Role of urokinase in colorectal neoplasia

The biofunctional activity of the plasminogen activators urokinase and tissue plasminogen activator has been measured in extracts from 50 colorectal carcinomas and 21 adenomas using a bioimmunoassay. Compared with control mucosa urokinase activity was significantly elevated in adenomas (P less than 0.001) and carcinomas, levels being significantly higher in carcinomas (P less than 0.05). In contrast tissue plasminogen activator activity was reduced in adenomas (P less than 0.01) and carcinomas, levels being significantly lower in carcinomas (P less than 0.01). Although enzyme activity did not relate to Dukes' stage or histological grade urokinase activity was higher in carcinomas with venous invasion (n = 17, P less than 0.05), in those with moderate or extensive local spread (n = 27, P less than 0.05) and in cases where a palliative resection only was feasible because of advanced disease (n = 8, P less than 0.05). Urokinase has been implicated in tissue degradation as well as fibrinolysis and may play a role in tumour invasion and metastasis in human colorectal neoplasia.     

Proactive teams yield exceptional care

Learn how a manager and her team used nine management principles to create a proactive nursing team while designing and opening a new inpatient unit.     

Longitudinal retention of families in the assessment of a prevention program targeting adolescent alcohol and tobacco use: the utility of an ecological systems framework

This study examined the association between ecological context (extrafamilial, familial, child factors) at baseline and longitudinal retention of families in the 36-month assessment of an adolescent alcohol and tobacco use prevention program that was conducted within a pediatric primary care setting. A total of 1,780 families were enrolled at baseline when the youth were in the fifth and sixth grades, and 1,220 of these families participated in the 36-month assessment. Findings indicated that familial and child, but not extrafamilial, factors were associated with the participation of families in the 36-month assessment. Clinical implications and future research directions are discussed.     

Analysis of maternal–offspring HLA compatibility,parent‐of‐origin effects,and noninherited maternal antigen effects for HLA–DRB1 in systemic lupus erythematosus

Objective

Genetic susceptibility to systemic lupus erythematosus (SLE) is well established, with the HLA class II DRB1 and DQB1 loci demonstrating the strongest association. However, HLA may also influence SLE through novel biologic mechanisms in addition to genetic transmission of risk alleles. Evidence for increased maternal–offspring HLA class II compatibility in SLE and differences in maternal versus paternal transmission rates (parent‐of‐origin effects) and nontransmission rates (noninherited maternal antigen [NIMA] effects) in other autoimmune diseases have been reported. Thus, we investigated maternal–offspring HLA compatibility, parent‐of‐origin effects, and NIMA effects at DRB1 in SLE.

Methods

The cohort comprised 707 SLE families and 188 independent healthy maternal–offspring pairs (total of 2,497 individuals). Family‐based association tests were conducted to compare transmitted versus nontransmitted alleles (transmission disequilibrium test) and both maternally versus paternally transmitted (parent‐of‐origin) and nontransmitted alleles (using the chi‐square test of heterogeneity). Analyses were stratified according to the sex of the offspring. Maternally affected offspring DRB1 compatibility in SLE families was compared with paternally affected offspring compatibility and with independent control maternal–offspring pairs (using Fisher's test) and was restricted to male and nulligravid female offspring with SLE.

Results

As expected, DRB1 was associated with SLE (P < 1 × 10⁻⁴). However, mothers of children with SLE had similar transmission and nontransmission frequencies for DRB1 alleles when compared with fathers, including those for the known SLE risk alleles HLA–DRB1*0301, *1501, and *0801. No association between maternal–offspring compatibility and SLE was observed.

Conclusion

Maternal–offspring HLA compatibility, parent‐of‐origin effects, and NIMA effects at DRB1 are unlikely to play a role in SLE.