Volume 103  ·   Issue 04  ·  1990

The dynamic changes of thyroid hormone levels in patients with severe head injury were observed. The results showed that the serum thyroid hormone levels changed rapidly within several hours after the injury and the mean levels of serum total T3 and T4 (TT3, TT4) decreased while high reverse triiodothyronine (rT3) increased significantly. Serum TT3, TT4 and rT3 levels returned to normal gradually in 2 to 3 weeks after the injury in the surviving group, whereas serum total T4 gradually declined and rT3 steadily increased in the fatal group. The mean levels of serum TSH remained unchanged in both groups. Therefore, the use of the levels of serum thyroid hormones as adjuvant indices can be helpful in making pertinent judgements of the severity and prognosis of severe head injuries.

Cadmium (Cd) is known to be closely related to the development of children's intelligence. To investigate the clinical significance of the hair cadmium content in the diagnosis of mental retardation (MR), 415 normal and 85 MR children's hair cadmium contents were measured by 79-1 anodic stripping voltmeter. The data were processed by an Apple-II microcomputer. Comparing the median value and using the Chi-square test the Cd contents in the hair of both male and female MR children were obviously higher than those of normal children (P less than 0.001). If the Cd content in the hair of male children is higher than 0.239 μg/g, and higher than 0.180 μg/g in the female, MR can be diagnosed. The sensitivity and specificity of the test are greater than 90%; false positive and false negative rates are lower than 10%. Hair Cd can be used as an additional criterion in the diagnosis of MR and may be important in the screening for MR.

Rapid, extensive loss of infected bone implies abnormal localized inflammatory cell activity. We have demonstrated, using a live bone Ca-45 release model, that polymorphonuclear leukocytes degrade bone in a dose dependent manner. Staphylococcus aureus-stimulated blood mononuclear leukocytes release soluble products in vitro that enhance that process. Despite the usually accepted roles of osteoclasts and their blood-borne monocytic precursors in normal bone remodelling, these results indicate that considerable early pathological infected bone loss may be attributable to inflammatory polymorphonuclear leukocytes.

A total of 11 techniques including 57 items for zygosity diagnosis was employed in two sets of triplet. Namely, placenta-fetal membrane, LDH isoenzymes, etc. The authors made an investigation in detail on the pedigree history of polyembryony and systematic analysis of two sets of male triplets. The conclusion was that the first triplet came from a single ovum, whereas the second triplet developed from double ova. Different methods for the zygosity diagnosis were discussed. It was considered that there was hereditary influence in the occurrence of triplets developing either from a single ovum or from multiple ova.

Platelet aggregation, platelet cAMP levels and thromboxane B2 (TXB2) synthesis had been investigated in 40 diabetics (20 with microangiopathy and 20 without) and 24 normal controls. The washed platelets, but not platelet rich plasma (PRP), from the diabetics show greater sensitivity to aggregation in response to thrombin, collagen and arachidonic acid than controls (P less than 0.05). Platelets from the diabetics contain the significantly decreased cAMP levels (P less than 0.01) and synthesize the significantly greater amount of TXB2 (P less than 0.01) when induced by thrombin or collagen. Conversion of exogenously added arachidonic acid to TXB2 remained unchanged (P greater than 0.05). cAMP levels in platelets from the diabetics exhibited a significant negative linear correlation with thrombin- and collagen-induced TXB2 synthesis. There was no significant difference in platelet aggregation, platelet cAMP levels and platelet TXB2 synthesis between the diabetics with and without microangiopathy. It was suggested that in the diabetic platelets: The observed increase in platelet thromboxane A2 (TXA2) synthesis should be due to the increased activity of arachidonic acid-metabolizing system, most likely at phospholipase site; the elevated platelet TXA2 levels should inhibit platelet membrane-associated adenylate cyclase which lowered the cAMP levels in platelets; and this alternation should be the mechanism of platelet hyperaggregability, which might contribute in some way to diabetic microangiopathy.

RIA method was used in this study to determine immunoreactive β-endorphin (ir-β-EP) in gastric mucosa of patients with benign and malignant gastric diseases. The results showed that the content of ir-β-EP in gastric mucosa in the peptic ulcer group was the highest (68±9.5 pg/mg wet weight tissue, P less than 0.01), while its content in gastric carcinoma was closely related to the degree of differentiation of the tumor, that is, in poorly differentiated carcinoma it was lower than that in well differentiated carcinoma (P less than 0.02), and was also lower than that in gastritis (P less than 0.05). At the same time, we found that β-endorphin can markedly augment the 3H-TdR incorporation of lymphocytes (P less than 0.01). This effect was not blocked by naloxone.

The patients suffering from Coxsackie B viral myocarditis with depressed natural killer (NK) activity were treated with Astragulas membranaceus (AM) intramuscularly for 3-4 months. After the treatment, the NK activity was increased significantly from 11.5±11.9% before therapy to 44.9±15.0%. Another 6 patients of Coxsackie B viral myocarditis with depressed NK activity were treated with conventional therapy. The NK activity remained unchanged in 12.9±6%. The general condition and symptoms improved in all patients with AM therapy, while the titers of neutralizing antibody remained at the same level. Two days after AM treatment, the mean titers of α- and γ-interferon (IFN) markedly increased in comparison with those before therapy and 3 weeks after AM therapy in 16 patients with Coxsackie B viral myocarditis, with left ventricular ejection fraction (LVEF) less than 65% and/or weak ventricular wall motion assayed by radionuclide angiocardiography. Whereas, in 12 patients treated with conventional therapy, there was no statistical difference among the results before and 2 days and 3 weeks after treatment. The results indicate that AM could partly regulate the lost of control of cellular immunity in patients with viral myocarditis.

The effects of direct sheath closure, partial sheath excision, and interposing sheath grafting at different repair stages were evaluated in the chicken model. Primary repair was done after sheath incision and tendon transection, and delayed primary repair was done 4 days after sheath and tendon injuries. The sheath grafting was accomplished by interposing a patch of sheath between the longitudinal incision of the plantar sheath. Six weeks later, biomechanical tests for measuring gliding excursions of the repaired tendons, morphological examinations of the extent of adhesions, and histological observations of the closed sheath or the grafted sheath were carried out. At the primary repair stage, the sheath interposing graft achieved more significant gliding excursion than the groups of direct sheath closure (P less than 0.01) and partial sheath excision (P less than 0.001), and no difference was found between the latter two groups (P greater than 0.05). At the delayed primary repair stage, the sheath interposing graft group was better than the partial excision graft group (P less than 0.05), and the partial excision group was better than the direct closure group (P less than 0.001). The sheath graft and sheath closure at the primary repair stage prevented adhesion formation, but the directly closed sheath did not keep intact after the delayed primary repair and extensive adhesion occurred. In this paper, the importance of volume of the repaired sheath tunnel and possible reasons for results of the delayed primary sheath closure were discussed and the management of flexor tendon sheath for different injuries at different repair stages was suggested.

The surface structure of four different articular cartilages of the femoral head was studied with scanning electron microscope in 12 cases of hip joint osteoarthritis. These articular cartilages were mink white, yellow, dusky red and hyperplastic and thickened. The osteoarthritic articular cartilage surface was uneven with puckerings of various height, width and orientation. The puckerings were covered with fibril network. The fibrils were exposed collagen fibrils and of different diameters. Wider fiber bundles without orientation were found on the fibril network. On the surface of the hyperplastic articular cartilage observed were many deep and oval spaces left behind after breakdown of the lacunae of cells in the clusters of articular chondrocytes. In the spaces, remnants of articular chondrocytes were seen.