Two cases of Robertsonian translocations in oligozoospermic males and their consequences for pregnancies induced by intracytoplasmic sperm injection

Two case histories are presented documenting structural chromosome abnormalities in infertile males. The abnormalities were detected only after application of intracytoplasmic sperm injection (ICSI) was repeatedly unsuccessful or resulted in an abnormal pregnancy. A mosaic Robertsonian translocation 45,XY,der(13;13)(q10; q10)/46,XY,t(13;13)(p10;p10), der(13p;13p) incompatible with normal offspring was found in a male with extreme oligozoospermia after three subsequent ICSI treatments were unsuccessful and one had resulted in a spontaneous abortion. A second case involved a Robertsonian translocation 45,XY,der(13;14)(q10;q10) which was detected in a male with extreme oligozoospermia after ultrasound abnormalities were found in an ICSI-induced twin pregnancy. Amniocentesis showed an unbalanced 46,XY,+13,der(13;14)(q10;q10) karyotype in one twin and a Robertsonian 45,XX,der(13;14)(q10;q10) karyotype in the other twin. Chromosome analysis of males with abnormal sperm characteristics is advised prior to ICSI.      

Tumor-associated trypsin participates in cancer cell-mediated degradation of extracellular matrix

We have recently demonstrated that many cancer cell lines produce a novel trypsinogen isoenzyme called tumor-associated trypsinogen 2 (TAT-2). It was found during a search of the target protease for tumor-associated trypsin inhibitor (TATI). We now show that degradation of subendothelial cell extracellular matrix (ECM) by four different cell lines (COLO 205 colon carcinoma, K-562 erythroleukemia, CAPAN-1 pancreatic carcinoma, and HT 1080 fibrosarcoma) can be partially inhibited by TATI or neutralizing trypsin antibodies. When cells were cultured in serum-free medium on ECM, TATI and trypsin antibodies inhibited the release of immunoreactive fibronectin fragments from ECM by 47-54 and 40%, respectively. Degradation of isotopically labeled ([3H]serine, [3H]proline, and [35S]sulfate) ECM was also significantly prevented by TATI. At its maximum, it exerted a 57% inhibition on the degradation of [3H]serine-labeled ECM. Plasminogen added exogenously to the culture medium further potentiated the proteolysis of ECM. Interestingly, addition of enteropeptidase, an activator of TAT-2, also enhanced cell-mediated proteolysis as assessed by degradation of purified fibronectin coated onto the surface of wells. Immunoblot analysis showed that enteropeptidase-mediated proteolysis generated a pattern of fibronectin fragments similar to that obtained by digestion of purified fibronectin by TAT-2. These results demonstrate the existence of a proteolytic system in tumor cells which is dependent on the activation of TAT-2. We suggest that TAT-2 is involved in a protease cascade-stimulating tumor cell invasion and degradation of extracellular matrix.     

Studies on the mechanism of ristocetin-induced platelet aggregation

Adenine nucleotide metabolism and the release reaction were studied during ristocetin-induced platelet aggregation. Decreasing platelet ATP by incubation with metabolic poisons did not decrease ristocetin- induced aggregation. ADP and ATP were released from platelets during ristocetin-induced aggregation, and ATP was converted to hypoxanthine. However, these occurred after aggregation was almost complete. Aggregation was inhibited by p-choromercuribenzoic acid. By studying platelet suspensions, we were able to determine that this effect was on platelets and not on the plasma cofactor needed for aggregation. We postulate that ristocetin and its cofactor aggregate platelets by binding platelet membranes and that the platelet plays a passive role in this reaction.     

小金胶囊抗炎、镇痛作用药效学试验

目的：考察小金胶囊在抗炎及镇痛方面的药效作用。方法：抗炎作用采用小鼠耳肿胀法、大鼠踝关节肿胀法，镇痛作用采用小鼠甲醛致痛法及醋酸扭体法。结果：小金胶囊对二甲苯所致的小鼠耳炎具有明显的抑制作用，可抑制角叉菜胶所致的大鼠踝关节肿胀，对甲醛所致的小鼠足疼痛具有抑制作用，并可减少醋酸引起的小鼠扭体次数。结论：小金胶囊具有明显的抗炎及镇痛作用。