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Objectives: To study the quantitative and qualitative differences of visual evoked potential (VEP) in monocular visual impairment after different parts of visual pathway injury., Methods: A total of 91 subjects with monocular visual impairment caused by trauma were selected and divided into intraocular refractive media-injury group (eyeball injury group for short), optic nerve injury group, central nervous system injury and intracranial combined injury group according to the injury cause and anatomical segment. Pattern Reversal visual evoked potential (PR-VEP) P100 peak time and amplitude, Flash visual evoked potential (F-VEP) P2 peak time and amplitude were recorded respectively. SPSS 26.0 software was used to analyze the differences of quantitative (peak time and amplitude) and qualitative indexes (spatial frequency sweep-VEP acuity threshold, and abnormal waveform category and frequency) of the four groups., Results: Compared with healthy eyes, the PR-VEP P100 waveforms of the intraocular eyeball injury group and the F-VEP P2 waveforms of the optic nerve group showed significant differences in prolonged peak time and decreased amplitude in injured eyes ( P <0.05). The PR-VEP amplitudes of healthy eyes were lower than those of injured eyes at multiple spatial frequencies in central nervous system injury group and intracranial combined injury group ( P <0.05).The amplitude of PR-VEP in patients with visual impairment involving central injury was lower than that in patients with eye injury at multiple spatial frequencies. The frequency of VEP P waveforms reaching the threshold of the intraocular injury group and the optic nerve injury group were siginificantly different from the intracranial combined injury group, respectively( P <0.008 3), and the frequency of abnormal reduction of VEP amplitude of threshold were significantly different from the central nervous system injury group, respectively( P <0.008 3)., Conclusions: VEP can distinguish central injury from peripheral injury, eyeball injury from nerve injury in peripheral injury, but cannot distinguish simple intracranial injury from complex injury, which provides basic data and basis for further research on the location of visual impairment injury.

Introduction: Inspired by application of platelet-rich plasma (PRP) in skin treatment during injuries, an extracting method was developed here to recover high amounts of cytokines and growth factors from PRP; this prepared extract was named as self-growth colony (SGC)., Methods: In optimization of SGC preparation, various parameters were tested, for example, centrifugation force, freeze-thaw, sonication, and inclusion of calcium chelator. The amounts of cytokines and growth factors, including platelet factor 4, β-thromboglobulin, epidermal growth factor, vascular endothelial growth factor, platelet-derived growth factor, were measured by ELISA assay., Results: By comparing to PRP, the prepared SGC contained a significant higher amount of measured growth factors. In addition, the degradation of growth factors within SGC during the storage was calibrated, which showed better stability as compared to that of PRP preparation. Having possible application in skin care, the optimized SGC was chemically standardized by using the enrichment of growth factors. Application of SGC in cultured keratinocytes stimulated the wound healing of injured cultures. In line to this notion, SGC was applied onto human skin, and thereafter the robust improvement of skin properties was revealed., Conclusions: The potential application of SGC in treating skin rejuvenation and ageing, as well as its elaborated application for medical purpose, that is, wound healing, was illustrated., (© 2021 S. Karger AG, Basel.)

Background: Vascular Endothelial Growth Factors (VEGFs) are a group of growth factor in regulating development and maintenance of blood capillary. The VEGF family members include VEGF-A, placenta growth factor (PGF), VEGF-B, VEGF-C and VEGF-D. VEGF receptor activation leads to multiple complex signaling pathways, particularly in inducing angiogenesis. Besides, VEGF is produced by macrophages and T cells, which is playing roles in inflammation. In macrophages, VEGF receptor-3 (VEGFR-3) and its ligand VEGF-C are known to attenuate the release of pro-inflammatory cytokines., Methods: Immunoprecipitation and molecular docking assays showed the binding interaction of kaempferol-3-O-rutinoside and VEGF-C. Western blotting and qRT-PCR methods were applied to explore the potentiating effect of kaempferol-3-O-rutinoside in VEGF-C-mediated expressions of proteins and genes in endothelial cells and LPS-induced macrophages. Enzyme-linked immunosorbent assay (ELISA) was employed to reveal the release of proinflammatory cytokines in LPS-induced macrophages. Immunofluorescence assay was performed to determine the effect of kaempferol-3-O-rutinoside in regulating nuclear translocation of NF-κB p65 subunit in the VEGF-C-treated cultures. In addition, Transwell® motility assay was applied to detect the ability of cell migration after drug treatment in LPS-induced macrophages., Results: We identified kaempferol-3-O-rutinoside, a flavonoid commonly found in vegetable and fruit, was able to act on cultured macrophages in inhibiting inflammatory response, and the inhibition was mediated by its specific binding to VEGF-C. The kaempferol-3-O-rutinoside-bound VEGF-C showed high potency to trigger the receptor activation. In LPS-treated cultured macrophages, applied kaempferol-3-O-rutinoside potentiated inhibitory effects of exogenous applied VEGF-C on the secretions of pro-inflammatory cytokines, i.e. IL-6 and TNF-α, as well as expressions of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). This inhibition was in parallel to transcription and translocation of NF-κB. Moreover, the binding of kaempferol-3-O-rutinoside with VEGF-C suppressed the LPS-induced migration of macrophage., Conclusion: Taken together, our results suggested the pharmacological roles of kaempferol-3-O-rutinoside in VEGF-C-mediated anti-inflammation., (Copyright © 2020. Published by Elsevier GmbH.)

Piceatannol is also named as trans -3,4,3',5'-tetrahydroxy-stilbene, which is a natural analog of resveratrol and a polyphenol existing in red wine, grape and sugar cane. Piceatannol has been proved to possess activities of immunomodulatory, anti-inflammatory, antiproliferative and anticancer. However, the effect of piceatannol on VEGF-mediated angiogenesis is not known. Here, the inhibitory effects of piceatannol on VEGF-induced angiogenesis were tested both in vitro and in vivo models of angiogenesis. In human umbilical vein endothelial cells (HUVECs), piceatannol markedly reduced the VEGF-induced cell proliferation, migration, invasion, as well as tube formation without affecting cell viability. Furthermore, piceatannol significantly inhibited the formation of subintestinal vessel in zebrafish embryos in vivo. In addition, we identified the underlying mechanism of piceatannol in triggering the anti-angiogenic functions. Piceatannol was proposed to bind with VEGF, thus attenuating VEGF in activating VEGF receptor and blocking VEGF-mediated downstream signaling, including expressions of phosphorylated eNOS, Erk and Akt. Furthermore, piceatannol visibly suppressed ROS formation, as triggered by VEGF. Moreover, we further determined the outcome of piceatannol binding to VEGF in cancer cells: piceatannol significantly suppressed VEGF-induced colon cancer proliferation and migration. Thus, these lines of evidence supported the conclusion that piceatannol could down regulate the VEGF-mediated angiogenic functions with no cytotoxicity via decreasing the amount of VEGF binding to its receptors, thus affecting the related downstream signaling. Piceatannol may be developed into therapeutic agents or health products to reduce the high incidence of angiogenesis-related diseases.

Kaempferol is a major flavonoid in Ginkgo Folium and other edible plants, which is being proposed here to have roles in angiogenesis. Angiogenesis is important in both physiological and pathological development. Here, kaempferol was shown to bind with vascular endothelial growth factor (VEGF), probably in the heparin binding domain of VEGF: this binding potentiated the angiogenic functions of VEGF in various culture models. Kaempferol potentiated the VEGF-induced cell motility in human umbilical vein endothelial cells (HUVECs), as well as the sub-intestinal vessel sprouting in zebrafish embryos and formation of microvascular in rat aortic ring. In cultured HUVECs, application of kaempferol strongly potentiated the VEGF-induced phosphorylations of VEGFR2, endothelial nitric oxide synthase (eNOS) and extracellular signal-regulated kinase (Erk) in time-dependent and concentration-dependent manners, and in parallel the VEGF-mediated expressions of matrix metalloproteinases (MMPs), MMP-2 and MMP-9, were significantly enhanced. In addition, the potentiation effect of kaempferol was revealed in VEGF-induced migration of skin cell and monocyte. Taken together, our results suggested the pharmacological roles of kaempferol in potentiating VEGF-mediated functions should be considered., (Copyright © 2020 Hu, Wang, Xia, Dai, Xiong, Dong, Duan, Chan, Qin and Tsim.)

Bile duct stones are a serious and the third most common complication of the biliary system that can occur following liver transplantation. The incidence rate of bile duct stones after liver transplantation is 1.8%-18%. The management of biliary stones is usually performed with endoscopic techniques; however, the technique may prove to be challenging in the treatment of the intrahepatic bile duct stones. We herein report a case of a 40-year-old man with rare, complex bile duct stones that were successfully eliminated with percutaneous interventional techniques. The complex bile duct stones were defined as a large number of bile stones filling the intra- and extrahepatic bile tracts, resulting in a cast formation within the biliary tree. Common complications such as hemobilia and acute pancreatitis were not present during the perioperative period. The follow-up period was 20 mo long. During the postoperative period, the patient maintained normal temperature, and normal total bilirubin and direct bilirubin levels. The patient is now living a high quality life. This case report highlights the safety and efficacy of the percutaneous interventional approach in the removal of complex bile duct stones following liver transplantation.

The adipocytokine apelin is a peptide, Apelin and its receptor are abundantly expressed in the nervous and cardiovascular systems. Previous studies had found apelin-13 reduces brain injuries and postischemic cerebral edema through blocking programmed cell death, Apelin-13 is also able to inhibit glucose deprivation induced cardiomyocyte autophagy in a concentration dependent fashion. To observe the effect of Apelin-13 on the brain injury induced by traumatic brain injury (TBI), and explore the effect of Apelin-13 on autophagy in TBI, We performed The neurological test, and the numbers of TBI-induced neural cell death were also counted by propidium iodide labeling. At last, the autophagy associated proteins LC3, Beclin-1, Bcl-2, p62 were also assessed with western-blotting. Compared with saline vehicle groups, the neural cell death, lesion volume, and neural dysfunction were attenuated by apelin-13 after TBI. In additionally, Apelin-13 also reversed TBI induced downregulation of LC3, Beclin-1, Bcl-2, p62 expression, compared with saline vehicle groups, at 24 and 48 h post TBI. Apelin-13 attenuates TBI induced brain damage by suppressing autophagy. All these results revealed that Apelin-13 suppressed autophagy. The autophagy may be involved in the mechanism of Apelin-13 rescue the subsequent damaged neuron in TBI.

Acute membrane damage due to traumatic brain injury (TBI) is a critical precipitating event. However, the subsequent effects of the mechanical trauma, including mitochondrial and lysosomal membrane permeability (MOMP and LMP) remain elusive. The main objective of the current study was to assess the role of a putative membrane-resealing agent poloxamer 188 (P188) in MOMP and LMP in response to a well-defined mechanical insult. Using an in vitro cell shearing device (VCSD), mechanical injury resulted in immediate disruption of membrane integrity in cultured primary neurons, and neurons were treated with P188 or a cathepsin B inhibitor (CBI) after VCSD 10 min. The protective effect of P188 on cultured primary neurons was first detected visually with a light microscope, and measured by MTT assay and LDH assay. The validity of monitoring changes in mitochondrial membrane potential (ΔΨm) was measured by JC-1 staining, and Western blot for cytochrome c and truncated Bid (tBid) in purified mitochondria was also performed. In addition, lysosomal integrity was detected by blotting for cathepsin B and tBid in purified lysosomes. Our results showed post-injury P188 treatment moderated the dissipation of ΔΨm in mitochondria, and inhibited VCSD-induced cytochrome c release from mitochondria as well as cathepsin B from lysosomes. Cathepsin B inhibition (CBI) could also increase cell viability, maintain mitochondrial membrane potential, and repress VCSD-induced release of cytochrome c from mitochondria to cytosol. Both P188 and CBI treatment decreased the cytosolic accumulation of tBid in supernatant of purified lysosomes, and the amount of mitochondrial localized tBid. These data indicate injured neurons have undergone mitochondrial and lysosomal membrane permeability damage, and the mechanism can be exploited with pharmacological interventions. P188's neuroprotection appears to involve a relationship between cathepsin B and tBid-mediated mitochondrial initiation of cell death.

NF-κB upregulation has been demonstrated in neurons and glial cells in response to experimental injury and neuropathological disorders, where it has been related to both neurodegenerative and neuroprotective activities. It has been generally recognized that NF-κB plays important roles in the regulation of apoptosis and inflammation as well as innate and adaptive immunity. However, the regulatory mechanism of NF-κB in apoptosis remained to be determined. The present study sought to first investigate the effect of a NF-κB inhibitor SN50, which inhibits NF-κB nuclear translocation, on cell death and behavioral deficits in our mice traumatic brain injury (TBI) models. Additionally, we tried to elucidate the possible mechanisms of the therapeutic effect of SN50 through NF-κB regulating apoptotic and inflammatory pathway in vivo. Encouragingly, the results showed that pretreatment with SN50 remarkably attenuated TBI-induced cell death (detected by PI labeling), cumulative loss of cells (detected by lesion volume), and motor and cognitive dysfunction (detected by motor test and Morris water maze). To analyze the mechanism of SN50 on cell apoptotic and inflammatory signaling pathway, we thus assessed expression levels of TNF-α, cathepsin B and caspase-3, Bid cleavage and cytochrome c release in SN50-pretreated groups compared with those in saline vehicle groups. The results imply that through NF-κB/TNF-α/cathepsin networks SN50 may contribute to TBI-induced extrinsic and intrinsic apoptosis, and inflammatory pathways, which partly determined the fate of injured cells in our TBI model.

Plasmalemma permeability plays an important role in the secondary neuronal death induced by traumatic brain injury (TBI). Previous works showed that Poloxamer 188 (P188) could restore the intactness of the plasma membrane and play a cytoprotective action. However, the roles of P188 in blood-brain barrier (BBB) integrity and TBI-induced neural cell death are still not clear. In this study, mice were induced TBI by controlled cortical impact (CCI), and cerebral water content was measured to explore the profile of brain edema after CCI. Further, the regimen of P188 in mouse CCI models was optimized. The neurological test and BBB integrity assessment were performed, and the numbers of TBI-induced neural cell death were counted by propidium iodide (PI) labeling. The expression of apoptotic pathway associated proteins (Bax, cyt-c, caspase-8, caspase-9, caspase-3, P53) and aquaporin-4 (AQP4) was assessed by RT-PCR or immunoblotting. The data showed that the brain edema peaked at 24 h after TBI in untreated animals. Tail intravenous injection of P188 (4 mg/ml, 100 μl) 30 min before TBI or within 30 min after TBI could attenuate TBI-induced brain edema. P188 pre-treatment restored BBB integrity, suppressed TBI-induced neural cell death, and improved neurological function. TBI induced an up-regulation of Bax, cyt-c, caspase-8, caspase-9, caspase-3, and the expression of p53 was down-regulated by P188 pre-treatment. AQP4 mainly located on endothelial cells and astrocytes, and its expression was also regulated by P188 pretreatment. All these results revealed that P188 attenuates TBI-induced brain edema by resealing BBB and regulating AQP4 expression, and suppressed apoptosis through extrinsic or intrinsic pathway. Plasmalemma permeability may be a potential target for TBI treatment.

Traumatic brain injury (TBI) results in neuronal apoptosis, autophagic cell death and necroptosis. Necroptosis is a newly discovered caspases-independent programmed necrosis pathway which can be triggered by activation of death receptor. Previous works identified that necrostatin-1 (NEC-1), a specific necroptosis inhibitor, could reduce tissue damage and functional impairment through inhibiting of necroptosis process following TBI. However, the role of NEC-1 on apoptosis and autophagy after TBI is still not very clear. In this study, the amount of TBI-induced neural cell deaths were counted by PI labeling method as previously described. The expression of autophagic pathway associated proteins (Beclin-1, LC3-II, and P62) and apoptotic pathway associated proteins (Bcl-2 and caspase-3) were also respectively assessed by immunoblotting. The data showed that mice pretreated with NEC-1 reduced the amount of PI-positive cells from 12 to 48 h after TBI. Immunoblotting results showed that NEC-1 suppressed TBI-induced Beclin-1 and LC3-II activation which maintained p62 at high level. NEC-1 pretreatment also reversed TBI-induced Bcl-2 expression and caspase-3 activation, as well as the ratio of Beclin-1/Bcl-2. Both 3-MA and NEC-1 suppressed TBI-induced caspase-3 activation and LC3-II formation, Z-VAD only inhibited caspase-3 activation but increased LC3-II expression at 24 h post-TBI. All these results revealed that multiple cell death pathways participated in the development of TBI, and NEC-1 inhibited apoptosis and autophagy simultaneously. These coactions may further explain how can NEC-1 reduce TBI-induced tissue damage and functional deficits and reflect the interrelationship among necrosis, apoptosis and autophagy.

Previous data demonstrate that traumatic brain injury (TBI) activates autophagy, and increases microtubule-associated protein 1 light chain 3 (LC3) immunostaining mainly in neurons. However, the role of autophagy in traumatic brain damage remains elusive. The aim of the present study was to investigate the autophagic mechanisms participating in traumatic brain injury. The autophagy inhibitors 3-methyladenine (3-MA) and bafliomycin A1 (BFA) were administered with a single i.c.v. injection before TBI. We first examined the protein levels of Beclin-1 and LC3 II, which have been found to promote autophagy previously. Immunoblotting analysis showed that 3-MA pretreatment reduced post-TBI Beclin-1 and LC3-II levels, and maintained p62/SQSTM1 (p62) levels. In addition, double immunolabeling showed that the increased punctate LC3-II dots colocalizing with Propidium Iodide (PI)-stained nuclei at 24 h after injury, were partially inhibited by 3-MA pretreatment. Furthermore, inhibition of autophagy could reduce TBI-induced cell injury assessed with i.p. injection of PI and lesion volume, and attenuate behavioral outcome evaluated by motor test and Morris water maze. The neuroprotective effects were associated with an inhibition on TBI-induced up-regulation of LC3, Beclin-1, cathepsin B, caspase-3 and the Beclin-1/Bcl-2 ratio. Taken together, these data imply that the autophagy pathway is involved in the pathophysiologic responses after TBI, and inhibition of this pathway may help attenuate traumatic damage and functional outcome deficits., (Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.)

Aim: To review percutaneous transhepatic portal venoplasty and stenting (PTPVS) for portal vein anastomotic stenosis (PVAS) after liver transplantation (LT)., Methods: From April 2004 to June 2008, 16 of 18 consecutive patients (11 male and 5 female; aged 17-66 years, mean age 40.4 years) underwent PTPVS for PVAS. PVAS occurred 2-10 mo after LT (mean 5.0 mo). Three asymptomatic patients were detected on routine screening color Doppler ultrasonography (CDUS). Fifteen patients who also had typical clinical signs of portal hypertension (PHT) were identified by contrast-enhanced computerized tomography (CT) or magnetic resonance imaging. All procedures were performed under local anesthesia. If there was a PVAS < 75%, the portal pressure was measured. Portal venoplasty was performed with an undersized balloon and slowly inflated. All stents were deployed immediately following the predilation. Follow-ups, including clinical course, stenosis recurrence and stent patency which were evaluated by CDUS and CT, were performed., Results: Technical success was achieved in all patients. No procedure-related complications occurred. Liver function was normalized gradually and the symptoms of PHT also improved following PTPVS. In 2 of 3 asymptomatic patients, portal venoplasty and stenting were not performed because of pressure gradients < 5 mmHg. They were observed with periodic CDUS or CT. PTPVS was performed in 16 patients. In 2 patients, the mean pressure gradients decreased from 15.5 mmHg to 3.0 mmHg. In the remaining 14 patients, a pressure gradient was not obtained because of > 75% stenosis and typical clinical signs of PHT. In a 51-year-old woman, who suffered from massive ascites and severe bilateral lower limb edema after secondary LT, PVAS complicated hepatic vein stenosis and inferior vena cava (IVC) stenosis. Before PTPVS, a self-expandable and a balloon-expandable metallic stent were deployed in the IVC and right hepatic vein respectively. The ascites and edema resolved gradually after treatment. The portosystemic collateral vessels resulting from PHT were visualized in 14 patients. Gastroesophageal varices became invisible on poststenting portography in 9 patients. In a 28-year-old man with hepatic encephalopathy, a pre-existing meso-caval shunt was detected due to visualization of IVC on portography. After stenting, contrast agents flowed mainly into IVC via the shunt and little flowed into the portal vein. A covered stent was deployed into the superior mesenteric vein to occlude the shunt. Portal hepatopetal flow was restored and the IVC became invisible. The patient recovered from hepatic encephalopathy. A balloon-expandable Palmaz stent was deployed into hepatic artery for anastomotic stenosis before PTPVS. Percutaneous transhepatic internal-external biliary drainage was performed in 2 patients with obstructive jaundice. Portal venous patency was maintained for 3.3-56.6 mo (mean 33.0 mo) and all patients remained asymptomatic., Conclusion: With technical refinements, early detection and prompt treatment of complications, and advances in immunotherapy, excellent results can be achieved in LT.

Objective: The aim of this study was to evaluate the efficacy of hepatic artery stenting with a balloon-expandable coronary stent for the treatment of hepatic artery stenosis (HAS) after orthotopic liver transplantation (OLT)., Patients and Methods: We performed retrospective review of all 11 patients who underwent hepatic artery stenting after a diagnosis of HAS., Results: A total of 13 balloon-expandable coronary stents were placed into 11 patients. The technical and immediate success rate was 100%; all stents remained patent during follow-up. One patient required 2 stents due to the length of the stenotic artery. Another underwent a second stenting after developing restenosis proximal to the original stenotic site. No procedure-related complications occurred, and no surgical revascularization or retransplantation was required during follow-up., Conclusions: A balloon-expandable coronary stent can play a role in the management of HAS. It can be used with great safety, with immediate as well as longer-term success.

Aim: To investigate and evaluate the technical feasibility and clinical effectiveness of fluoroscopically guided peroral uncovered expandable metal stent placement to treat gastric outlet and duodenal obstructions., Methods: Fifteen consecutive patients underwent peroral placement of Wallstent(TM) Enteral Endoprosthesis to treat gastric outlet and duodenal obstructions (14 malignant, 1 benign). All procedures were completed under fluoroscopic guidance without endoscopic assistance. Follow-up was completed until the patients died or were lost, and the clinical outcomes were analyzed., Results: The technique success rate was 100%, and the oral intake was maintained in 12 of 14 patients varying from 7 d to 270 d. Two patients remained unable to resume oral intake, although their stents were proven to be patent with the barium study. One patient with acute necrotizing pancreatitis underwent enteral stenting to treat intestinal obstruction, and nausea and vomiting disappeared. Ten patients died during the follow-up period, and their mean oral intake time was 50 d. No procedure-related complications occurred. Stent migration to the gastric antrum occurred in one patient 1 year after the procedure, a tumor grew at the proximal end of the stent in another patient 38 d post-stent insertion., Conclusion: Fluoroscopically guided peroral metal stent implantation is a safe and effective method to treat malignant gastrointestinal obstructions, and complications can be ignored based on our short-term study. Indications for this procedure should be discreetly considered because a few patients may not benefit from gastrointestinal insertion, but some benign gastrointestinal obstructions can be treated using this procedure.

Portal vein stenosis after liver transplantation is a relatively uncommon vascular complication that may result in graft loss if not promptly treated. The purpose of this study was to evaluate the midterm result of the use of intravascular stents for portal vein stenosis after liver transplantation. From April 2004 to September 2005, percutaneous transhepatic balloon dilation with stent deployment was performed in nine cases. Varices were embolized with stainless steel coils in two cases. No procedure-related complication occurred. Portal venous patency was maintained in all nine patients from 6 to 19 months (mean 10 months). In conclusion, an intravascular stent is an effective treatment for the portal vein stenosis after liver transplantation with excellent midterm patency.

Aim: To evaluate the utility of local tumor therapy combined with percutaneous transhepatic biliary drainage (PTBD) for malignant obstructive biliary disease., Methods: A total of 233 patients with malignant biliary obstruction were treated in our hospital with PTBD by placement of metallic stents and/or plastic tubes. After PTBD, 49 patients accepted brachytherapy or extra-radiation therapy or arterial infusion chemotherapy. The patients were followed up with clinical and radiographic evaluation. The survival and stent patency rate were calculated by Kaplan-Meier survival analysis., Results: Twenty-two patients underwent chemotherapy (11 cases of hepatic carcinoma, 7 cases of pancreatic carcinoma, 4 cases of metastatic lymphadenopathy), and 14 patients received radiotherapy (10 cases of cholangiocarcinoma, 4 cases of pancreatic carcinoma), and 13 patients accepted brachytherapy (7 cases of cholangiocarcinoma, 3 cases of pancreatic carcinoma, 4 cases of metastatic lymphadenopathy). The survival rate of the local tumor treatment group at 1, 3, 6, and 12 months was 97.96%, 95.92%, 89.80%, and 32.59% respectively, longer than that of the non treatment group. The patency rate at 1, 3, 6, and 12 months was 97.96%, 93.86%, 80.93%, and 56.52% respectively. The difference of patency rate was not significant between treatment group and non treatment group., Conclusion: Our results suggest that local tumor therapy could prolong the survival time of patients with malignant biliary obstruction, and may improve stent patency.