PURPOSE: Postpancreatectomy hemorrhage (PPH) is a life-threatening complication after pancreatoduodenectomy. Stent-graft implantation is an emerging treatment option for PPH. This study reports the outcome of PPH treated with stent-graft implantation. METHODS: This was a single-center, retrospective study. Between April 2020 and December 2023, 1723 pancreatectomy cases were collected while we screened 12 cases of PPH after pancreatoduodenectomy treated with stent-graft implantation. Patients' medical and radiologic images were retrospectively reviewed. Technical and clinical success, complications, and stent-graft patency were evaluated. Continuous data are reported as means ± standard deviation when normally distributed or as median (Q₁, Q₃) when the data is non-normal distributed. Categorical data are reported as n (%). A p < 0.05 was considered statistically significant. Kaplan-Meier estimates were used for stent patency and patients' survival. RESULTS: Pancreatic fistula was identified in 6 cases (50.0%), and pseudoaneurysm was identified in 3 cases (25.0%), including pancreatic fistula together with pseudoaneurysm in 1 case (8.3%). All pseudoaneurysm or contrast extravasation sites were successfully excluded with patent distal perfusion, thus technical success was achieved in all cases. The overall survival rate at 6 months and 1 year was 91.7% and 78.6%, respectively. One patient had herniation of the small intestine into the thoracic cavity, which caused a broad thoracic and abdominal infection and died during hospitalization. Rebleeding occurred at the gastroduodenal artery stump in 1 case after stent-graft implantation for the splenic artery and was successfully treated with another stent-graft implantation. Two cases of asymptomatic stent-graft occlusion were observed at 24.6 and 26.3 after the operation, respectively. CONCLUSIONS With suitable anatomy, covered stent-graft implantation is an effective and safe treatment option for PPH with various bleeding sites and causes.
Humans ; Pancreaticoduodenectomy/adverse effects* ; Stents ; Male ; Retrospective Studies ; Female ; Middle Aged ; Postoperative Hemorrhage/surgery* ; Aged ; Adult

Objective To investigate the mechanism of mitochondrial autophagy regulating the expression of NLRP3 inflammasome in prostate tissue in experimental autoimmune prostatitis(EAP)rats and to provide a theoretical basis for the study of new drug development.Methods A numerical table of 40 SD male rats was randomly divided into 8 groups.Namely,normal group(N),model group(M),rapamycin group(RAP),rapamycin+mitochondrial autophagy inhibitor group(RAP+Mdivi-1),autophagy inhibitor group(3MA),mitochondrial autophagy inhibitor group(Mdivi-1),Caspase1 inhibitor group(Caspase1),NLRP3 inhibitor group(NLRP3),5 animals per group.After drug intervention,HE staining,immunofluorescence,colorimetry,and WB method were used to observe the relevant indexes.Results Compared with group N,the structural damage of prostate gland was obvious in group M.Compared with the M group,the prostate gland structure in RAP group,Caspase-1 group and NLRP3 group were improved.However,that in 3-MA group and Mdivi-1 group was not improved,and even destroyed more obvi-ously.Compared with group N,the co-expression of LC3-II and LAMP-1 was enhanced,mitochondrial membrane potential was decreased,ROS release level was significantly increased in prostate tissue of rats in group M.Com-pared with the M group,the above indexes in RAP group and NLRP3 group were significantly improved.However,the above indexes in 3-MA group and Mdivi-1 group became worse.Compared with group N,the protein expressions of DRP1,PINK1 and Parkin in prostate mitochondria of rats in group M were increased,and the protein expres-sions of OPA1 was decreased.Compared with group M,the protein expressions of DRP1,PINK1 and Parkin in RAP group and NLRP3 group were significantly increased,while those in 3-MA group and Mdivi-1 group were sig-nificantly decreased.OPA1 protein expression was significantly decreased in the RAP group.The protein expression of Parkin in Caspase-1 group was decreased,but the protein expression of DRP1,OPA1 and PINK1 had no significant difference.Compared with group N,the protein expressions of LC3II/LC3I,Beclin1,NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β,and IL-18 in prostate tissue of rats in group M were increased,while the protein expres-sions of P62 was decreased.Compared with M group,LC3II/LC3I and Beclin1 protein expressions in RAP group and NLRP3 group were significantly increased,while those in 3-MA group and Mdivi-1 group were significantly decreased.Compared with M group,P62,NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β and IL-18 protein expressions in RAP group and NLRP3 group were significantly decreased,while those in 3-MA group and Mdivi-1 group were significantly increased.Compared with M group,the protein expressions of NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β,and IL-18 in Caspase-1 group were significantly reduced,but the protein expressions of LC3Ⅱ/LC3Ⅰ,Beclin1,and P62 were not statistically significant.Conclusions NLRP3 inflammatosome is involved in the progression of chronic prostatitis in EAP rats.Mitochondrial autophagy mediates the occurrence and development of prostatitis in EAP by regulating the activation of NLRP3 inflammasome in prostate tissue.

Objective To investigate the effect and mechanism of miR-155-5p targeting suppressor of cytokine signaling 1(SOCS1)in regulating the Janus kinase 2(JAK2)/signal transducer and activator of transcrip-tion 3(STAT3)signaling pathway in renal injury associated with lupus nephritis(LN).Methods Thirty female MRL-faslpr lupus model mice were randomly divided into five groups(n=6 per group):the model group,the antagomir NC group,the miR-155-5p antagomir group,the miR-155-5p antagomir+shRNA control group,and the miR-155-5p antagomir+SOCS1 shRNA group.The mice were treated with adeno-associated virus vectors carrying miR-155-5p antagomir,antagomir NC,SOCS1 shRNA,or shRNA control.Additionally,six age-matched C57BL/6 mice served as a control group and received an equivalent volume of saline.Serum blood urea nitrogen(BUN)and creatinine(Scr)levels,renal histopathological changes,and the expression levels of miR-155-5p,SOCS1,phosphorylated JAK2(p-JAK2),and phosphorylated STAT3(p-STAT3)in renal tissues were evaluated.Results Compared with the normal group,the model group exhibited significantly elevated levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins in the kidneys(P<0.01),while the expression level of SOCS1 was markedly reduced(P<0.01).Compared with both the model group and the antagomir NC group,the miR-155-5p antagomir group showed decreased levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins(P<0.01),along with a significant increase in SOCS1 expression(P<0.01).Similarly,compared with the miR-155-5p antagomir group and the miR-155-5p antagomir+shRNA control group,the miR-155-5p antagomir+SOCS1 shRNA group demon-strated significantly higher levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins(P<0.01),while SOCS1 expression was notably decreased(P<0.01).Renal pathology analysis revealed that,compared to the normal group,the model group exhibited glomerular atrophy,extensive infiltration of inflammatory cells in the renal tubulointerstitial region,and partial renal tubular necrosis.In contrast,the miR-155-5p antagomir group showed marked improvements in glomerular atrophy,tubular necrosis,and inflammatory cell infiltration compared with the model group and antagomir NC group.Furthermore,compared with the miR-155-5p antagomir group and the miR-155-5p antagomir+shRNA control group,the miR-155-5p antagomir+SOCS1 shRNA group exhibited more severe glomerular atrophy,tubular necrosis,and inflammatory cell infiltration.Conclusion MiR-155-5p exacerbates renal damage in MRL-faslpr lupus model mice by targeting SOCS1,potentially through the activation of the JAK2/STAT3 signaling pathway.

Objective The pathogenesis of EAP in rats based on the TLR4/NF-κB-NLRP3 inflammasome signaling pathway was explored.Methods Randomly divide 12 male SD rats into 4 groups using the number table,namely normal group(N),model group(M),Caspase-1 inhibitor group(Caspase-1),and NLRP3 inhibitor MCC950 group(NLRP3),with 3 rats in each group.After drug intervention,relevant indicators were observed by using HE staining,ELISA,WB methods.Results Compared with the N group,the M group rats had showed significant damage in prostate gland structure and infiltration of inflammatory cells.Compared with group N,the expression of TLR4,P-NF-κB P65,NLRP3,ASC,Cleaced-Caspase-1,Cleaced-IL-1β,and IL-18 proteins in the prostate tissue of group M rats had increased(P<0.01).Compared with group M,the expression of TLR4,P-NF-κB P65,NLRP3,ASC,Cleaced-Caspase-1,Cleaced-IL-1β,and IL-18 proteins in the NLRP3 and Caspase-1 groups had significantly reduced(P<0.01).The serum levels of IL-1 β,IL-6,IL-8,IL-17A,IL-18,IFN-γ,and TNF-α in group M rats had been significantly higher than those in group N(P<0.01).But the serum levels of IL-10 had been slightly lower and no statistical significance.The serum levels of IL-1β,IL-6,IL-8,IL-17A,IL-18,IFN-γ,and TNF-α in group M rats had been lower than those in group N(P<0.01 or P<0.05),the serum IL-10 level had increased(P<0.01).Conclusion The activation of TLR4/NF-κB-NLRP3 inflammasome signaling path-way promotes the occurrence and development of prostatitis in EAP rats.

Objective To investigate the mechanism of mitochondrial autophagy regulating the expression of NLRP3 inflammasome in prostate tissue in experimental autoimmune prostatitis(EAP)rats and to provide a theoretical basis for the study of new drug development.Methods A numerical table of 40 SD male rats was randomly divided into 8 groups.Namely,normal group(N),model group(M),rapamycin group(RAP),rapamycin+mitochondrial autophagy inhibitor group(RAP+Mdivi-1),autophagy inhibitor group(3MA),mitochondrial autophagy inhibitor group(Mdivi-1),Caspase1 inhibitor group(Caspase1),NLRP3 inhibitor group(NLRP3),5 animals per group.After drug intervention,HE staining,immunofluorescence,colorimetry,and WB method were used to observe the relevant indexes.Results Compared with group N,the structural damage of prostate gland was obvious in group M.Compared with the M group,the prostate gland structure in RAP group,Caspase-1 group and NLRP3 group were improved.However,that in 3-MA group and Mdivi-1 group was not improved,and even destroyed more obvi-ously.Compared with group N,the co-expression of LC3-II and LAMP-1 was enhanced,mitochondrial membrane potential was decreased,ROS release level was significantly increased in prostate tissue of rats in group M.Com-pared with the M group,the above indexes in RAP group and NLRP3 group were significantly improved.However,the above indexes in 3-MA group and Mdivi-1 group became worse.Compared with group N,the protein expressions of DRP1,PINK1 and Parkin in prostate mitochondria of rats in group M were increased,and the protein expres-sions of OPA1 was decreased.Compared with group M,the protein expressions of DRP1,PINK1 and Parkin in RAP group and NLRP3 group were significantly increased,while those in 3-MA group and Mdivi-1 group were sig-nificantly decreased.OPA1 protein expression was significantly decreased in the RAP group.The protein expression of Parkin in Caspase-1 group was decreased,but the protein expression of DRP1,OPA1 and PINK1 had no significant difference.Compared with group N,the protein expressions of LC3II/LC3I,Beclin1,NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β,and IL-18 in prostate tissue of rats in group M were increased,while the protein expres-sions of P62 was decreased.Compared with M group,LC3II/LC3I and Beclin1 protein expressions in RAP group and NLRP3 group were significantly increased,while those in 3-MA group and Mdivi-1 group were significantly decreased.Compared with M group,P62,NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β and IL-18 protein expressions in RAP group and NLRP3 group were significantly decreased,while those in 3-MA group and Mdivi-1 group were significantly increased.Compared with M group,the protein expressions of NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β,and IL-18 in Caspase-1 group were significantly reduced,but the protein expressions of LC3Ⅱ/LC3Ⅰ,Beclin1,and P62 were not statistically significant.Conclusions NLRP3 inflammatosome is involved in the progression of chronic prostatitis in EAP rats.Mitochondrial autophagy mediates the occurrence and development of prostatitis in EAP by regulating the activation of NLRP3 inflammasome in prostate tissue.

Objective The pathogenesis of EAP in rats based on the TLR4/NF-κB-NLRP3 inflammasome signaling pathway was explored.Methods Randomly divide 12 male SD rats into 4 groups using the number table,namely normal group(N),model group(M),Caspase-1 inhibitor group(Caspase-1),and NLRP3 inhibitor MCC950 group(NLRP3),with 3 rats in each group.After drug intervention,relevant indicators were observed by using HE staining,ELISA,WB methods.Results Compared with the N group,the M group rats had showed significant damage in prostate gland structure and infiltration of inflammatory cells.Compared with group N,the expression of TLR4,P-NF-κB P65,NLRP3,ASC,Cleaced-Caspase-1,Cleaced-IL-1β,and IL-18 proteins in the prostate tissue of group M rats had increased(P<0.01).Compared with group M,the expression of TLR4,P-NF-κB P65,NLRP3,ASC,Cleaced-Caspase-1,Cleaced-IL-1β,and IL-18 proteins in the NLRP3 and Caspase-1 groups had significantly reduced(P<0.01).The serum levels of IL-1 β,IL-6,IL-8,IL-17A,IL-18,IFN-γ,and TNF-α in group M rats had been significantly higher than those in group N(P<0.01).But the serum levels of IL-10 had been slightly lower and no statistical significance.The serum levels of IL-1β,IL-6,IL-8,IL-17A,IL-18,IFN-γ,and TNF-α in group M rats had been lower than those in group N(P<0.01 or P<0.05),the serum IL-10 level had increased(P<0.01).Conclusion The activation of TLR4/NF-κB-NLRP3 inflammasome signaling path-way promotes the occurrence and development of prostatitis in EAP rats.

Objective To investigate the effect and mechanism of miR-155-5p targeting suppressor of cytokine signaling 1(SOCS1)in regulating the Janus kinase 2(JAK2)/signal transducer and activator of transcrip-tion 3(STAT3)signaling pathway in renal injury associated with lupus nephritis(LN).Methods Thirty female MRL-faslpr lupus model mice were randomly divided into five groups(n=6 per group):the model group,the antagomir NC group,the miR-155-5p antagomir group,the miR-155-5p antagomir+shRNA control group,and the miR-155-5p antagomir+SOCS1 shRNA group.The mice were treated with adeno-associated virus vectors carrying miR-155-5p antagomir,antagomir NC,SOCS1 shRNA,or shRNA control.Additionally,six age-matched C57BL/6 mice served as a control group and received an equivalent volume of saline.Serum blood urea nitrogen(BUN)and creatinine(Scr)levels,renal histopathological changes,and the expression levels of miR-155-5p,SOCS1,phosphorylated JAK2(p-JAK2),and phosphorylated STAT3(p-STAT3)in renal tissues were evaluated.Results Compared with the normal group,the model group exhibited significantly elevated levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins in the kidneys(P<0.01),while the expression level of SOCS1 was markedly reduced(P<0.01).Compared with both the model group and the antagomir NC group,the miR-155-5p antagomir group showed decreased levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins(P<0.01),along with a significant increase in SOCS1 expression(P<0.01).Similarly,compared with the miR-155-5p antagomir group and the miR-155-5p antagomir+shRNA control group,the miR-155-5p antagomir+SOCS1 shRNA group demon-strated significantly higher levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins(P<0.01),while SOCS1 expression was notably decreased(P<0.01).Renal pathology analysis revealed that,compared to the normal group,the model group exhibited glomerular atrophy,extensive infiltration of inflammatory cells in the renal tubulointerstitial region,and partial renal tubular necrosis.In contrast,the miR-155-5p antagomir group showed marked improvements in glomerular atrophy,tubular necrosis,and inflammatory cell infiltration compared with the model group and antagomir NC group.Furthermore,compared with the miR-155-5p antagomir group and the miR-155-5p antagomir+shRNA control group,the miR-155-5p antagomir+SOCS1 shRNA group exhibited more severe glomerular atrophy,tubular necrosis,and inflammatory cell infiltration.Conclusion MiR-155-5p exacerbates renal damage in MRL-faslpr lupus model mice by targeting SOCS1,potentially through the activation of the JAK2/STAT3 signaling pathway.

Objective Taking Sortilin as the entry point,this study aims to explore the mechanism of vascular calcification in chronic renal failure(CRF)and explore the influence of Sanqi on Sortilin,TLRs and vascular calcification,and to provide an effective method for clinical reduction of cardiovascular events in CRF.Methods Thirty-six male SD rats were randomly divided into normal group,model group,low-,medium-and high-dose Sanqi group and calcitriol group,with 6 rats in each.The replicative CRF vascular calcification rat model was fed with adenine combined with high phosphorus diet.Aortic calcium salt deposition,serum creatinine(Scr),urea nitrogen(BUN),blood calcium(Ca),blood phosphorus(P),total cholesterol(TC),triglyceride(TG),TLRs and Sortilin protein in aorta and inflammatory factors were detected.Results In the model group,renal fibrosis was obvious and many adenine crystals were found in renal interstitium.Large deposits of calcium salts were found.Renal fibrosis and calcium salt deposition were alleviated in different degrees in all treatment groups.Compared with those in the normal group,the level of BUN,Cr,P,TG,TC,IFN-γ,IL-6,IL-10 and IL-17A in the serum of the model group was ascended(P<0.01),while the level of Ca was descended(P<0.01).Compared with those in the model group,the level of BUN,Cr,P,TG,TC,IFN-γ,IL-6,IL-10 and IL-17A in the serum of rats in the Sanqi medium and high dose group and calcitriol group was significantly decreased(P<0.01),and the contents of Ca were significantly increased(P<0.05 or P<0.01).Compared with those in the normal group,the protein expression of BMP2,RUNX2,Sortilin,TLR7 and TLR9 in aortic tissue of rats in the model group was elevated(P<0.01),while the protein expression of SM22α was declined(P<0.01).Compared with those in the model group,the protein expression of BMP2,RUNX2,Sortilin,TLR7,and TLR9 in the low-,medium-,and high-dose Sanqi group and calcitriol group was decreased significantly(P<0.01);the protein expression of SM22α was increased significantly(P<0.05 or P<0.01),and the high-dose Sanqi group and calcitriol group had more significant effects.Conclusion Sanqi can improve renal fibrosis and vascular calcification in CRF model rats,and its mechanism may be related to the regulation of biological functions of Sortilin and TLRs.

Objective To evaluate the dosimetric characteristics of base dose plan compensation (BDPC) optimization method applied on the intensity-modulated radiotherapy (IMRT) for upper esophageal carcinoma,based on the Eclipse treatment planning system.Methods Nineteen patients were included.For each case initial IMRT plan was generated and further optimized respectively by the two following methods:the BDPC method and hot and cold spot control (HCSC) method.Then the BDPC and HCSC plans were compared concerning planning-target-volume (PTV) coverage,conformity index (CI),and homogeneity index (HI),as well as organ-at-risk (OAR) sparing,planning time,monitor unit (MU) and delivery time.Results Compared with the HCSC plans,the BDPC plans provided superior CI and HI (Z =-3.662,-3.745,P ＜ 0.05),as well as lower D2％ (near-maximum dose) (Z =-3.823,P ＜ 0.05) and comparable D98％ (near-minimum dose) (P ＞ 0.05) for PTV64 (high-risk PTV),and provided superiorCI (Z=-3.340,P＜0.05),lower D95％ and D98％ (Z=-3.582,-2.616,P＜0.05) for PTV54 (low-risk PTV).The BDPC plans also provided slightly lower doses to the spinal cord and lung compared with the HCSC plans (Z =-3.625--3.369,P ＜ 0.05).Moreover,the planning time [(26.05 ±0.88) min] for BDPC plans was less than that of the HCSC plans [(33.73 ± 3.24) min] (Z =-3.823,P ＜0.05).The MU of the BDPC plans (1 019 ± 167) was higher than that of the HCSC plans (1 003 ±159) (Z=-2.616,P＜0.05),while the delivery time [(3.52 ±0.29) min] was more than that of the HCSC plans [(3.50±0.28) min] (Z=-2.548,P＜0.05).Conclusions The BDPC optimization method can significantly improve target dose homogeneity and conformity with effective reduction of the dose to OARs for upper esophageal carcinoma.Moreover,it is simple and can improve the treatment planning efficiency.

Objective To evaluate open and endovascular procedures for the treatment of visceral arterial naeurysms.Methods Clinical data of 93 cases were reviewed from Jan 2001 to Jan 2011,including 47 males,and 46 females.Splenic artery aneurysm in 45 cases,superior mesenteric artery aneurysm in 15 cases,renal artery aneurysms in 10 cases,common hepatic artery aneurysm in 7,celiac artery aneurysms in 11 and gastroduodenal artery aneurysm in 5 cases.All cases had either open procedures or endovascular procedures after comprehensive evaluation.Results Surgical open procedures were performed on 34 cases,and endovascular procedures were performed on 59 cases.The perioperative complication rate were 52.9％ and 13.6％ for open and endovascular groups respectively.The mean follow-up time was 36.8 months ( 11 months to 10 years).1 -year survival rate and 5-year survival rate were 100％and 60.6％ in open surgery group,compared with 100％ and 84.5％ in endovascular group.Conclusions Endovascular repair is effective for visceral artery aneurysm with lower perioperative complication rate and better long-term survival rate.