High-flow priapism due to bilateral cavernous artery fistulas treated by unilateral embolization:A case report

BACKGROUND High flow priapism(HFP)is a rare type of priapism.Perineal trauma is the most common cause of HFP.Trauma-induced penile artery injury may lead to an arterial-cavernosal fistula,whereas persistent irregular arterial blood flow entering the corpora cavernosum can cause a persistent penile erection.The routine treatment of HFP focuses on addressing the abnormal penile erectile status and avoiding post-treatment erectile dysfunction.Interventional embolization is an important therapeutic modality for HFP,and bilateral embolization therapy is currently the most commonly used technique for patients with bilateral cavernous artery fistulas;however,unilateral embolization therapy has yet to be reported.CASE SUMMARY Herein,we report of the case of a 26-year-old Chinese male who presented with a persistent abnormal erection for 12 h after perineal impact injury.Medical history,cavernous arterial blood gas analysis and radiological examinations led to a diagnosis of HFP caused by bilateral cavernous artery fistulas.We performed routine conservative treatment(compression therapy and ice application)for the patient after admission;however,10 d later,his symptoms had not been relieved.After completion of the preoperative workup,right(severe side)selective perineal artery embolization was performed;the left cavernous artery fistula was left untreated.After postoperative continuation of conservative treatment for 72 h,the patient experienced complete penile thinning.The patient had no symptoms of erectile dysfunction over a follow-up period of 12 mo.CONCLUSION Compared with bilateral cavernous artery fistula embolization,we believe that unilateral cavernous artery fistula embolization can achieve positive clinical efficacy and reduce the risk of postoperative erectile dysfunction secondary to penile ischemia.

Alleviation of acute pancreatitis-associated lung injury by inhibiting the p38 mitogen-activated protein kinase pathway in pulmonary microvascular endothelial cells

BACKGROUND Previous reports have suggested that the p38 mitogen-activated protein kinase signaling pathway is involved in the development of severe acute pancreatitis(SAP)-related acute lung injury(ALI).Inhibition of p38 by SB203580 blocked the inflammatory responses in SAP-ALI.However,the precise mechanism associated with p38 is unclear,particularly in pulmonary microvascular endothelial cell(PMVEC)injury.AIM To determine its role in the tumor necrosis factor-alpha(TNF-α)-induced inflammation and apoptosis of PMVECs in vitro.We then conducted in vivo experiments to confirm the effect of SB203580-mediated p38 inhibition on SAP-ALI.METHODS In vitro,PMVEC were transfected with mitogen-activated protein kinase kinase 6(Glu),which constitutively activates p38,and then stimulated with TNF-α.Flow cytometry and western blotting were performed to detect the cell apoptosis and inflammatory cytokine levels,respectively.In vivo,SAP-ALI was induced by 5%sodium taurocholate and three different doses of SB203580(2.5,5.0 or 10.0 mg/kg)were intraperitoneally injected prior to SAP induction.SAP-ALI was assessed by performing pulmonary histopathology assays,measuring myeloperoxidase activity,conducting arterial blood gas analyses and measuring TNF-α,interleukin(IL)-1βand IL-6 levels.Lung microvascular permeability was measured by determining bronchoalveolar lavage fluid protein concentration,Evans blue pulmonary cells was confirmed by performing a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling analysis and examining the Bcl2,Bax,Bim and cle-caspase3 levels.The proteins levels of P-p38,NFκB,IκB,P-signal transducer and activator of transcription-3,nuclear factor erythroid 2-related factor 2,HO-1 and Myd88 were detected in the lungs to further evaluate the potential mechanism underlying the protective effect of SB203580.RESULTS In vitro,mitogen-activated protein kinase(Glu)transfection resulted in higher apoptotic rates and cytokine(IL-1βand IL-6)levels in TNF-α-treated PMVECs.In vivo,SB2035080 attenuated lung histopathological injury,decreased inflammatory activity(TNF-α,IL-1β,IL-6 and myeloperoxidase)and preserved pulmonary function.Furthermore,SB203580 significantly reversed changes in the bronchoalveolar lavage fluid protein concentration,Evans blue accumulation,terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cell numbers,apoptosis-related proteins(cle-caspase3,Bim and Bax)and endothelial microstructure.Moreover,SB203580 significantly reduced the pulmonary P-p38,NFκB,P-signal transducer and activator of transcription-3 and Myd88 levels but increased the IκB and HO-1 levels.CONCLUSION p38 inhibition may protect against SAP-ALI by alleviating inflammation and the apoptotic death of PMVECs.

Coupling effect of the conductivities of Li ions and electrons by introducing LLTO@C fibers in the LiNi0.8Co0.15Al0.05O2 cathode

To probe the coupling effect of the electron and Li ion conductivities in Ni-rich layered materials(LiNi0.8Co0.15Al0.05O2,NCA),lithium lanthanum titanate(LLTO)nanofiber and carbon-coated LLTO fiber(LLTO@C)materials were introduced to polyvinylidene difluoride in a cathode.The enhancement of the conductivity was indicated by the suppressed impedance and polarization.At 1 and 5 C,the cathodes with coupling conductive paths had a more stable cycling performance.The coupling mechanism was analyzed based on the chemical state and structure evolution of NCA after cycling for 200 cycles at 5 C.In the pristine cathode,the propagation of lattice damaged regions,which consist of high-density edge-dislocation walls,destroyed the bulk integrity of NCA.In addition,the formation of a rock-salt phase on the surface of NCA caused a capacity loss.In contrast,in the LLTO@C modified cathode,although the formation of dislocation-driven atomic lattice broken regions and cation mixing occurred,they were limited to a scale of several atoms,which retarded the generation of the rock-salt phase and resulted in a pre-eminent capacity retention.Only NiO phase“pitting”occurred.A mechanism based on the synergistic transport of Li ions and electrons was proposed.

C型槽参数对NACA0009翼型间隙流动的影响

间隙流动广泛存在于流体机械转子位置,其存在会直接影响内部流态的稳定性,降低效率的同时降低水力机械的寿命。该文采用数值计算方法研究了C型槽对NACA0009翼型叶顶间隙泄漏涡的抑制机理,并使用正交试验法对C型槽的槽数、槽宽、槽深和内侧面偏斜角度对翼型的影响进行了研究。研究结果表明:C型槽产生低速涡流,有效降低了间隙位置泄漏流的流速,从而抑制高速泄漏流的产生,且C型槽深度和偏斜角度的选取对于翼型的水动力性能影响较大。并借助正交试验结果提出了两种最优C型槽设置方法,有效抑制了间隙泄漏涡。