自控微动带锁髓内钉内固定对骨折愈合影响的扫描电镜观察与生化分析

目的:观察自控微动带锁髓内钉[AMLN]内固定对骨折愈合的影响及机制。方法:对12只山羊两侧股骨干横断截骨,分别采用AMLN和GK钉固定,术后7、14、28、56d分批处死,行生物化学测量,扫描电镜观察。结果(1)电镜观察术后7～14d AMLN固定组骨痂丰富、层叠状有序排列,骨小梁的吸收陷窝内有胶原纤维不断形成;术后28～56d骨胶原纤维在吸收陷窝内外形成丰富,互相平行束状排列,与骨干主应力轴相一致,骨吸收和骨生成活跃,骨塑形改建迅速,哈佛氏系统结构完整,结构网架在骨质钙盐结晶沉积下十分坚韧;而GK钉固定组则无上述特征现象发生;(2)AMLN钉固定组的骨痂胶原、不溶性胶原、钙、磷含量均高于GK钉固定组(P<0.05)。结论:AMLN钉固定使骨折端局部稳定、有轴向生理性应力刺激与应力传导,增加了成骨细胞的代谢活性,使骨小梁沿压应力轴线发育,促进了骨胶原生成、骨盐的沉积及转化、骨痂的形成和强度的提高,加快了骨质重建的速度。     

重症急性胰腺炎的临床营养支持治疗

重症急性胰腺炎(SAP)常出现代谢紊乱及肠道功能紊乱,严重感染和多脏器功能障碍综合征(MODS)是主要死因。在SAP病程的不同时期采取不同的营养(肠内及肠外营养)支持单独或者联合应用可以改善患者的营养状况,维护肠道黏膜屏障及机体免疫功能,避免或减轻炎性细胞因子的过量释放和瀑布样级联反应(cascade)造成的全身炎性反应综合征(SIRS)和MODS,从而显著降低SAP的感染率和病死率。因肠外营养易发生导管相关性感染及“过度营养”的问题,故强调早期放置鼻空肠管到Treitz韧带下方进行肠内免疫营养支持是安全有效的。     

Medical chemistry: evaluation of active and problem-oriented teaching methods

In the preclinical phase of basic medical education at the Karolinska Institute in Stockholm, Sweden, chemistry extends over 16 weeks and changes were made to the teaching methods during 7 of those weeks--one in organic chemistry and 6 in intermediary metabolism. The number of lectures was reduced and problem-oriented group tasks wee introduced instead which required a higher level of student responsibility for individual learning. Teaching and group tasks were designed to give the students a better understanding of the biochemical processes in their entirety as well as the way these are controlled in the human body. From this base the students will be enabled to discuss and understand physiological, pathological and medical phenomena. Experience and results show that student performance in examinations improved significantly, that students acquired a better understanding and a more comprehensive grasp of the subject, and a noticeably more positive interest in medical chemistry. They remember approximately 60% more a few years after completing the course than do students who have been instructed in a more traditional manner, and although the load of the teachers has increased by some 20% in respect of scheduled time, the instructors have gained in improved student contact and a wider knowledge of their subjects. The results have remained the same for each course since the change was introduced in 1977. Due to new admission criteria, more students now have less knowledge of mathematics and chemistry, and more students have social circumstances that make independent studies more attractive (family obligations and financial obligations).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hypoglycemic brain injury

Summary Profound hypoglycemia causing the disappearance of spontaneous EEG activity was induced by insulin in rats. For analysis of cerebral cortical concentrations of labile phosphates, glycolytic metabolites and amino acids, the brain was frozen in situ. For microscopic analysis of the corresponding cerebral cortical areas the brain was fixed by perfusion. Hypoglycemia with an isoelectric EEG for 30 and 60 min caused severe perturbation of the cerebral energy metabolites. After both 30 and 60 min of isoelectric EEG, two microscopically different types of nerve cell injury were seen. Type I injury was characterized by angulated, darkly stained neurons with perineuronal vacuolation, mainly affecting small neurons in cortical layer 3. Type II injured neurons, mainly larger ones in layers 5–6, were slightly swollen with vacuolation or clearing (depending on the histotechnique used) of the peripheral cytoplasm, but had no nuclear changes.Recovery was induced by glucose injection. Improvement in the cerebral energy state occurred during the 30 min recovery period even after 60 min of hypoglycemia. However, the persisting reduction in the size of adenine nucleotide and amino acid pools after 30 or 180 min recovery suggested that some cells remained damaged. In confirmation many type I injured neurons persisted during the recovery suggesting an irreversible injury. The disappearance of virtually all type II injuries indicated reversibility of these histopathological changes.The microscopic changes in hypoglycemia were different from those in anoxia-ischemia suggesting a dissimilar pathogenesis in these states despite the common final pathway of energy failure.     

Mechanism of xylitol toxicity in the rabbit

Xylitol toxicity was evaluated by intravenous infusion of varying doses of xylitol at different concentrations into rabbits. Acute toxicity was observed with the administration of 50% xylitol solutions. Striking increases of SGOT and serum LDH levels, along with an increase of urine volume were observed. The LD₅₀ of a 50% solution infused at a rate of 87 mg/kg/min was estimated to be between 4–6 g xylitol/kg body wt. The toxicity correlated well with the concentration of the xylitol solution used or the infusion rate. Both determined serum xylitol concentration and serum osmolality. At a constant infusion rate, the total dose became the important factor in toxicity. The effects of xylitol were compared with those seen after the administration of isosmolar urea, mannitol, or glucose. The acute toxicity of xylitol appears to be mainly due to a hyperosmolar effect. A 5% xylitol solution, essentially isotonic, is nontoxic to the animal in a dose up to 1 g/kg body wt/12 hr even for multiple infusions.     

高原地区与平原地区新入伍战士尿生化指标的对比性研究

目的：探讨高原缺氧对初上高原人员健康的损害情况。方法：对北京地区（海拔３１．２ｍ）和青海省西宁西川地区（海拔２２６０ｍ）及海南州（海拔２８００ｍ）共３００名入伍２８天￣３０天的新战士，进行尿生化十项检测。结果：北京地区（Ａ组）总阴性率为７％，高原地区（Ｂ组）为４２％。两组相比有非常显著的差异（Ｐ〈０．０１）。主要阳性项目，ＰＲＯ（尿蛋白）、ＢＬＤ（尿潜血）和ＵＲＯ（尿胆红素）在Ｂ组分别占高原地区总     

Plasma phenylalanine levels in phenylketonuric heterozygous and normal adults administered aspartame at 34 mg/kg body weight

Following administration of aspartame (34 mg/kg body wt) in orange juice, plasma concentrations of free amino acids were measured in 12 female subjects known to be heterozygous for phenylketonuria and 22 normal subjects (12 male, 10 female). No change in fasting plasma aspartate concentrations were noted after aspartame loading in either group. In normal male subjects, the mean (±S.D.) plasma phenylalanine concentration increased from a fasting value of 5.86 ± 1.25 μmol/dl to a mean peak value of 12.0 ± 3.79 μmol/dl. Plasma phenylalanine levels in normal female subjects increased from a mean fasting concentration of 4.83 ± 0.84 μmol/dl to a mean peak value of 8.95 ± 1.49 μmol/dl suggesting a more rapid absorption, metabolism, and/or clearance of phenylalanine by females. In female heterozygous subjects, the mean peak plasma phenylalanine concentration was significantly higher than in normal females. Plasma phenylalanine values increased from a mean fasting value of 5.92 ± 1.51 μmol/dl to a mean peak value of 15.1 ± 4.67 μmol/dl. Similarly, the area under the plasma phenylalanine concentration-time curve was significantly greater in heterozygous female subjects (21.36 ± 5.10 IU) than in normal female subjects (10.84 ± 2.32 IU). However, peak plasma phenylalanine levels were well below those associated with toxic effects in all cases.     

Pierre Robin Syndrome

Summary Clinical, light and electron-microscopic, and biochemical observations are presented in an 11 years old boy with Pierre Robin Syndrome; micrognathia, cleft palate and glossoptosis. Respiratory distress and feeding difficulties were early and serious complications of the glossoptosis. Cachexia, a striking physical underdevelopment, profound psychomotor retardation and epilepsy constituted the prominent clinical features. The neuropathology of the syndrome was characterized by the following: 1. Arrest in cerebral growth and maturation; 2. Mild diffuse and laminar cortical neuronal losses and astrocytic fibrosis; and 3. Minor histogenetic anomaly in the cerebellar cortex.The arrest in cerebral development was reflected grossly by microencephaly and, histologically by immaturity of numerous cortical neurons, poverty of intracortical fibrillary plexuses, poor establishment of cytoarchitectonic characteristics and hypoplasia of hemispheric white matter. At subcellular level, there was diminution of cytoplasmic organelles, particularly the rough endoplasmic reticulum. A marked deficiency in myelin lipids and severe diminution of total ganglioside concentration in the cerebral cortex were the major biochemical findings.In the pathogenesis of cerebral alterations congenital factors and the complications of glossoptosis were considered. It was suggested that the early undernutrition played an important role in the impediment of cerebral growth and maturation. The cerebral hypoxic insults further curtailed the development of already compromised neurons and depressed their functional activities, particularly in the more susceptible cerebral cortex. It was proposed that the arrested brain development provided a substantial structural basis for the psychomotor retardation.     

Dietary protein intake and dynamic aspects of whole body nitrogen metabolism in adult humans.

The constant isotope-infusion method of Picou and Taylor-Roberts was used to study rates of total body protein synthesis and breakdown in adult subjects following acute changes in the level of dietary protein intake. Six healthy adults, four males and two females, were studied after adaptation to dietary protein intakes of 1.5 and 0.38 g of protein/kilogram body weight/day. Dietary periods were from 7 to 15 days duration. 15N-glycine was used as a tracer, and was administered orally for 60 hr at 3-hr intervals, or by continuous intravenous infusion for 48 hr. Results were similar for both routes of isotope administration for the comparison conducted at the higher protein intake. At the 1.5-g protein level the mean N flux was 28.2 mg nitrogen/kg/hr, with total body protein (N x 6.25) synthesis and breakdown rates being 3.0 g/kg/day and 2.7 g/kg/day, respectively. Reducing the protein intake to 0.38 g/kg/day caused an 8% decrease (p less than 0.05) in N flux, a 27% increase (p less than 0.005) in the rate of total body protein breakdown, and a 15% increase (p less than 0.05) in the rate of protein synthesis. Endogenous amino acids were reutilized more efficiently under these conditions. The findings are discussed in relation to the way in which adult subjects adapt to acute changes in dietary protein intake.