猴株五日热巴尔通体药敏及生化特性研究

目的 了解猴株五日热巴尔通体的生化特性和药物敏感性, 为进一步研究五日热巴尔通体的耐药机制奠定基础。方法 采用E test法, 检测1株五日热ATCC参考株及10株五日热巴尔通体猴分离株的生化特性及对14种抗生素的最低抑菌浓度(MIC)。结果 H15SC对利福平高度耐药(MIC256), 其余菌株敏感;H98SC对克林霉素耐药, 其余菌株敏感;除S13外, 其余10株菌株对丁胺卡那霉素、多粘菌素MICs值较高;全部菌株对阿奇霉素、头孢他啶、环丙沙星、庆大霉素、红霉素、妥布霉素、氯霉素、强力霉素、苄星青霉素敏感。结论 首次发现巴尔通体菌株对利福平高度耐药, 需要进一步了解其耐药机制, 减少不合理用药, 预防利福平耐药在人分离株中发生。     

Characterization of kallikrein from human saliva isolated by use of affinity chromatography

Kallikrein was isolated from paraffin stimulated saliva by use of two steps affinity chromatography. A 610-fold purification of the enzyme was achieved by use of Sepharose 4B conjugated with soy bean trypsin inhibitor and pancreatic trypsin inhibitor. The isoelectric point of kallikrein was found to be pH 4.3 and the molecular weight was calculated to be about 38.000 by gel filtration on a AcA 44 Ultrogel column. The enzyme had a pH optimum at pH 8.6 using BAEE and TAME as substrates. The michaelis constant for kallikrein on these two substrates was 4.0. 10^?4M and 5.5. 10^?4M. respectively.     

振动性血管损伤的生物监测指标的实验研究

目的探讨振动性血管损伤的生物监测指标。方法将新西兰兔分为A组（接振强度3．04m／s^2）、B组（接振强度6．13m／s^2）、c组（接振强度12．26m／s^2）和1个对照组，分别于不同接振时间测定各组新西兰兔血浆内皮素、血管紧张素Ⅱ和一氧化氮的浓度。结果随接振时间的延长和接振强度的增高，血浆内皮素和血管紧张素Ⅱ的浓度有升高的趋势（P〈0．05，P〈0．01），而一氧化氮的浓度有降低的趋势（P〈0．05，P〈0．01）。结论振动导致内皮素、血管紧张素Ⅱ浓度的增高和一氧化氮浓度的降低，可能与振动性血管损伤有一定的关系，因此，选择内皮素、血管紧张素Ⅱ、一氧化氮作为振动性血管损伤的生物监测指标有一定意义。     

Studies on the hepatotoxicity induced by bis (tributyltin) oxide

The toxic effects of bis (tributyltin) oxide (TBTO) on the rat liver were studied with an electron microscope and the accumulation sites of tin were determined with an X-ray microanalyzer. The activities of serum enzymes and the concentration of serum bilirubin were also analyzed. Male Wistar rats received an intramuscular injection of 0.5 ml/kg of TBTO. Marked swelling of the mitochondria appeared in the hepatocytes 4 h after injection of TBTO. Cytoplasmic vacuoles, which contained degenerated mitochondria, gradually increased in number in these hepatocytes. This in turn may have caused a decrease in the volume of hepatic cell cords and an enlargement of sinusoids in the entire hepatic lobule. However, fine structures of intrahepatic bile ducts were not altered. By X-ray microanalysis, tin peaks were preferentially obtained from swollen mitochondria of the hepatocytes. By polarographic analysis of the respiratory responses of mitochondria, it was demonstrated that rates of state 4 respiration and respiratory control ratio were significantly disturbed in TBTO-treated rats in comparison with those of controls. The activities of AST (aspartate aminotransferase) and ALT (alanine aminotransferase) were significantly increased after TBTO treatment, but those of ALP (alkaline phosphatase), LAP (leucine aminopeptidase) and total bilirubin were not changed. These results indicated that parenterally administered TBTO accumulated in the liver cell mitochondria and disturbed oxidative phosphorylation. Mitochondrial dysfunction might induce severe damage of the hepatocytes. Four days after injection of TBTO, hepatic structures and chemical indices were almost restored by the regeneration of hepatocytes.     

The contribution of alpha1-antitrypsin to the total antitrypsin activity of human serum. A study of two phenotype PI OO individuals.

Comparison of the levels of alpha1-AT, alpha2-M, inter alpha-AT, C1 inactivator and antiplasmin and global antitrypsin activity in a group of normal phenotype PI MM individuals, a group of normal individuals with phenotypes with intermediate alpha1 AT activities and alpha2-AT-deficient persons show that alpha1-AT contributes more than 90 percent of the total antitrypsin activity of normal plasma. AT III and fast reacting antiplasmin are shown to contribute to the remaining activity. It can be assumed that due to test conditions the antitrypsin activity of alpha2-M is not assessed. C1 inactivator and inter alpha1-AT do not contribute to a perceptible extent to the overall antitrypsin activity estimated according to the method of Eriksson (Eriksson, S. (1965) Acta Med. Scand. 177, 1).     

Response to trauma of protein, amino acid, and carbohydrate metabolism in injured and uninjured rat skeletal muscles

Soft tissue injury to one hindlimb produced trauma in rats without affecting their food intake or weight gain. Histologic examination showed damage to the soleus and gastrocnemius muscles but not to the extensor digitorum longus muscle. The protein content of the injured soleus muscle was lower than that of the contralateral soleus at one day after injury, and was reflected in vitro by a faster rate of protein degradation. The injured soleus also showed greater rates of protein synthesis, glucose uptake, glycolysis, oxidation of glucose, pyruvate, and leucine, and de novo synthesis of alanine. During three days after the injury, urinary nitrogen excretion increased progressively and was paralleled by a faster rate of protein degradation in uninjured muscles incubated with glucose, insulin, and amino acids. In these muscles, the inhibition of protein degradation by insulin diminished, while its stimulation of protein synthesis was unaffected. This insensitivity of proteolysis to insulin in trauma can explain the increased rate of this process. The oxidation of glucose and pyruvate were lower in the diaphragms of traumatized than of normal rats incubated with leucine, while glycolysis and uptake of 2-deoxyglucose did not differ. The degradation of leucine and isoleucine was greater in the diaphragms of traumatized animals and was associated with a faster de novo synthesis of alanine. For the uninjured soleus muscles of the traumatized rats, the slower rates of oxidation of glucose, glycolysis, and uptake of 2-deoxyglucose in the presence of insulin showed an insensitivity of glucose metabolism to this hormone. In contrast, no differences were seen in these various metabolic processes between the extensor digitorum longus muscles of traumatized and normal rats. These data suggest that the response of skeletal muscles to trauma may depend on their physiologic and biochemical characteristics.     

Multiple forms of acid phosphatase activity in Gaucher's disease.

Although the primary genetic defect in all individuals with Gaucher's disease is a deficiency in glucocerebrosidase activity, the finding of marked elevations in splenic and serum acid phosphatase activity is almost as consistent a finding. Gaucher spleen and serum contain at least two forms of acid phosphatase that can be readily separated by chromatography on columns containing the cation exchange resin Sulphopropyl Sephadex. The major species of acid phosphatase (designated SP-I) contained in Triton X-100 (1% v/v) extracts of Gaucher spleen accounts for 65%--95% of the total activity and has the following properties: (1) it does not bind to the cation exchange column; (2) it exhibitis a pH optimum of 4.5--5.0; (3) it is inhibited by sodium fluoride (15 mM), L(+)-tartaric acid (20 mM), and beta-mercaptoethanol (2.1 M), and (4) it is resistant to inhibition by sodium dithionite (10 mM). The minor acid phosphatase activity (designated SP-II) present in extracts of Gaucher spleen has properties similar to those of the major species of acid phosphatase activity contained in serum from patients with Gaucher's disease: (1) it binds firmly to cation exchange columns (eluted by 0.5 M sodium chloride); (2) it exhibits a pH optimum of 5.0--6.0; (3) it is inhibited by sodium fluoride and sodium dithionite; and (4) it is resistant to inhibition by beta-mercaptoethanol (2.1 M) and L(+)-tartaric acid (20 mM). In addition, a second form of acid phosphatase that is tartrate resistant was found to be elevated in Gaucher serum. This form of serum acid phosphatase did not bind to Sulphopropyl Sephadex, was found to be significantly resistant to beta-mercaptoethanol (2.1 M), and was only partially inhibited by sodium dithionite (10 mM). The findings reported here indicate that at least three distinct forms of acid phosphatase activity are elevated in Gaucher's disease. Furthermore, the minor acid phosphatase activity contained in spleen homogenates has properties very similar to those of the major acid phosphatase activity observed to be present in serum of patients with Gaucher's disease. These data indicate that simple spleen spillage cannot account for the increased levels of serum acid phosphatase in patients with Gaucher's disease.     

Effect of bone-derived growth factor on DNA, RNA, and proteoglycan synthesis in cultures of rabbit costal chondrocytes

Calvariae and chondrocytes in culture have been reported to release growth factors which stimulate bone and cartilage growth respectively. In the present studies, we examined the effects of bone-derived growth factor (BDGF) on DNA, RNA and proteoglycan synthesis in cultured rabbit chondrocytes. Two partially purified fractions of BDGF were tested, one with an approximate molecular weight (MW) of 20-30,000 and with greater activity on calvarial DNA labeling (BDGF I) and another with an approximate MW 6-13,000 and greater activity on bone collagen labeling (BDGF II). Both fractions had a similar effect and increased the incorporation of -3H-uridine into acid insoluble residues in chondrocytes and the incorporation of 35SO4(2-), 3H-glucosamine and 3H-serine into proteoglycans. However, BDGF II had a greater stimulatory effect on the incorporation of 3H-thymidine than BDGF I. These findings suggest that factor(s) released by bone cells are capable of stimulating cartilage metabolism and growth.