骨折延迟愈合和骨不连接治疗的进展

本文综述了骨折延迟愈合和骨不连接治疗的进展。文中将治疗延迟愈合和骨不连接的方法分为二类,即非手术治疗和手术治疗。简要介绍了非手术治疗的各种方法、原理以及实验研究和临床应用。手术治疗是通过手术达到骨折断端的牢固固定,同时进行骨移植或不加骨移植。固定分为外固定和内固定,一般都主张加压固定;骨移植分为游离骨移植和带血运的骨移植,后者明显优于前者。     

2型糖尿病与钙,磷代谢及相关激素的关系

目的 观察２型糖尿病患者钙、磷代谢及相关激素的变化及对骨代谢的影响。方法 测定２０例健康对照者和６０例２型糖尿病患者血甲状旁腺素（ＰＴＨ）、降钙素（ＣＴ）、２５羟维生素Ｄ３「「２５（ＯＨ）Ｄ３」」、环磷酸腺苷（ｃＡＭＰ）和血、尿钙（Ｃａ）、磷（Ｐ）、镁（Ｍｇ）,糖基化血红蛋白（ＨｂＡｌｃ）、２４ｈ尿和２４ｈ尿白蛋白定量等指标。结果 ２型糖尿病患者血ＰＴＨ水平显著高于对照组（Ｐ〈０．０１）,ＣＴ水平     

必然与自由—对人与自然的辩证思考

随着科技迅速发展,人在自然面前有了更多的“自由”,但与此同时,“全球问题”的出现又时时困扰着人们。人类要摆脱“困境”,更大限度地获得自由,迫切需要从认识上、实践中摆脱正人与自然的关系,自然地把改造自然和改造人自身结合起来,实现从必然王国向自由王国的飞跃。     

产时保健对母婴健康的影响

目的：了解产妇及胎儿在医院分娩过程中产时保健情况对母婴健康的影响。方法：对１１６６４例产妇接产情况,采用χ＾２检验对不同年份不同分娩方式及母婴分娩并发症发生率进行对比分析。结果：剖宫产率为４１．８４％,围产儿死亡率为１０．６８‰,产妇分娩并发症的发生率为５．９９％,其中产后出血占９５．４２％,剖宫产与阴式分娩产后出血率差异无显著性（χ＾２＝０．６６,Ｐ＞０．０５）,新生儿并发症发生率为８．５８％,     

INHIBITORY EFFECT OF FLUVASTATIN ON AORTIC INTIMAL THICKENING IN NORMOCHOLESTEROLEMIC RABBITS

Objective, The anti-atherosclerotic effect of fluvastatin at doses insufficient to lower serum cholesterol on the catheter-induced intimal thickening and possible mechanism were investigated in abdominal aorta of rabbits. Methods. Fifty-six rabbits were randomly divided into eight groups( n = 7, each). Fluvastatin was given mixed with food at daily dose of 8mg/kg starting 5 days before catheterization. Light microscope, immanohistochemistry, transmis-sion electron microscope and RT-PCR assay were applied to assess vascular smooth muscle cell (VSMC) proliferation and apoptosis, as well as oncogene expression in vascular wall. Results. At day 10 and day 15 after catheter induced denudation intima/media( I/M) thickness ratio was obviously higher, and also the percentage of PCNA-positive cells and TUNEL-positive cells in media was significantly higher compared with controls. The intimal hyperplasia was mostly composed of α-SM-actin-pesitive cells. In rabbits given flu-vastatin I/M ratio and the percentage of these positive cells significantly decreased compared with those without fluvas-tatin.The overexpression of proto-oncogene H-ras mRNA and decreased expression of anti-oncogene p53 mRNA were found after vascular injury, whereas fluvastatin significantly reduced H-ras mRNA and increased p53 mRNA expres-sion. Conclusion. Proliferation of VSMC in the media and the migration to the intima can be inhibited, and apoptosis of VSMC be induced by short-term use of fluvastatin after balloon catheter denudation, independent of serum lipid change. The underlying mechanism is presumably associated With the influence of fluvastatin on oncogene expression in the injured vascular Wall.     

114例慢性肺心病并发冠心病的临床分析

目的 :探索慢性肺心病并发冠心病 (以下称肺冠病 )的临床特点。方法 :总结了 1996～ 1999年 12月间收治的 43 7例慢性肺心病的临床表现 ,并结合有关资料进行分析。结果 :在 43 7例慢性肺心病中 ,有 114例合并冠心病 ,并且从中发现肺心病年龄越大 ,肺冠病发生的可能性越大。本组 114例中 ,老年人占 92 1%,表明肺冠病并不少见。结论 :肺心病和冠心病均系老年人的常见病。本组 43 7例肺心病中并发冠心病发生率为 2 3 8%,临床治疗肺冠病时要两病同时合理用药     

Metabolism of saikosaponin c and naringin by human intestinal bacteria

By human intestinal bacteria, saikosaponin c was transformed to four metabolites, prosaikogenin E1 (E1) prosaikogenin E2 (E2), prosaikogenin E3 (E3) and saikogenin E. Metabolic time course of saikosaponin c was as follows; in early time, saikosaponin c was converted to E1 and E2, and then these were transformed to saikogenin E via E3. Also, this metabolic pathway was similar to the metabolism of saikosaponin c by rat intestinal bacteria.Bacteroides JY-6 andBacteroides YK-4, the bacteria isolated from human intestinal bacteria, could transform saiko-saponin c to E via E1 (or E2) and E3. However, these bacteria were not able to directly transform E1 and E2 to saikogenin E. Naringin was mainly transformed to naringenin by human intestinal bacteria. The minor metabolic pathway transformed naringin to naringenin via prunin. By JY-6 or YK-4, naringin was metabolized to naringenin only via prunin.     

Interactions between loreclezole,chlormethiazole and pentobarbitone at GABAA receptors: functional and binding studies

1. Interations were investigated between loreclezole, chlormethiazole and pentobarbitone as potentiators of depolarization responses mediated by γ-aminobutyric acid_A (GABA_A) receptors on afferent nerve terminals in the rat cuneate nucleus in vitro. These drugs were also compared as modulators of [³H]-flunitrazepam (FNZ) binding to synaptic membranes prepared from rat whole brain homogenate.
2. In rat cuneate nucleus slices, the drugs shifted muscimol log dose–response lines to the left in an approximately parallel fashion with the result that 200 μM chlormethiazole potentiated muscimol responses by 0.567±0.037 log unit (mean±s.e.mean, n=4) while loreclezole gave a maximal potentiation at 10 μM of only 0.121±0.037 (n=6) log unit and 0.071±0.039 (n=22) at 50 μM.
3. While 50 μM chlormethiazole and 30 μM pentobarbitone showed no significant interactions between each other when potentiating muscimol responses in combination, 50 μM loreclezole in combination with either chlormethiazole or pentobarbitone attenuated their potentiating effects, possibly by inducing desensitization of GABA_A receptors.
4. In the [³H]-FNZ binding studies on well-washed membranes, loreclezole enhanced binding to a maximum of 47.3±2.83% of control (mean±s.e.mean, n=3) at 300 μM. Scatchard analysis revealed no change in B_max but a decrease in K_D for [³H]-FNZ from 3.9±0.29 nM to 2.7±0.10 nM (mean±s.e.mean, n=4) in the presence of 100 μM loreclezole. In contrast, 100 μM chlormethiazole caused no potentiation. A small component of the enhancement by loreclezole could be blocked by 100 μM bicuculline and could also be blocked by 100 μM chlormethiazole. It seems likely that the effects on [³H]-FNZ binding are due predominantly to direct actions of the drugs on the GABA_A receptor and are separate from the GABA-potentiating effects.
5. The results indicate distinctly different profiles of action for loreclezole, chlormethiazole and pentobarbitone on GABA_A receptors.

     

Nonhereditary p53 mutations in T-cell acute lymphoblastic leukemia are associated with the relapse phase

We have previously reported that greater than 60% of human leukemic T- cell lines possess mutations in the p53 tumor suppressor gene. To determine whether T-cell acute lymphoblastic leukemia (T-ALL) patient samples possess p53 mutations, we screened peripheral blood-and bone marrow-derived leukemia samples, taken at diagnosis and at relapse, for p53 mutations. Exons 4 through 9 and selected intron regions of the p53 gene were analyzed using polymerase chain reaction-single-strand conformation polymorphism and direct sequencing. p53 mutations were found in 0 of 15 T-ALL diagnosis samples, as compared with 10 of 36 (28%) T-ALL relapse samples. To determine whether p53 mutations play a role in the recurrence (relapse) of T-ALL, two special groups of T-ALL patients were studied: (1) a group of 8 relapse patients whose disease was refractory to chemotherapeutic treatment, and (2) a group of 6 "paired" T-ALL cell samples from patients for whom we possess both diagnosis and relapse samples. Three of 8 relapsed patients (37.5%) whose disease was refractory to the reinduction of remission by chemotherapy possessed missense mutations of the p53 gene. All 3 cases had mutations in exon 5. Among the paired samples, 3 of 6 patients harbored p53 mutations at disease recurrence, but possessed only wild- type p53 alleles at diagnosis. One case had mutation on exon 4, 1 case in exon 5, and 1 case in exon 8 with loss of heterozygosity. These data clearly indicate that recurrence of T-ALL is associated with missense mutations in p53. Our results indicate that (1) mutations of p53 do occur in T-ALL in vivo, and such mutations are associated with the relapse phase of the disease; and (2) p53 mutation is involved in the progression of T-ALL. This conclusion is supported by our observation that the introduction of T-ALL-derived mutant p53 expression constructs into T-ALL cell lines further increases their growth rate in culture, enhances cell cloning in methylcellulose, and increases tumor formation in nude mice.     

Recurrence after resection ofα-fetoprotein-positive hepatocellular carcinoma

The long-term prognosis of surgery for hepatocellular carcinoma (HCC) is not yet satisfactory, the main reason being the high recurrence rate. The authors report the results of a long-term follow-up of 308 patients with HCC who became -fetoprotein-(AFP)-negative after resection between 1975 and 1991. By March 1992, there was recurrence in 134 patients (43.5%). The 1-, 3-, 5- and 10-year recurrence rates were 9.2%, 38.8%, 54.9% and 85.0%, respectively. The 5-year survival rate was 49.7% for patients who had undergone a second hepatic resection (n=48). Analysis of factors influencing postoperative recurrence indicated that patients subjected to mass survey, with a lower -glutamyltransferase level, at an early stage of TNM classification, with a tumour of less than 5 cm, without tumour embolus, and with postoperative immunotherapy had a lower incidence of recurrence. It is concluded that the earlier the disease is diagnosed, the less the recurrence rate; adjuvant immunotherapy may reduce postoperative recurrence, and the early detection and resection of a recurrent tumour are important to prolonging survival further after curative resection of HCC.Abbreviations HCC hepatocellular carcinoma - AFP -fetoprotein - HBsAg hepatitis B surface antigen Presented in part at the 4th Wilson T. S. Wang International Surgical Symposium, 11–13 December 1992, Hong Kong.