Effect of interleukin-8 on glomerular sulfated compounds and albuminuria

To evaluate the effect of interleukin-8 (IL8) on glomerular basement membrane (GBM) sulfated compounds and albuminuria, we infused IL8 in 1% bovine serum albumin (BSA) for 5 days into the left renal artery of Holtzman male rats at the rate of 10 μl/h using an osmotic pump. Control rats received 1% BSA. A significant increase in urinary albumin/creatinine ratio was seen on the last day of IL8 infusion (0.38±0.11, mean ± SEM) when compared with albumin/creatinine ratio prior to infusion (0.19±0.04, P = 0.04). No significant differences in urinary albumin excretion prior to and after infusion of 1% BSA were observed. On the last day of infusion, rats were injected with ³⁵sulfate (1.0 mCi/200 g body weight) intraperitoneally and killed after 8 h. Glomeruli were isolated and GBM obtained. After 5 days of IL8 administration, there was a significant increase in ³⁵sulfate uptake by GBM of the infused kidney (76±10 cpm/dry glomerular weight, mean ± SEM) compared with the uptake seen in the contralateral kidney (53±9, P = 0.05). The in vivo infusion of IL8 increased the ³⁵sulfate uptake by GBM and augmented the urinary albumin/creatinine ratio, suggesting that IL8 may induce albuminuria by altering the metabolism of the GBM sulfated compounds. This hypothesis needs to be confirmed by studies on glomerular charge selectivity and GBM anionic sites during the course of the infusion. Moreover, the persistence of the effect needs to be evaluated by prolonging the infusion for more than 5 days. Received June 3, 1996; received in revised form and accepted October 18, 1996     

Voltage-gated Currents in Rabbit Retinal Astrocytes

The voltage-gated currents of the astrocytes associated with the retinal capillaries of the rabbit retina were studied using whole-cell patch clamp recording. The resting potential of these cells was −70 ± 4.8 mV (mean ± SEM; n = 54), and the input resistance and cell capacitance were 558 ± 3.6 MΩ and 19.5 ± 1.8 pF respectively. Depolarization to potentials positive to −50 mV evoked rapidly activating inward and outward currents. The inward current was transient, eliminated by substitution of choline for Na⁺ in the bathing solution, and reduced by 50% in the presence of 1 μM tetrodotoxin. The time-to-peak of the Na⁺ current was more than twice that for the Na⁺ current found in retinal neurons. The glial Na⁺ current was half-inactivated at −55 mV. A transient component of the outward K⁺ current was blocked by external 4-aminopyridine while a more sustained component was blocked by external tetraethylammonium. At potentials between −150 and −50 mV the membrane behaved Ohmically. Voltage-gated currents in retinal astrocytes recorded in situ appear qualitatively similar to those described for some glial cells in vitro.     

The assembly of the factor X-activating complex on activated human platelets

Summary.  Platelet membranes provide procoagulant surfaces for the assembly and expression of the factor X-activating complex and promote the proteolytic activation and assembly of the prothrombinase complex resulting in normal hemostasis. Recent studies from our laboratory and others indicate that platelets possess specific, high-affinity, saturable, receptors for factors XI, XIa, IX, IXa, X, VIII, VIIIa, V, Va and Xa, prothrombin, and thrombin. Studies described in this review support the hypothesis that the factor X-activating complex on the platelet surface consists of three receptors (for the enzyme, factor IXa; the substrate, factor X; and the cofactor, factor VIIIa), the colocalization of which results in a 24 million-fold acceleration of the rate of factor X activation. Whether the procoagulant surface of platelets is defined exclusively by procoagulant phospholipids, or whether specific protein receptors exist for the coagulant factors and proteases, is currently unresolved. The interaction between coagulation proteins and platelets is critical to the maintenance of normal hemostasis and is pathogenetically important in human disease.     

羊膜负载骨髓间充质干细胞与表皮细胞对放创性皮肤损伤促愈合研究

目的探讨治疗放创性全厚皮肤缺损创面的方法及效果. 方法贵州小香猪8只,每只背部脊柱两侧均有放创性全层皮肤缺损圆形创面(Ф3.67cm)各3个,共48个创面.将经处理的人羊膜(human amniotic mambrane, HAM)分别负载自体骨髓间充质干细胞(mesenchymal stem cells, MSCs)和表皮细胞,移植到其左侧24个创面作为实验组(A组);以单纯无种植细胞的HAM敷盖其右侧前16个创面(B组);以单纯油纱布敷盖其右侧后8个创面(C组).B、C作为对照组.观察移植后1～3周内各组创面愈合、肉芽组织生长及上皮化等情况,并进行创面组织HE染色及vWF免疫组织化学检测.用图像分析法测算各组各时间点创面平均面积(cm2),并计算其愈合百分率. 结果 C组于伤后 22～23天愈合,B组于伤后19～21天愈合;A组于伤后15～17天愈合,较B、C组分别提前6～7天和5～6天,愈合质量好.移植15～17天,A组与B、C组创面平均残留面积及愈合面积百分率比较,差异有统计学意义(P＜0.01). A组创面的新生上皮已完全覆盖整个创面,肉芽组织生长旺盛,肉芽组织中vWF、成纤维细胞和毛细血管含量丰富,可见胶原沉积;B、C组创面仍见许多炎性细胞浸润,肉芽组织中vWF、成纤维细胞和毛细血管含量少,胶原沉积不明显. 结论 HAM负载自体MSCs和表皮细胞植入对放创性全厚皮肤缺损创面有较好的促愈合作用,愈合质量较高.     

红细胞膜通道力学效应的探讨

在考察红细胞双凹碟形体形成的基础上,讨论了红细胞的输氧功能与红细胞变形的关系,揭示了红细胞膜通道的力学效应:当红细胞呈双凹碟形时,PiPo的地方,红细胞膜通道有释放出氧的现象,其氧的总流率为 J=Lo_2(Pio_2-Poo_2) Lp(Pi-Po) 式中Lo_2为O_2分压差引起的膜通道对氧的流导,PiO_2、Poo_2为膜内外的氧分压;Lp为由于压差引起的膜通道对氧的流导。     

PNH者患红细胞膜结构损伤及膜脂与膜蛋白关系的探索

本文分析了20例PNH患者红细胞膜总脂,Ch/PIM比及磷脂组分,并比较了10例PNH红细胞膜AChE在PBS系统和生理盐水中的酶活性。发现PNH红细胞膜脂缺失严重,比正常少22％,但Ch/PIM比值及各磷脂相对含量均无明显改变。在PBS中AChE活性接近正常红细胞,但在生理盐水中明显低于正常红细胞,仅为正常的40％。表明PNH红细胞对补体敏感而溶血可能是由于补体导致膜脂缺失,进而破坏了红细胞膜结构的完整性而引起的,这也是AChE活性在低pH环境中酶活性比正常红细胞低的原因。     

人鼻粘膜表面超微结构及纤毛输送功能的研究

研究结果表明:①人鼻粘膜的上皮在胚胎期的发育并不完善。在新生儿,纤毛上皮细胞的融合刚刚开始,其表面的纤毛呈微绒毛状。②在最常见的四种鼻粘膜炎症病变中,其超微结构的损害程度以伴有化脓性感染者最重,慢性肥厚性鼻炎与萎缩性鼻炎次之,变态反应性鼻炎最轻。③上述四种炎症病人的鼻纤毛输送能力均较正常人差,其中以伴有化脓性感染者最差,慢性肥厚性鼻炎和萎缩性鼻炎次之,变态反应性鼻炎最轻。     

High-frequency ventilation (HFV) in hyaline membrane disease —a preliminary report

Eight premature babies affected by hyaline membrane disease and needing mechanical respiratory support were ventilated by means of a VDR 1 (Bird Space Technology) respirator at 10 Hz during a mean time of 51 h. Before HFV 7 infants had been on conventional mechanical ventilation (CMV) and one on nasal CPAP. The values of mean airway pressure (MAP) and oxygenation index (PaO₂/FIO₂) on CMV and HFV were (mean and range): 1. CMV: MAP 15 (4–29) mm Hg, ox. index 15.47 (5.07–23.19) kPa; 2. HFV after 1 h: MAP 15 (10–19) mm Hg, ox. index 24.13 (9.07–46.12) kPa. Improved oxygenation allowed rapid reduction of FIO₂ in the following hours. Only 3 infants were weaned directly from VDR 1, 5 were switched back to CMV mainly because of technical failures of the respirator. The change from HFV to CMV was associated with a fall of PaO₂/FIO₂ from 35.99 (15.86–74.52) to 22.39 (7.33–31.46) kPa. The mean time of artificial ventilation (CMV+HFV) was 121 h (range 46–166). Except for 1 pneumothorax no medical complications were seen during HFV, and all patients survived. Despite impressive improvements in oxygenation it is cautioned against the use of the VDR 1 because of the high incidence of technical problems.     

Pathology of the lung in the fetus and neonate, with particular reference to problems of growth and maturation

The major forms of lung pathology in the perinatal period are reviewed with emphasis on disturbances of growth and maturation. Lung hypoplasia results from impairment in the physiological control of lung growth during the fetal period. It is more common than organogenetic defects which are discussed only briefly. Hyaline membrane disease is now seldom seen in a pure form due to improvements in perinatal care. However, its complications and sequelae such as interstitial emphysema, pneumothorax and bronchopulmonary dysplasia are encountered more frequently. In addition, a wide variety of pathological processes may localize to, or be expressed in, the lung of the newborn, notably asphyxial changes, persistent pulmonary hypertension, haemorrhage and infection.