ObjectiveTo evaluate the efficacy of intra-arterial chemotherapy (IAC) for advanced retinoblastoma (RB) after failure of intravenous chemotherapy (IVC). MethodsFifteen eyes of 13 patients with advanced RB were treated with IAC (1-5 cycles) after failure of IVC (2-8 cycles). The patients included 10 boys and 3 girls, with the mean age of (15.67±8.16) months. Six patients had bilateral RB and 7 patients had unilateral RB. There were 14 eyes (93.33%) in stage D, 1 eye (6.67%) in stage E according to the International Classification of intraocular retinoblastoma. The main reasons for failure of IVC were recurrent primary tumor in 3 eyes (20.00%), subretinal seeds recurrence in 9 eyes (60.00%), viable vitreous seeds in 2 eyes (13.33%) and poor response of primary tumor in 1 eye (6.67%). The mean interval between IVC completion and IAC start was 3 months. The mean follow-up was 19 months (ranged from 3 to 52 months). ResultsAfter IVC and secondary IAC, the retinoblastoma and seeds were regressed in 12 eyes (80.00%). Three eyes required enucleation for severe vitreous seeds, subretinal seeds recurrence and primary tumor recurrence. There was no evidence of metastasis in any case. ConclusionIAC can achieve high global salvage rate (80.00%) for patients with advanced retinoblastoma after failure of IVC.
Objective To observe the influence of resveratrol on superoxide dismutase (SOD), malondialdehyde (MDA), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) of intestinal mucosal ischemia-reperfusion injury protection in rats with severe acute pancreatitis (SAP). Methods Fifty-four rats were divided into three groups randomly: sham operation group (SO group), SAP model group (SAP group) and resveratrol-treated group (Res group). SAP model was made by injecting sodium taurocholate 50 mg/kg to pancreatic bile duct and resveratrol was given intravenously at 5 min after inducing SAP model. The rats were sacrificed at 3 h, 6 h and 12 h after inducing SAP model respectively by equal number. The levels of MDA, SOD, ICAM-1 and VCAM-1 and histological changes of small intestine were measured. Results The level of MDA in small intestine tissue in SAP group was significantly higher than that in SO group (P＜0.05), while the activity of SOD was significantly lower in the relevant tissues (P＜0.05). The expressions of ICAM-1 and VCAM-1 in SAP group were higher than those of SO group (P＜0.05). The activity of SOD in small intestine tissue in Res group was significantly higher than that in SAP group (P＜0.05); while the level of MDA was significantly lower in the relevant tissues (P＜0.05). The expressions of ICAM-1 and VCAM-1 in Res group were lower than those of SAP group (P＜0.05). Conclusions Oxygen free radicals are concerned with the process of pathological changes in intestinal mucosal ischemia-reperfusion in rats with SAP. Resveratrol might increase SOD activity and decrease MDA level to attenuate lipid peroxidation in small intestine of SAP, and reduce the expressions of ICAM-1 and VCAM-1 in intestine, thus diminish the damage of the intestine in SAP. And it acts as a protective effect to small intestinal ischemia-reperfusion injury.
Objective To evaluate the phenomena of apoptosis and its relevant mechanism during ischemia-reperfusion period. Methods The published papers to explore the apoptotic phenomena and its mechanism in organs or tissues which experienced ischemia-reperfusion injury were reviewed. Results Apoptosis was common in ischemia-reperfusioned organ or tissue. The severity of apoptosis was influenced by many factors such as ischemia, hypoxia, oxygen free radials, intracellular free calcium ion overloading, various cytokines, et al; and also was regulated by bcl-2 family, caspase family and NF-κB，et al. Conclusion Apoptosis is a common phenomenum in ischemiareperfusioned organ or tissue which is affected and regulated by various factors.
Objective To investigate the expression of nuclear factor (NF)-κB and intercellular adhesion molecule (ICAM)-1 in rat′s retina injured by ischemia-reperfusion, and the effect of pyrrolidine dithiocarbamate (PDTC) on the expression of NF-κB and ICAM-1. Method The model of retinal ischemia-reperfusion was set up in 60 SD rats, which were divided into two groups with 30 rats in each: ischemia-reperfusion group and ischemia-reperfussion with injection of PDTC group. The left cephalic artery of each rat was ligated, and the right side was the control. Every group was subdivided into group 1 hour, 6, 12, 24, 48, and 72 hours after ischemia-reperfusion injury, and with 5 rats in each group. mRNA of NF-κB and ICAM-1 mRNA was measured by in situ hybridization (ISH) method in rat′s retina. Every rat underwent electroretinography (ERG) at the corresponding time before executed by neck breaking. Results In ischemia-reperfusion group, expression of NF-κB and ICAM-1 was detected at the 6th hour after ischemia-reperfusion, reached the highest level at the 24th hour, and weakened gradually later. In ischemia-reperfusion with injection of PDTC group, expression of NF-κB and ICAM-1 was detected at the 12th hour after ischemia-reperfusion, and reached the highest level at the 24th hour but lower than that in ischemia-reperfusion group. No expression of NF-κB and ICAM-1 was found in the control group. The relative recovery rate of ERG a and b wave amplitude in ischemia-reperfusion groups was lower than that in ischemia-reperfusion with injection of PDTC group at every stage(P＜0.01 ). The lowest relative recovery rate of ERG a and b wave amplitude in different stages in both of the 2 groups was at the 24th hour(P＜0.01). Conclusions NF-κB and ICAM-1 may play an important role in retinal ischemia-reperfusion injury, as the inhibitor of NF-κB, PDTC may relieve the retinal ischemia-reperfusion injury. (Chin J Ocul Fundus Dis，2004，20：175-178)
The high incidence and mortality rates existed in chronic pulmonary thromboembolism(PTE), with considerable misdiagnosis and missed diagnosis rate. The prognosis for patients with chronic thromboembolic pulmonary hypertension was poor with medical therapy. But the pulmonary thromboendarterectomy was well established.The postoperative pulmonary hypertension and reperfusion pulmonary edema are main complications and death causes. The key management after pulmonary thromboendarterectomy is important which decreases pulmonary hypertension , and prevents reperfusion pulmonary edema and re thromboembolism.
ObjectiveTo observe the effect of Crocin on structure and the expression of tumor necrosis factor-alpha; (TNF-alpha;) and interleukin-1beta; (IL-1beta;) in rat retina after injury by ischemia-reperfusion. Methods A total of 80 Sprague-Dawley male rats at the age of 8 -10 weeks were divided into control group, model group, low-dose Crocin group and high-dose Crocin group, with 20 rats in each group. The rats of control group were not treated. The rats in model, low-dose Crocin and high-dose Crocin group were induced with normal saline by anterior chamber perfusion creating a retinal ischemia-reperfusion (RIR) model. The rats of the low-dose Crocin and highdose Crocin group received intraperitoneal injection with different doses of Crocin solution (5 mg/kg, or 50 mg/kg) 30 minutes prior to ischemic injury and one time per day after successful RIR. Optical microscopy was used to observe the retinal structure. Enzymelinked immunosorbent assay (ELISA) was used to measure the expression of TNF-alpha; and IL-1beta; 6, 12, 24 and 48 hours after RIR. ResultsThe retinal structure of control group was normal. Pathological changes were found in the RIR model and low-dose Crocin group, such as retinal edema, disorganized structure and loosely packed cells. The degree of pathological changes in lowdose Crocin group was less than the RIR model group. The retinal structure of high-dose Crocin group was similar to the control group. The expression of TNF-alpha; was the highest at 24 hours after modeling, while the expression of IL-1beta; was the highest at 12 and 48 hours after RIR modeling. Six, 12, 24 and 48 hours after RIR modeling, compared with the control group, the TNF-alpha; expression of model (t=5.42, 7.94, 9.32, 9.18;P＜0.05 ), low-dose Crocin (t=3.94, 4.12, 4.98, 3.84;P＜0.05) and high-dose Crocin group (t=2.13, 2.34, 2.96, 2.78;P＞0.05) were increased. Compared with the RIR model group, the TNF-alpha; expression of low-dose Crocin (t=3.95, 4.56, 4.01, 5.12) and high-dose Crocin group (t=5.23, 7.65, 7.74, 7.63) was decreased. Compared with the control group, the IL-1beta; expression of model (t=7.23, 7.87, 7.15, 15.60), low-dose Crocin (t=5.65, 5.10, 5.54, 6.87;P＜0.05) and high-dose Crocin group (t=4.38, 5.21, 4.56, 4.75) was increased (P＜0.05). Compared with the model group, the IL-1beta; expression of low.dose Crocin group was decreased significantly 48 hours after RIR modeling (t=7.56,P＜0.05); but it decreased significantly at each time point in high-dose Crocin group (t=6.94, 5.36, 6.05, 10.50;P＜0.05). Conclusion Crocin can improve the retinal pathologic changes, while down-regulating TNF-alpha; and IL-1beta; expression in RIR rats.
ObjectiveTo investigate the protective effects of glycine on rat sinusoidal endothelial cells (SECs) after hepatic warm ischemiareperfusion and its mechanism.MethodsSeventytwo male SD rats were randomly divided into the normal control,ischemiareperfusion,glycine plus strychnine treated and glycine treated groups. The changes of endothelin (ET),hyaluronic acid (HA),tumor necrosis factorα (TNFα) content and alanine aminotransterase (ALT), superoxide dismutase (SOD) activity as well as morphology of SECs under light microscope were observed at the time point 1,3,24 h after hepatic reperfusion. The effects of glycine on the above parameters were also observed. ResultsThe group using glycine treated, the abnormal changes of all above parameters were improved remarkably (P＜0.01 or P＜0.05). Strychnine can antagonize these effects partly.ConclusionGlycine can prevent the injury to rat SECs after hepatic warm ischemiareperfusion.It most likely acts through glycine receptor on SECs and Kupffer cells.
Objective To evaluate the clinical efficacy of two-stage retrograde hybrid repair for acute aortic dissection involving the aortic arch complicated with distal malperfusion syndrome. Methods From May 2019 to December 2022, the patients presented with acute aortic dissection involving the aortic arch complicated with distal malperfusion syndrome treated in the Department of Cardiovascular Surgery of West China Hospital, Sichuan University were enrolled. After preoperative evaluation, all patients underwent priority emergency interventional surgery to improve distal malperfusion, and then underwent two-stage hybrid surgery to repair proximal aortic lesions. The perioperative clinical and imaging data were retrospectively analyzed. Results Five patients were collected, including 4 males and 1 female, with a median age of 58 years. The main manifestations were lower limb ischemia and renal insufficiency in 3 patients, and poor intestinal perfusion in 2 patients. All patients were given priority to interventional surgery to implant graft stents or bare stents and necessary branch artery intervention, and then successfully performed two-stage hybrid surgery, including type Ⅰhybrid surgery for 2 patients, type Ⅱ hybrid surgery for 1 patient and type Ⅲ hybrid surgery for the other 2 patients, with a success rate of 100.0%. All patients were discharged successfully, and the function of the organs with poor perfusion returned to normal. Only 1 patient recovered to grade 4 muscle strength of the diseased lower limbs upon discharge. No adverse events such as amputation, exploratory laparotomy and intestinal resection or long-term hemodialysis occurred. Conclusion The application of two-stage retrograde hybrid repair in the surgical treatment of acute aortic dissection involving the aortic arch complicated with distal malperfusion syndrome is safe and effective, and is helpful to improve the perioperative survival rate, and clinical outcomes of such patients.
Objective To study the effect of Kupffer cell on the liver ischemia/reperfusion injury.Methods The literature in recent years on the liver ischemia/reperfusin injury were reviewed.Results The activated kupffer cell can generate and release a variety of soluble toxic mediators, affect the liver microcirculation directly or indirectly. Conclusion Kupffer cell have important effect on liver ischemia/reperfusion injury.
ObjectiveTo summarize the research advances of pyroptosis in hepatic ischamia-reperfusion injury (IRI).MethodThe literatures about the studies of mechanism of pyroptosis in hepatic IRI were retrieved and analyzed.ResultsPyroptosis, also known as inflammatory necrocytosis, was proven to play an important role in the hepatic IRI. When hepatic ischemia-reperfusion occurred, the classical pathway of pyroptosis dependenting on caspase-1 and the non-classical pathway of pyroptosis dependenting on caspase-11 were initiated by specific stimulants, and leaded to the activation of gasdermin D, releases of proinflammatory factors such as interleukin-1β, interleukin-18, etc., and the recruitment and activation of neutrophils. Consequently, pyroptosis caused more severe hepatic inflammation and aggravated existing cell injury and dysfunction of liver during hepatic IRI.ConclusionsPyroptosis plays an important role in liver IRI. Further researches about mechanism of pyroptosis will be beneficial to the prevention and treatment of the pyroptosis of related diseases.