The effect of Brugia pahangi infection on survival of susceptible and refractory species of the Aedes scutellaris complex

Life table statistics were used to examine the survival functions of filarial susceptible and refractory species of the Aedes scutellaris (Walker) group of mosquitoes, following infection with high and moderate doses of Brugia pahangi (Buckley & Edeson). Survivorship curves and hazard function curves were generated, and the median survival times and the proportions of mosquitoes surviving beyond the extrinsic incubation period of the parasite were determined. In the susceptible populations of Aedes polynesiensis Marks, Ae. pseudoscutellaris (Theobald) and Ae.tabu Ramalingam & Belkin a dose-response relationship was detected between parasite load and mortality. This relationship was characterized by a significant reduction in the proportions of infected female mosquitoes surviving at days 1 and 9 postinfection, reduction in the median survival times and an increase in the hazard rates as the infectious dose increased. The survival of the refractory species, Ae.alcasidi Huang and Ae.katherinensis Woodhill was not significantly affected by the infection. A positive correlation between microfilaraemia in the vertebrate host and parasite load in the susceptible mosquito populations was also observed. Regression analysis of the number of parasites recovered from susceptible mosquitoes at the time of death showed that mosquitoes at highest risk of dying harboured from 11.6 to 19.4 infective larvae when fed on a gerbil with sixty-five microfilariae per 20 microliters blood; this resulted in 34.4-40.2% mortality by day 9 postinfection. A mean number of 32.6-46.9 infective larvae was observed when these populations were exposed to a gerbil with a microfilaraemia of 150 mf/20 microliters and resulted in 72.8% to 80% mortality in these populations. Viable infective larvae were recovered from infected mosquitoes up to 50 days postinfection.     

内毒素对人血小板聚集,释放的体外作用

大肠杆菌 O55B5内毒素在体外可抑制人血小板自发性聚集,并使血小板内 cAMP、钙调素明显增高,但对肾上腺素诱发的血小板聚集无作用,也不能引起血小板致密颗粒和α-颗粒的释放。此外还观察到内毒素组无血小板上清液中5-HT 含量减少。     

Differences in reactivity of confluent and nonconfluent cultures of human endothelial cells toward thrombin-stimulated platelets or heparinized salt solution

Summary This study examined whether nonconfluent endothelial cell cultures reacted differently than confluent ones toward thrombin-stimulated platelets or a heparinized salt solution. The adherence to the endothelial cell cultures of⁵¹Cr-labeled human platelets stimulated at different thrombin concentrations was studied. There was significantly higher adherence of stimulated platelets to nonconfluent cultures compared with confluent ones. This was confirmed by scanning electron microscopy, which also revealed a tendency for the platelets to adhere at the cell periphery. Electron microscopy also showed that thrombin-stimulated platelets induced endothelial cell contraction. Part of the peripheral endothelial cell surface toward the bottom of the culture dish was inverted, facing the lumen of the dish. This phenomenon was particularly seen in nonconfluent cultures. When⁵¹Cr-labeled endothelial cultures were incubated with a mildly injurious fluid as heparinized sodium acetate and 20% serum, at 20° C for 30 min, the nonconfluent cultures showed significantly more cell detachment and release of⁵¹Cr than the confluent ones. We conclude that under the conditions of the present experiments there are differences in the reactivity of confluent and nonconfluent endothelial cell cultures. These differences probably reflect biological dissimilarities. In experiments where properties of cultured endothelium are studied, care should be taken that the degree of confluency is standardized.     

Effects of intravenous epinephrine on macaque platelets

Blood was obtained from three species of macaques for a study of platelets. A rapidly mobilizable platelet pool was demonstrated in rhesus macaques given intravenous epinephrine. The number of platelets/ml of blood increased about 30% 3 to 5 min after epinephrine was given. The size distributions of the platelets were similar before and after injection. Platelet aggregability was increased after injection. Basal platelet aggregabilities, as measured by platelet aggregate ratios, were similar in rhesus macaques. Celebes black macaques, and human subjects, but were significantly greater in cynomolgus macaques than in the other three species.     

急性低氧对大鼠血液中儿茶酚胺及血小板聚集性的影响

健康ＳＤ雄性大鼠,体重２５０－３００ｇ,麻醉、气管插管,用人工呼吸机经气袋供气,自发吸入氧浓度为９％的氧氮混合气,用高效液相色谱－电化学联合检测法及电阻法检测循环血液中儿茶酚胺及全血血小权聚集性的动态变化。结果：急性低氧１５ｍｉｎ时血液中肾肾上腺素（Ａ）浓度及全血血小板聚集性显著增加（Ｐ〈０．０１）,而去甲肾上腺素（ＮＡ）浓度虽有所增加,但无统计学意义（Ｐ〉０．０５）;复氧１５ｍｉｎ时血液中儿茶酚     

Platelet calcium pump activity in essential hypertensives and their first-degree relatives

Intracellular free Ca²⁺ concentration has been shown to be elevated in platelets of patients with essential hypertension. This study was designed to characterize Ca²⁺-pump activity of the platelet membranes (surface and intracellular) in these patients. A double-blind study was carried out. Untreated and treated (on R-blockers) essential hypertensives were studied in comparison with normotensive control subjects. First degree blood relatives of essential hypertensives were also studied. The Ca²⁺-activation kinetics of the enzyme showed a significant decrease in the V_max. (for the plasma- and intracellular membranes) and Km (for the intracellular membranes) in the essential hypertensive patients. Increased platelet membrane cholesterol content was observed in these patients. Lowered Ca²⁺-efflux by Ca²⁺-ATPase may lead to elevated intracellular free Ca²⁺-levels in platelets of essential hypertensives. A lowered Ca²⁺-ATPase activity may emerge as a marker for essential hypertension.     

Platelet activating factor (PAF) stimulates release of PGI2 from inflamed rabbit gallbladder cell cultures

This study examines the hypothesis that PAF stimulates release of PGI₂ from inflamed rabbit gallbladder explant cell cultures. New Zealand white rabbits underwent bile duct ligation for 72 h (72 h BDL), or sham operation, Sham and 72 h BDL gallbladder explants were placed in culture, and the cells grown to 75% confluence. The cells were exposed to increasing concentrations of PAF for 60 min. The media analyzed for eicosanoid release by EIA and the cells analyzed for cyclooxygenase and prostacyclin synthase content by immunoblot analysis. PAF increased release of 6-keto-PGF_1α from the 72 h BDL gallbladder cell cultures in a dose-related manner which was inhibited by indomethacin preincubation by 90%. The increased 72 h BDL cell release of 6-keto-PGF_1α was not associated with changes in the content of cyclooxygenase or prostacyclin synthase. PAF did not alter eicosanoid release from sham control cell cultures. These data suggest that PAF can only up-regulate endogenous 6-keto-PGF_1α release from the 72 h BDL cells that had been previously stimulated by inflammation. PAF may thus contribute to gallbladder distention and injury by chronic stimulation of inflamed gallbladder PGI₂ release.     

大鼠血小板中的神经肽Y及其对血管收缩的影响

特异性放射免疫分析显示大鼠血小板与富血小板血浆(PRP)分别含NPY免疫活性物质90±16ng/10~7血小板与93±19ng/ml,大大高于普通血浆(1.2±0.1ng/ml)与贫血小板血浆(PPP)(1.7±0.3 ng/ml)中的含量(P<0.001)。血小板样品HPLC各馏分的NPY放免活性峰位与标准NPY的峰位相符。PRP经胶原最大程度聚集后,血小板内的NPY浓度降为34±5 ng/10~7血小板,而PPP中的NPY浓度则升高到26±4 ng/ml。1.6 ml PRP经胶原作用产生最大程度聚集,由此分离所得的PPP引起离体灌流大鼠尾动脉收缩,张力上升380±80 mg;上述PPP经NPY抗血清处理后引起尾动脉收缩的幅度显著减小(190±40 mg,P<0.001)。而1 nmol/L人工合成NPY并不引起血管收缩。结果表明大鼠血小板中含有大量NPY,在不可逆聚集时可以释放,释放的NPY可能参与血小板聚集时释放物质的缩血管效应。     

Exposure of preterm neonates to toxic metals during their stay in the Neonatal Intensive Care Unit and its impact on neurodevelopment at 2 months of age

BackgroundPremature neonates might be exposed to toxic metals during their stay in the neonatal intensive care unit (NICU), which could adversely affect neurodevelopment; however, limited evidence is available. The present study was therefore designed to assess the exposure to mercury, lead, cadmium, arsenic, and manganese of preterm neonates who received total parenteral nutrition (TPN) and/or red blood cell (RBC) transfusions during their NICU stay and the risk of neurodevelopment delay at the age of 2 months.MethodsWe recruited 33 preterm neonates who required TPN during their NICU admission. Blood samples were collected for metal analysis at two different time points (admission and before discharge). Metals in the daily TPN received by preterm neonates were analyzed. Neurodevelopment was assessed using the Ages and Stages Questionnaire Edition 3 (ASQ-3).ResultsAll samples of TPN had metal contamination: 96% exceeded the critical arsenic limit (0.3 μg/kg body weight/day); daily manganese intake from TPN for preterm neonates exceeded the recommended dose (1 µg/kg body weight) as it was added intentionally to TPN solutions, raising potential safety concerns. All samples of RBC transfusions exceeded the estimated intravenous reference dose for lead (0.19 µg/kg body weight). Levels of mercury, lead and manganese in preterm neonates at discharge decreased 0.867 µg/L (95% CI, 0.76, 0.988), 0.831 (95%CI, 0.779, 0.886) and 0.847 µg/L (95% CI, 0.775, 0.926), respectively. A decrease in ASQ-3-problem solving scores was associated with higher levels of blood lead in preterm neonates taken at admission (ß = −0.405, 95%CI = −0.655, −0.014), and with plasma manganese (ß = −0.562, 95%CI = −0.995, −0.172). We also observed an association between decreased personal social domain scores with higher blood lead levels of preterm neonates before discharge (ß = −0.537, 95%CI = −0.905, −0.045).ConclusionOur findings provide evidence to suggest negative impacts on the neurodevelopment at 2 months of preterm infants exposed to certain metals, possibly related to TPN intake and/or blood transfusions received during their NICU stay. Preterm neonates may be exposed to levels of metals in utero.