discussion. RevMan 5.3 software will be utilized for statistical analysis. RESULTS: This study will summarize the most recent studies and will provide a deeper understanding about using the effect of RYGBS for patients with T2DM. CONCLUSIONS: The findings of this study will present the existing evidence for the effect of RYGBS for patients with T2DM. SYSTEMATIC REVIEW REGISTRATION: INPLASY202040127.

Efficacy of laparoscopic sleeve gastrectomy in obese patients with type 2 diabetes mellitus: A protocol of systematic review and meta-analysis.

BACKGROUND: A numerous studies have reported that obese patients (OP) are easily to have type 2 diabetes mellitus (T2DM). Although a variety of managements are available to treat such disorder, their efficacy is still limited. Previous studies have reported that laparoscopic sleeve gastrectomy (LSGT) can benefit OP with T2DM. However, no study specifically and systematically explores this topic. Thus, this study will assess the efficacy and complications of LSGT for the management of OP with T2DM. METHODS: The search strategy will be performed in the electronic databases from inception to the March 31, 2020 without limitations of language and publication time: PUBMED, EMBASE, Cochrane Library, Scopus, Web of Science, CINAHL, AMED, WANGFANG, VIP, and CNKI. Two authors will independently identify the articles, collect the data, and assess the risk of bias using Cochrane risk of bias tool. We will invite a third author to solve any differences between two authors. We will use RevMan 5.3 software to investigate the statistical analysis. RESULTS: This study will supply a high-quality synthesis of randomized controlled trials (RCTs) on the analysis of LSGT for the management of OP with T2DM. CONCLUSIONS: This study will help to build proposals that aim at providing high quality RCTs in the management of LSGT in OP with T2DM. SYSTEMATIC REVIEW REGISTRATION: INPLASY202040128.

Circulating Neutrophils Predict Poor Survival for HCC and Promote HCC Progression Through p53 and STAT3 Signaling Pathway.

Background: Tumor-associated neutrophils (TANs) contribute to tumor progression, invasion, and angiogenesis. However, most studies focus on tumor infiltration neutrophils while the roles of circulating neutrophils in tumor progression remain unclear. This study was aimed to verify the pro-tumor effects of circulating neutrophils and its' mechanism in HCC. Methods: We collected clinical data of 127 HCC patients underwent TACE. The prognostic factors for overall survival (OS) were analyzed by Kaplan-Meier curve and Cox models. Circulating neutrophils of HCC patients were sorted and co-cultured with human HCC cell lines MHCC-97H and SMMC-7721. Then we detected tumor cells' proliferation, migration, and invasion. Phosphokinase array was used to determine the kinase profile on MHCC-97H and SMMC-7721 cultured with or without circulating neutrophils. Results: The result of multivariate analyses of 127 patients showed that increased circulating neutrophils was an independent poor prognostic factor for OS of HCC patients underwent TACE. Circulating neutrophils promoted migration and invasion of HCC cell lines but had no impact on proliferation. The kinase profile on HCC cell lines showed that p-p53S46 and p-STAT3Y705 were up-regulated after co-cultured with circulating neutrophils. Repeated scratch tests and transwell tests showed a reversed impact on migration and invasion of circulating neutrophils after we treated HCC cell lines with inhibitors of p53 or STAT3. Conclusion: Circulating neutrophils was an independent poor prognostic factor for OS of HCC patients underwent TACE. It had pro-tumor effect on HCC through p53 and STAT3 signaling pathway.

Long Non-Coding RNA (lncRNA) SNHG5 Participates in Vertical Sleeve Gastrectomy for Type II Diabetes Mellitus by Regulating TGR5.

BACKGROUND Due to its remarkable effect in controlling glycometabolism, relatively simple operation, and low risk of complications, sleeve gastrectomy (SG) has become the preferred surgical treatment for type II diabetes mellitus. Increased blood glucose in the body can cause damage to functional cells. MATERIAL AND METHODS Long non-coding RNA SNHG5 expression and TGR5 in serum were analyzed by real-time PCR. A diabetic cell model was established by culturing normal human intestinal epithelial cells NCM460 and DLD-1 with high-glucose and high-fat medium. CCK-8 assay, TUNEL assay, and flow cytometry were used to assess cell growth and apoptosis, respectively. The secretion of lactate dehydrogenase (LDH) was detected using the LDH Cytotoxicity Kit. lncRNA SNHG5 was downregulated by siRNA. The changes in expression of SNHG5, TGR5, Akt, p65, and Bcl-2 were analyzed by real-time PCR assay or Western blot. RESULTS In 40 type II diabetes patients who underwent sleeve gastrectomy, the expression of SNHG5 decreased and the expression of TGR5 increased compared with that before the operation. After high-glucose and high-fat culture, cell growth was inhibited and cell apoptosis increased significantly. The expression of SNHG5 was increased and TGR5 was decreased with high-glucose and high-fat culture. However, high glucose and high fat showed an opposite trend for cell growth, apoptosis, and LDH release under inhibition of SNHG5. The expression levels of TGR5 and Akt, p65, and Bcl-2 were also returned to normal by SNHG5 inhibition. CONCLUSIONS By downregulating expression of the SNHG5 gene and then altering expression of the TGR5 gene, the damage to colorectal cells induced by high glucose was alleviated. This may be one of the mechanisms underlying the effect of sleeve gastric surgery in treatment of diabetes mellitus.

Silencing of IL13RA2 promotes partial epithelial-mesenchymal transition in hepatocellular carcinoma via ERK signaling pathway activation.

Lack of insight into the mechanisms underlying hepatocellular carcinoma (HCC) metastasis has hindered the development of curative treatments. Overexpression of interleukin-13 receptor alpha 2 (IL13RA2) has been reported to contribute to invasion and metastasis in several tumors. However, the role of IL13RA2 in HCC remains to be characterized. In this study, we identified that low expression of IL13RA2 is associated with poor survival of patients with HCC, and demonstrated that IL13RA2 knockdown endows HCC cells with invasive potential. Mechanistically, silencing of IL13RA2 promotes partial epithelial-mesenchymal transition via increasing extracellular signal-regulated kinase phosphorylation in HCC. Collectively, our results suggest that IL13RA2 may have potential as a prognostic biomarker for HCC.

IDO and intra-tumoral neutrophils were independent prognostic factors for overall survival for hepatocellular carcinoma.

BACKGROUND: Both Indole-amine-2,3-dioxygenase (IDO) and neutrophils were proved to have pro-tumor effect in some kinds of solid tumors by immune suppression. However, little is known about their effect on hepatocellular carcinoma (HCC) and the relationship between these two immune-suppressive factors. The aim of this study was to evaluate the prognostic significance of IDO and intra-tumoral neutrophils and their correlations in HCC. METHODS: Specimens' tissue microarray (TMA) for 153 HCC patients was used in this study. We examined intra-tumoral expression of IDO and CD66b in TMA. The Kaplan-Meier method and Cox regression models were used to evaluate the prognostic value of IDO expression and CD66b. RESULTS: Multivariate analysis showed both IDO expression and intra-tumoral neutrophils infiltration were independent prognostic factors for overall survival (OS). In high IDO expression group, the percentage of intra-tumoral neutrophils infiltration was higher than that in low IDO expression group. CONCLUSION: Both IDO and intra-tumoral neutrophils were independent prognostic factors for overall survival for HCC.

Angiogenesis enhanced by treatment damage to hepatocellular carcinoma through the release of GDF15.

Transarterial chemoembolization (TACE) is the standard treatment for unresectable hepatocellular carcinoma (HCC). Hypoxia-induced angiogenesis by TACE is linked to treatment failure; however, whether the chemotherapeutic damage of TACE to HCC could increase tumor angiogenesis has not been explored. The molecular effects of chemotherapy-damaged HCC cells on the neo-angiogenesis were investigated in vitro and in vivo. The expression of growth differentiation factor 15 (GDF15) was significantly upregulated in HCC cells exposed to chemotherapeutic agents. GDF15 from chemotherapy-damaged HCC cells promoted the in vitro proliferation, migration, and tube formation of endothelial cells. The pro-angiogenic effect of GDF15 was through the activation of Src and its downstream AKT, MAPK, and NF-κB signaling, which was blocked by thalidomide. The use of thalidomide significantly attenuated the in vivo chemotherapy-damaged HCC cells-promoted angiogenesis in nude mice. In conclusion, the chemotherapeutic damage in TACE to HCC could promote tumor angiogenesis via the increased release of GDF15. Thalidomide could reverse these pro-angiogenic effects.

M2-polarized tumor-associated macrophages facilitated migration and epithelial-mesenchymal transition of HCC cells via the TLR4/STAT3 signaling pathway.

BACKGROUND: M2-polarized macrophages are tumor-associated-macrophages (TAMs), which are important contents of tumor-infiltrating immune cells. Toll-like receptor 4 (TLR4) is a molecular biomarker of tumor aggressiveness and poor prognosis. Toll-like receptors (TLRs) have important roles in the immune system and M2-polarized macrophages. However, the effects of TLR4 on M2-polarized macrophages in hepatocellular carcinoma (HCC) are unknown. Here, TLR4 expressed on HCC cells mediates the pro-tumor effects and mechanisms of M2-polarized macrophages. METHODS: THP-1 cells were induced to differentiate into M2-like macrophages through treatments with IL-4, IL-13, and phorbol myristate acetate (PMA). We used the HCC cell lines SMMC-7721 and MHCC97-H cultured in conditioned medium from M2-like macrophages (M2-CM) to investigate the migration potential of HCC cells and epithelial-mesenchymal transition (EMT)-associated molecular genetics. Signaling pathways that mediated M2-CM-promoted HCC migration were detected using western blotting. RESULTS: HCC cells cultured with M2-CM displayed a fibroblast-like morphology, an increased metastatic capability, and expression of EMT markers. TLR4 expression was markedly increased in M2-CM-treated HCC cells. TLR4 overexpression promoted HCC cell migration, and a TLR4-neutralizing antibody markedly inhibited HCC EMT in cells cultured with M2-CM. Furthermore, the TLR4/(signal transducer and activator of transcription 3 (STAT3) signaling pathway contributed to the effects of M2-CM on HCC cells. CONCLUSIONS: Taken together, M2-polarized macrophages facilitated the migration and EMT of HCC cells via the TLR4/STAT3 signaling pathway, suggesting that TLR4 may be a novel therapeutic target. These results improve our understanding of M2-polarized macrophages.

Increased matrix stiffness promotes tumor progression of residual hepatocellular carcinoma after insufficient heat treatment.

Aggravated behaviors of hepatocellular carcinoma (HCC) will occur after inadequate thermal ablation. However, its underlying mechanisms are not fully understood. Here, we assessed whether the increased matrix stiffness after thermal ablation could promote the progression of residual HCC. Heat-treated residual HCC cells were cultured on tailorable 3D gel with different matrix stiffness, simulating the changed physical environment after thermal ablation, and then the mechanical alterations of matrix stiffness on cell phenotypes were explored. Increased stiffness was found to significantly promote the proliferation of the heat-treated residual HCC cells when the cells were cultured on stiffer versus soft supports, which was associated with stiffness-dependent regulation of ERK phosphorylation. Heat-exposed HCC cells cultured on stiffer supports showed enhanced motility. More importantly, vitamin K1 reduced stiffness-dependent residual HCC cell proliferation by inhibiting ERK phosphorylation and suppressed the in vivo tumor growth, which was further enhanced by combining with sorafenib. Increased matrix stiffness promotes the progression of heat-treated residual HCC cells, proposing a new mechanism of an altered biomechanical environment after thermal ablation accelerates HCC development. Vitamin K1 plus sorafenib can reverse this protumor effect.

Activated hepatic stellate cells secrete periostin to induce stem cell-like phenotype of residual hepatocellular carcinoma cells after heat treatment.

Some evidences show that residual tumor after thermal ablation will progress rapidly. However, its mechanisms remain unclear. Here, we assessed whether activated HSCs could regulate stem cell-like property of residual tumor after incomplete thermal ablation to promote tumor progression. Human HCC cell lines were exposed to sublethal heat treatment to simulate the peripheral zone of thermal ablation. After residual HCC cells were cultured with conditional medium (CM) from activated HSCs, parameters of the stem cell-like phenotypes were analyzed. Nude mice bearing heat-exposed residual HCC cells and HSCs were subjected to metformin treatment to thwarter tumor progression. CM from activated primary HSCs or LX-2 cells significantly induced the stem cell-like phenotypes of residual HCC cells after heat treatment. These effects were significantly abrogated by neutralizing periostin (POSTN) in the CM. POSTN regulated the stemness of heat-exposed residual HCC cells via activation of integrin ß1/AKT/GSK-3ß/ß-catenin/TCF4/Nanog signaling pathway. Metformin significantly inhibited in vivo progression of heat-exposed residual HCC via suppressing POSTN secretion and decreasing cancer stem cell marker expression. Our data propose a new mechanism of activated HSCs promoting the stemness traits of residual HCC cells after incomplete thermal ablation and suggest metformin as a potential drug to reverse this process.

Over expression of hyaluronan promotes progression of HCC via CD44-mediated pyruvate kinase M2 nuclear translocation.

Hyaluronan is expressed in hepatocellular carcinoma (HCC) as HCC generally arises from a cirrhotic liver in which excessive production and accumulation of HA leads to developing cirrhosis. Though it has been suggested HA is involved in progression of HCC, the mechanisms underlying the connection between HA and HCC progression are unclear. Since increased aerobic glycolysis is a metabolic trait of malignant cells and HA-CD44 can modulate glucose metabolism, we aim to investigate the roles of PKM2, a key enzyme in glucose metabolism, in the HA-CD44 axis facilitated the progress of HCC. We shown PKM2 was required for HA-promoted HCC progression, which was not modulated by PKM2 kinase activity but by nuclear translocation of PKM2. PKM2 translocation was Erk (Thr202/Tyr204) phosphorylation dependent, which functioned at the downstream of HA-CD44 binding. Furthermore, elevated HA expression significantly correlated with PKM2 nuclear location and was an independent factors predicting poor HCC prognosis. In conclusions PKM2 nuclear translocation is required for mediating the described HA biological effects on HCC progression and our results imply that inhibition of HA may have therapeutic value in treating HCC.

Clostridium perfringens infection after transarterial chemoembolization for large hepatocellular carcinoma.

We report an unusual case of Clostridium perfringens liver abscess formation after transcatheter arterial chemoembolization (TACE) for large hepatocellular carcinoma. Severe deterioration in liver and renal function accompanied with hemocytolysis was found on the 2(nd) day after TACE. Blood culture found Clostridium perfringens and abdominal computed tomography revealed a gas-containing abscess in the liver. Following antibiotics administration and support care, the infection was controlled and the liver and renal function turned normal. The 2(nd) TACE procedure was performed 1.5 mo later and no recurrent Clostridium perfringens infection was found.