BackgroundDiabetic retinopathy (DR) associated with this disease closely approximates the oxidative damage inflicted on retinal pigment epithelial (RPE) cells by high glucose,in recent years,people devote themselves to the protection of RPE cells extensively.ObjectiveTo investigate the protective effect of pancreatic β MIN-6 cells on retinal pigment epithelial(RPE) cells from high glucose-induced damage.MethodsRPE cells were incubated with normal medium for 4 d and divided into 3 groups:normal glucose group,high glucose group and MIN-6 cells group.RPE cell were exposed with 5 mmol/L normal glucose in normal glucose group,exposed with 30 mmol/L high glucose in high glucose group,and exposed with 5 × 104 MIN-6 cells and 30 mmol/L high glucose in MIN-6 cells group.After 24 h,cell viability of RPE cells was determined by MTT cell viability assay.Results More than 95％ cells showed the brown staining by ABC method.After incubation for another 24 hours,the A550 value was 0.44±0.02,0.30±0.01 and 0.41±0.01 in the normal glucose group,high glucose group and MIN-6 cells group respectively with a significant difference among these three groups (F =19.94,P＜ 0.01 ).The A55o value was significantly higher in the normal glucose group and the MIN-6 cells group compared with the high glaucose group (t =6.85,5.62,P＜0.01 ).The survival rate of RPE cells in the normal glucose group was(97.5±3.3 )％,and that in the high glucose group was ( 68.2 ± 4.5 ) ％,showing significant difference between them ( t =11.30,P＜0.01 ).ConclusionsHigh glucose-induced damage of RPE cells is abrogated,and MIN-6 cells can protect RPE cells from high glucose-induced damage.

We present a case of Marfan's syndrome with acute aortic dissection during the trimester of her pregnancy, who underwent a Bentall operation 2 days after emergency cesarean section. A 24-year-old woman during the 31st week of pregnancy visited our emergency room due to sudden onset of chest and back pain, though she had no abnormality until this event. Because of her tall height, spider fingers, positive wrist sign, visual disorder and scoliosis, she was given a diagnosis of Marfan's syndrome. Enhanced CT and cardiac ultrasonography revealed that she was suffering from acute aortic dissection with annulo-aortic ectasia. Since it was difficult for her to continue with her pregnancy, she underwent emergency cesarean section and gave birth to a male baby weighted 1, 706g. Although there was little likelifood of early thrombus formation in the false lumen or significant aortic regurgitation indicating an emergency operation, fear of massive bleeding from her uterus and the exfoliated surface of the placenta after cesarean section required an observation period of 2 days. We performed a Bentall operation successfully after careful sedation, ventilation and blood pressure control for 2 days.

Protein C (PC) deficiency is an inherited thrombotic disorder with a prevalence of 0.19% among the general population. PC deficiency is associated with an increased risk of thrombosis when other risk factors are present, such as trauma, surgery, or infection, and is an important cause of mechanical valve thrombosis. We performed tricuspid valve replacement with a 29mm Carpentier-Edwards Perimount valve in a 20-year-old man with PC deficiency. The patient had corrected transposition of the great vessels with severe tricuspid insufficiency, as well as a history of cerebral infarction. In the perioperative period, we used only heparin sodium as the anticoagulant. When we restarted administration of warfarin, changing over from heparin, transient increases of serum plasmin inhibitor-plasmin complex (PIC) and thrombin antithrombin complex (TAT) levels were observed. Despite an increased dose of heparin, an appropriate activated partial thromboplastin time (APTT) was not obtained. This suggested a hypercoagulatory state, but the postoperative course was uneventful. Management of perioperative anticoagulation, prevention of late thrombotic events, and prosthetic valve selection in this particular situation are discussed.

A 56-year-old woman suffering from mitral stenosis had underwent PTMC (percutaneous transvenous mitral commissurotomy) at age 46. After she developed congestive heart failure, mitral valve replacement (MVR) with Carbomedics 29M and tricuspid annuloplasty (TAP) was carried out. Four hours after admission to the ICU, massive bleeding was noticed. Cardiopulmonary bypass was restarted in the operating room. Laceration and hematoma were found at the posterolateral wall of the left ventricle. Under cardiac arrest with removal of the prosthetic valve, an internal tear was detected about 2cm below the anterolateral commissure (Miller Type III). The tear was covered with a horse pericardial patch (2×3cm) using 6-0 running sutures with reinforcement with gelatin-resorcine-formaline (GRF) glue between the laceration and the patch. MVR sutures in the annulus above the ventricular tear were first passed through the annulus, the pericardial patch and then the prosthetic cuff. Additionally, an epicardial tear was covered and reinforced with the fibrin sheet, GRF glue and pericardial patch in turn. Cardiopulmonary bypass was weaned easily without bleeding. The patient was intentionally on respiratory support with sedation for 3 days. The subsequent postoperative course was uneventful.

A man in his 70s was transported to our hospital for acute exacerbation of chronic kidney disease. After arrival, he began having visual hallucinations, which were attributed to cognitive decline. We subsequently found that he had been taking amantadine 100 mg/day prescribed by another hospital. We thought that the visual hallucinations were caused by overdose of amantadine and discontinued the drug. Since abrupt discontinuation of antiparkinsonian drugs has a risk of neuroleptic malignant syndrome, tapering the dosage is desirable in most cases. However, the half-life of amantadine in patients with severe renal dysfunction is estimated to be 7-10 days, and thus the blood concentration of amantadine can be inferred to decrease slowly. Therefore, we chose to discontinue amantadine without tapering in the expectation of rapid improvement of the visual hallucinations, considering that the risk of neuroleptic malignant syndrome would be lower than that in patients with normal renal function who discontinued amantadine immediately. After the discontinuation of amantadine, no increase in creatine kinase level or muscle rigidity was observed, and the visual hallucinations improved on day 7 after discontinuation.