Postmortem cardiac troponin T levels in the blood and pericardial fluid. Part 2: analysis for application in the diagnosis of sudden cardiac death with regard to pathology

Although previous forensic pathological studies have suggested the possible application of cardiac troponins in the diagnosis of myocardial infarction, there appears to be insufficient data with regard to its cardiac pathology. The present study analyzed the heart blood, peripheral blood and pericardial fluid levels of cardiac troponin T (cTnT) in sudden cardiac deaths (n = 96) within 48h postmortem in relation to pathological findings of acute myocardial infarction (AMI, n = 34), recurrent myocardial infarction (RMI, n = 23), ischemic heart disease without any pathological evidence of infarction (IHD, n = 24) and other heart diseases (OHD, n = 15). Control groups (n = 75, survival time <24 h) within 48 h postmortem consisted of asphyxiation (n = 35), drowning (n = 27) and cerebrovascular diseases (n = 13). There was a marked correlation in the cTnT levels between right and left heart blood samples. The pericardial level was usually higher than either heart blood level, and the external iliac venous blood level was the lowest. Although postmortem time-dependent increases in heart and pericardial blood cTnT levels were observed in most groups, they were most evident for AMI and asphyxiation. In the early postmortem period (<12 h) there was no significant difference between AMI or RMI and the other groups except for drowning. After 12 h postmortem, significantly elevated heart blood and pericardial cTnT levels were observed for AMI and RMI showing multiple interstitial hemorrhages and necrosis compared to those with localized eosinophilic changes or patchy interstitial hemorrhages, IHD and OHD. These differences were the smallest for peripheral blood. For sudden cardiac death cases, the difference in cTnT level at each site among the causes of death was independent of gender, age, heart or lung weight and pathologies of affected coronary artery and severity of coronary stenosis. These observations suggest that the elevation in postmortem blood and pericardial cTnT levels in sudden cardiac death may depend on the severity of ischemic myocardial damage including the size and intensity of myocardial lesions involving multiple interstitial hemorrhages and necrosis, and also the postmortem period for heart and pericardial levels.     

Changes in levels of hepatitis B virus markers in patients positive for low-titer hepatitis B surface antigen

Aim: Recently, patients positive for the low-titer hepatitis B surface antigen (HBsAg) have been found occasionally owing to the increase in the accuracy of detection methods. The aim of this study is to clarify the clinical status of acute hepatitis B virus (HBV) infection in patients positive for low-titer HBsAg. Method: Eight patients, who were positive for HBsAg at low titers and diagnosed as having acute HBV infection, were enrolled in this study. Assays of HBsAg, hepatitis B core antibody (anti-HBc), hepatitis B e-antigen (HBeAg), hepatitis B e-antibody (anti-HBe), hepatitis B surface antibody (anti-HBs) and HBV DNA, and biochemical tests were basically conducted every 4 weeks for at least 24 weeks. Result: The average cut-off index of HBsAg was 8.7 ± 9.6 (range, 1.0–25.7). All the patients were negative for anti-HBc, HBeAg, anti-HBe and HBV DNA on their initial visit. The genotype of HBV could be determined in four patients: two were infected with genotype B/HBV, one was infected with genotype A/HBV, and the remaining patient was infected with genotype C/HBV. Although HBsAg clearance was observed within 4 months in all the patients, none of the other HBV markers seroconverted during the observation period. Conclusion: HBV infection terminating with seronegativity for HBV markers may occur in transient HBV infection.     

Effects of poly(ethyleneglycol)-modified hemoglobin vesicles on agonist-induced platelet aggregation and RANTES release in vitro

We studied the effects of hemoglobin-vesicles modified with PEG (PEG-HbV), a type of liposome-encapsulated hemoglobin (LEH), on human platelet functions in vitro. The effect of a low concentration of PEG-HbV (Hb; 5.8 mg/dl) was assessed by examining an agonist-induced aggregation response, and that of relatively high concentrations of PEG-HbV (Hb; 0.29, 1 and 2 g/dl) by measuring the release of RANTES (Regulated upon activation, normal T-cell expressed and presumably secreted) from platelets, which is regarded as a marker of platelet activation. The preincubation of platelets with PEG-HbV at 5.8 mg/dl of Hb did not affect platelet aggregation induced by collagen, thrombin and ristocetin. The pretreatment of platelet-rich plasma (PRP) with PEG-HbV at concen trations up to 2 g/dl of Hb had no aberrant effects on the collagen-induced RANTES release. Furthermore, the collagen-induced release of RANTES from PRP was not affected by longer incubation with PEG-HbV at 2 g/dl of Hb. The basal levels of RANTES from PRP were unchanged in the presence of PEG-HbV. These results suggest that PEG-HbV, at the concentrations studied, have no aberrant effects on platelet functions in the presence of plasma.     

Novel technique of overlaying a poly-l-lactic acid nanosheet for adhesion prophylaxis and fixation of intraperitoneal onlay polypropylene mesh in a rabbit model

Background

One problem with polypropylene mesh (PPM) used to repair abdominal wall hernias is dense adhesions to the visceral surface. The authors developed the biocompatible poly-l-lactic acid (PLLA) nanosheet (thickness?Methods The PLLA nanosheet was fabricated by the spin-coating method and peeling technique with polyvinyl alcohol (PVA) as a supporting film. Two 1.5-cm-square pieces of mesh were implanted on each peritoneal side of the midline incision. The mesh was fixed to the peritoneum with a suture and then overlaid with a 4-cm-square piece of Seprafilm or nanosheet. To examine the fixative property, mesh was overlaid with Seprafilm or nanosheet without a fixed suture. After 4?weeks, mesh adhesion, inflammatory reaction, fixation, and dislocation of mesh were evaluated.

Results

Nanosheet-overlaid meshes were flexible and fit over the peritoneum. Adhesion was observed in 10% of the nanosheet-overlaid meshes and in 50% of the Seprafilm-overlaid meshes. The adhesion tenacity grade was significantly lower with the nanosheet-overlaid meshes (0.1?±?0.1) than with the Seprafilm-overlaid meshes (1.0?±?0.4) (p?=?0.029), and the percentage of the adhesion area also was lower with the nanosheet-overlaid meshes (1.0?±?1.0% vs 8.5?±?3.2%; p?=?0.037). The mean inflammatory cell counts were lower with the nanosheet-overlaid meshes (p?=?0.0023). Regarding the fixative property, 37.5% of the nanosheet-overlaid meshes were fixated on the peritoneum, but no Seprafilm-overlaid mesh was fixated.

Conclusion

Overlaying of a PLLA nanosheet was effective for adhesion prophylaxis of intraperitoneal mesh. It also may have a possible beneficial effect on fixation of mesh.     

Activation of human complement by rat peritoneal mast cells and its inhibition by a rat serum factor

The effects of normal sera from humans, rats, and guinea pigs on unsensitized rat peritoneal mast cells were studied in vitro. Five to 20% fresh human sera induced mast cell death and substantial histamine release. The factor was heat labile. Neither hereditary C3-deficient sera nor experimentally C1q-depleted sera showed cytotoxicity. The CH50 activity of human serum was decreased to about one half after a 15-min incubation with 2 X 10(6) mast cells/ml at 37 degrees C. The cytotoxic activity and CH50 reduction were completely eliminated by an addition of 10 mM Mg-EGTA to the serum. These data demonstrated that unsensitized rat mast cells served as both the initiator and target of complement activity when human serum was used as a complement source. Requirements of both Ca++ and C1q suggested the activation of the classical pathway of complement. Fresh 5-20% sera from rats and guinea pigs, on the other hand, showed neither cytotoxicity nor CH50 reduction. Furthermore, these sera strongly inhibited the human serum-induced reaction. The latter results indicated the presence of a modulating factor in rat and guinea pig sera, which inhibits mast cell associated complement activation.     

The novel roles of liver for compensation of insulin resistance in human growth hormone transgenic rats

Chronic excess of GH is known to cause hyperinsulinemia and insulin resistance. We developed human GH transgenic (TG) rats, which were characterized by high plasma levels of human GH and IGF-I. These TG rats showed higher levels of plasma insulin, compared with control littermates, whereas plasma glucose concentrations were normal. Insulin-dependent glucose uptake into adipocytes and muscle was impaired, suggesting that these rats developed insulin resistance. In contrast, insulin-independent glucose uptake into hepatocytes from TG rats was significantly increased, and glycogen and lipid levels in livers of TG rats were remarkably high. Because the role of liver in GH-induced insulin resistance is poorly understood, we studied insulin signaling at early stages and insulin action in liver and primary cultures of hepatocytes prepared from TG rats. There was no difference in insulin receptor kinase activity induced by insulin between TG and control rats; however, insulin-dependent insulin receptor substrate-2 tyrosine phosphorylation, glycogen synthase activation, and expression of enzymes that induce lipid synthesis were potentiated in hepatocytes of TG rats. These results suggest that impairment of insulin-dependent glucose uptake by GH excess in adipose tissue and muscle is compensated by up-regulation of glucose uptake in liver and that potentiation of insulin signaling through insulin receptor substrate-2 in liver experiencing GH excess causes an increase in glycogen and lipid synthesis from incorporated glucose, resulting in accumulation of glycogen and lipids in liver. This novel mechanism explains normalization of plasma glucose levels at least in part in a GH excess model.     

从人参叶中得到的两个微量皂甙成分

从有参叶中分离得到两种微量皂甙成分，分别为3β，12β，20（S）－三羟基达玛－24（25）－烯－（20－O－α－L-呋喃阿拉伯糖基（1→6）－β－D－吡喃葡萄糖基）－3－O－β-D-吡喃葡萄糖甙（1），和3β，12β，20（S）-三羟基达玛-24（25）－烯－（20－O－α-L－吡喃阿拉伯糖基（1→6）-β-D－吡喃葡萄糖基－3－O－β-D吡喃葡萄糖甙（2），前者为三七参甙－Fe(notoginsenoside-Fe）,后者为一新的天然产物，命名为人参皂甙－Rd2(ginsenoside-Rd2）。     

Effect of sumatriptan on gastric emptying: a crossover study using the BreathID system

AIM:To determine the effect of oral sumatriptan on gastric emptying using a continuous 13 C breath test(BreathID system).METHODS:Ten healthy male volunteers participated in this randomized,2-way crossover study.The subjects fasted overnight and were randomly assigned to receive a test meal(200 kcal/200 mL) 30 min after pre-medication with sumatriptan 50 mg(sumatriptan condition),or the test meal alone(control condition).Gastric emptying was monitored for 4 h after administration of the test meal by the 13 C-acetic acid breath test performed continually using the BreathID system.Then,using Oridion Research Software(β version),the time taken for emptying of 50% of the labeled meal(T 1/2) similar to the scintigraphy lag time for 10% emptying of the labeled meal(T lag),the gastric emptying coefficient(GEC),and the regression-estimated constants(β and κ) were calculated.The statistical significance of any differences in the parameters were analyzed using Wilcoxon’s signed-rank test.RESULTS:In the sumatriptan condition,significant differences compared with the control condition were found in T 1/2 [median 131.84 min(range,103.13-168.70) vs 120.27 min(89.61-138.25);P = 0.0016],T lag [median 80.085 min(59.23-125.89) vs 61.11 min(39.86-87.05);P = 0.0125],and β [median 2.3374(1.6407-3.8209) vs 2.0847(1.4755-2.9269);P = 0.0284].There were no significant differences in the GEC or κ between the 2 conditions.CONCLUSION:This study showed that oral sumatriptan significantly delayed gastric emptying of a liquid meal.