Increased type III/I collagen and α1(I)/α2(l) chain in a bronchopulmonary dysplastic lung

The type ratio of collagen III/I and molecule ratio of α₁(I)/α₂(I) were analysed in lungs from five infants with bronchopulmonary dysplasia (BPD) and seven control infants. All five BPD lungs showed typical characteristics, with pulmonary fibrosis and irregular cystic formation at postmortem examination. A pepsin digestion technique followed by interrupted gel electrophoresis was performed for the determination and molecular analysis of collagens III and I. The ratio of collagen types III and I were significantly increased in BPD lung (P < 0.005). The ratio of α₁(I) and α₂(I) were also significantly increased in BPD lung (P < 0.05). It is likely that collagen III is predominantly increased and that the α₁(I) trimer is formed in the active stage of BPD lungs.     

ENDOTOXIN CLEARANCE BY EXCHANGE BLOOD TRANSFUSION IN SEPTIC SHOCK NEONATES

ABSTRACT. The role of exchange transfusion with fresh whole blood in septic shock infants was evaluated. Endotoxin was positive in 8 of 10 infants and completely removed from 6 by exchange transfusion. All 6 infants with negative endotoxins after exchange transfusions survived, but 2 with positive reactions died despite the exchange transfusion. Staphylococcus aureus was cultured in the blood from 2 infants with negative reactions and one of them survived. These findings suggested that the clearance of endotoxin has an important role in exchange transfusion among septic shock neonates.     

Expression of Human Placental Cell Surface Antigens on Peripheral Blood Lymphocytes and Lymphoblastoid Cell Lines

The expression of human placental cell surface antigens was examined in cells of lymphoid origin, including peripheral blood lymphocytes and cultured lymphoblastoid cells of bone marrow or thymus derivation. A select group of this. defined set of surface antigens was detected on all three cell preparations. The most remarkable observation was the conspicuous absence of three subunits previously demonstrated to be present on all human cell surfaces examined to date. Antiserum directed against several placental components prevents adhesion and spreading of cell which grow attached to surfaces. These results suggest a role for these three glycoproteins in mediating cellular adhesion.     

Quantitative Electroencephalography of Medetomidine,Medetomidine‐Midazolam and Medetomidine‐Midazolam‐Butorphanol in Dogs

The purpose of this study was to evaluate the effects of the administration of an α₂‐adrenoceptor agonist alone and in combination with other derivatives on brain wave activity. In addition, the diagnostic values of the electroencephalogram (EEG) for judging the depth of the balanced anaesthesia with an α₂‐adrenoceptor agonist was evaluated. The treatments comprised 20 μg/kg medetomidine (Me‐20), 80 μg/kg medetomidine (Me‐80), 20 μg/kg medetomidine and 0.5 mg/kg midazolam (Me‐Mi) administered intramuscularly, and 20 μg/kg medetomidine with 0.5 mg/kg midazolam and 0.1 mg/kg butorphanol (Me‐Mi‐Bu). The EEG was recorded continuously at pre‐administration, and at 7, 10, 20, 30, 45 and 60 min after administration. The recorded data were analysed by separating the power spectrum into 1–3, 4–7, 8–13 and 14–30 Hz bands. Spectral‐edge analysis was used to calculate the spectral edge frequency 90 (SEF90) and the median edge frequency (MEF). Time‐related changes in power spectrum analysis showed a significant increase in the Me‐80 group in the 1–3 Hz band. The power for 1–3 Hz in the Me‐80 group was significantly higher than in all the other groups. In the 14–30 Hz band, there was a significant reduction of power in all groups following administration of the agents. The SEF90 frequencies were significantly reduced in all groups except for the Me‐20 group after administration of the agents. The SEF90 frequencies in the Me‐20, Me‐Mi and Me‐Mi‐Bu were all significantly higher than those in the Me‐80 group. However, there was no significant difference between the Me‐20, Me‐Mi and Me‐Mi‐Bu groups in any analyses. Our results demonstrated that the changes in quantitative EEG made by the Me‐Mi‐Bu and Me‐Mi groups were similar to those made by Me‐20 groups. Present results suggest that the EEG should be interpreted with caution in assessing the anaesthetic level in balanced anaesthesia in dogs.     

The prognostic value of p53, Ki-67 and matrix metalloproteinases MMP-2 and MMP-9 in transitional cell carcinoma of the renal pelvis and ureter

AIM: To investigate the prognostic and predictive relevance of p53 protein, Ki-67 antigen, MMP-2 and MMP-9 in patients with transitional cell carcinoma (TCC) of the upper urinary tract. METHODS: The expression of p53 protein, Ki-67 antigen, MMP-2 and MMP-9 was examined by immunohistochemistry in 69 patients with TCC of the upper urinary tract. Correlation of p53, Ki-67, MMP-2 and MMP-9 over-expression with conventional pathological parameters and patient survival was examined. RESULTS: p53 over-expression was significantly correlated with histological grade (P < 0.05), but not with pathological stage, vascular invasion, lymphatic invasion or lymph node metastasis. Ki-67 over-expression was significantly correlated with stage, grade, lymphatic invasion and vascular invasion (P < 0.05). In survival analyses, Ki-67 over-expression was a significant prognostic factor in the univariate analysis (P < 0.05), but it did not have a significant impact on survival in the multivariate analysis. Ki-67 labeling index was a significant prognostic factor in patients with a low p53 labeling index, but not in patients with a high p53 labeling index. CONCLUSION: Ki-67 over-expression is of prognostic value in TCC of the upper urinary tract, while p53, MMP-2 and MMP-9 are of limited value.     

Comparison of disseminated intravascular coagulation in trauma with coagulopathy of trauma/acute coagulopathy of trauma‐shock

Gando S, Wada H, Kim HK, Kurosawa S, Nielsen JD, Thachil J, Toh C‐H, Scientific and Standardization Committee on DIC of the ISTH. Comparison of disseminated intravascular coagulation in trauma with coagulopathy of trauma/acute coagulopathy of trauma‐shock. J Thromb Haemost 2012; 10: 2593–5.