Atherosclerotic rabbit aortas: expandable intraluminal grafting

Balloon-expandable intraluminal grafts that ranged in diameter from 2 to 4 mm were placed in the atherosclerotic abdominal aortas of 24 rabbits. The animals were killed 1, 3, 8, or 24 weeks after placement of the graft. All grafts retained patency without altering the luminal diameter. The small degree of neointimal thickening covering the graft's inner surface was not detectable on conventional in vivo arteriograms. Aortic atherosclerotic plaque external to the graft was markedly compressed 1 week after graft placement. The plaque regained full thickness 24 weeks after grafting when the plaque expanded outside the graft as a result of relaxation or atrophy of the surrounding arterial media.     

多环胺化合物HH01抗实验性大鼠胃溃疡作用

HH01(A和B)在60mg·kg^-1剂量下,对无水乙醇型、冷应激型和幽门结扎型胃溃疡模型有较好的预防作用;大剂量时对胃液分泌有一定的抑制作用,并可减少胃酸分泌,同时减少胃液中DNA的含量,作用特点与甲氰脒胍不同;在同样剂量下对消炎痛型胃溃疡模型无效。     

Metabolic bone disease in pseudohypoparathyroidism: radiologic features

We reviewed the radiographs of six patients with pseudohypoparathyroidism (PHP) manifested by variable renal and skeletal resistance to parathyroid hormone (PTH). Features compatible with hyperparathyroid bone disease, osteomalacia, and rickets were observed. Skeletal changes of hyperparathyroidism included (a) subperiosteal bone resorption, (b) radiolucent lesions, caused by either brown tumors or bone cysts, (c) slipped capital femoral epiphyses, (d) focal areas of osteosclerosis, (e) periosteal neostosis, and (f) osteopenia with reduced cortical and trabecular bone volume. Histologic bone features were compatible with osteitis fibrosa in all patients, which suggests that the skeleton responded to the bone-remodeling effects of PTH despite hormonal resistance at other target sites. Skeletal changes of rickets included metaphyseal irregularities, cupping, and widening of the growth plates. Osteomalacia was indicated by Looser zones in one patient and confirmed by histologic evidence in three patients.     

Respiratory effects of pregnancy and progesterone in Jersey cows

Unanesthetized Jersey cows were studied during both pregnant (5-9 months) nonlactating states, and nonpregnant lactating states; and also following treatment with progesterone (Pr). The pH, PCO2 and PO2 of aortic blood, VE and f were measured and the mixed expired gas was analyzed. The following significant changes from the nonpregnant state occurred during pregnancy: PaCO2 = -3.2 mm Hg, pHa = +0.02 unit, VT = -0.44 L, f = +7 breaths/min, and VE/VCO2 = +9.7. Concomitant with the respiratory studies, serum Pr levels were determined by radioimmunoassay (RIA) in 11 nonpregnant and 5 pregnant cows, and in 6 nonpregnant, lactating cows prior to and on days 3, 5 and 10 of treatment with Pr (500 mg, i.m., twice daily). Minute ventilation (VE, L X min-1 X kg-1, BTPS) was positively correlated (r = +0.59) and PaCO2 was negatively correlated (r = -0.64) with endogenous serum Pr levels of non-pregnant and pregnant cows. However, exogenous Pr did not significantly alter these parameters or pHa, despite mean serum levels nearly twice (23.6 +/- 10.2 ng/ml) those observed in pregnant cows (12.7 +/- 3.7 ng/ml). The increased ventilation during pregnancy in Jersey cows, shown in this study, does not appear to be related to Pr as exogenous Pr failed to induce hyperventilation. The correlation of increased ventilation with endogenous Pr levels therefore suggests that the mode of in vivo Pr release, or different compound, simultaneously released, could be the stimulus.     

芹菜甲素保护脑细胞的作用

以每周定时im马桑内酯0.9～1.5mg/kg三个月为实验性癫痫慢性发作模型。ig芹菜甲素700mg/kg能明显降低大鼠癲痫发作的程度和次数,延长潜伏期。脑形态学结果表明,芹菜甲素对大脑顶叶皮层细胞、胶质细胞和小脑蚓部蒲肯野细胞有一定的保护作用。同时观察的安定1.5～5mg/kg则无此作用。     

Hypothesis: vitamin E complements polyunsaturated fatty acids in essential fatty acid deficiency in cystic fibrosis

While several studies have demonstrated essential fatty acid (EFA) deficiency in plasma and tissue lipids of cystic fibrosis (CF) patients, the reasons for this deficiency are not well established. It is believed that reduced EFA intake, malabsorption of fat, altered desaturase/lipase activity and defective cystic fibrosis transmembrane conductance regulator (CFTR) altering utilisation of EFA in epithelial cells contribute to the development of EFA deficiency in CF. It is likely that increased metabolism of arachidonic acid to eicosanoids such as leukotrienes, thromboxane and prostaglandins may also be a contributing factor. Evidence is presented that elevated oxidative damage to EFA and impaired antioxidant defences, in particular vitamin E, may contribute to the development of EFA deficiency in CF. Furthermore, antioxidant supplementation in CF may improve EFA status.