Aims: To assess and compare the self perceived work related stress among emergency department (ED) and general ward (GW) nurses, and to investigate its relation with salivary IgA and lysozyme. Methods: One hundred and thirty two of 208 (63.5%) registered female ED and GW nurses participated in the study. A modified mental health professional stress scale (PSS) was used to measure self perceived stress. ELISA methods were used to determine the salivary IgA and lysozyme levels. Results: On PSS, ED nurses had higher scores (mean 1.51) than GW nurses (1.30). The scores of PSS subscales such as organisational structure and processes (OS), lack of resources (RES), and conflict with other professionals (COF) were higher in ED than in GW nurses. ED nurses had lower secretion rates of IgA (geometric mean (GM) 49.1 µg/min) and lysozyme (GM 20.0 µg/min) than GW nurses (68.2 µg/min, 30.5 µg/min). Significant correlations were observed between PSS and log IgA and lysozyme secretion rates. OS, RES, and COF were correlated with log IgA and lysozyme levels. Conclusion: ED nurses, who reported a higher level of professional stress, showed significantly lower secretion rates of salivary IgA and lysozyme compared to GW nurses. Salivary IgA and lysozyme were inversely correlated with self perceived work related stress. As these salivary biomarkers are reflective of the mucosal immunity, results support the inverse relation between stress and mucosal immunity.

Salivary immunoglobulin A (IgA) and lysozyme have been studied as possible biomarkers of stress. This study examined the stress levels among female nurses in various units and the relationship between these stress levels and salivary IgA and lysozyme secretion. One hundred ninety-five (43%) of 457 eligible female nurses from surgical wards/operating theaters (SURG), medical wards (MED), and outpatient clinics/day-surgery theaters (OPD) completed a self-administered questionnaire. From this group of 195 nurses, 124 provided a salivary sample accumulated over 5 minutes. Stress levels were assessed with a ten-point Stress Assessment Score (SAS) for Asians and a direct question on perceived life stress. Enzyme-linked immunosorbent assay and lyso-plate methods were used to determine salivary IgA and lysozyme levels. Forty-five percent of SURG, 35% of MED, and 17% of OPD nurses scored at least four points on the SAS. SURG nurses had the lowest IgA secretion (geometric mean; 95% confidence interval [CI]) rates (43 micrograms/min; 36 to 51 micrograms/min). The other groups had significantly higher salivary IgA secretion rates: MED (96 micrograms/min; 80 to 116 micrograms/min) and OPD (77 micrograms/min; 60 to 98 micrograms/min) Findings for salivary lysozyme (microgram/min) were similar; SURG (9 micrograms/min; 6 to 13 micrograms/min) MED (19 micrograms/min; 12 to 28 micrograms/min) and OPD (16 micrograms/min; 9 to 28 micrograms/min). The salivary IgA (Spearman's r = -0.22, P = 0.01) but not the lysozyme (Spearman's r = -0.01, P = 0.9) secretion rate correlated negatively with SAS. Nurses working in various units under different conditions experienced dissimilar levels of stress. Salivary IgA, but not lysozyme, correlated inversely with self-reported levels of stress. It may thus be a potential biomarker in future studies on stress.

Summary: Arterial thrombosis and renal vein thrombosis occurred in two men and one woman, respectively, treated with steroids for the nephrotic syndrome. Raised serum cholesterol occurred in one patient only. Though bleeding, clotting, and prothrombin times, as well as the platelet counts, were normal, the rate of thromboplastin generation was increased in all three patients. Adding heparin to the plasma of one patient slowed the rate, and suggested that the raised rate could be due to removal or suppression of such normal circulating coagulation inhibitors. The thromboplastin generation test seems to be useful in diagnosing and managing such hypercoagulable states, and may help in further investigations of their causes.

Autosomal dominant polycystic kidney disease (ADPKD) is a common Mendelian disorder that affects approximately 1 in 1000 live births. Linkage studies have shown that the majority (approximately 85%) of cases are due to mutations in PKD1 on chromosome 16p, while mutations in PKD2 on chromosome 4q account for most of the remaining cases. Locus heterogeneity in ADPKD is known to contribute to differences in disease severity, with PKD1-linked families having earlier onset of end-stage renal disease (ESRD) than PKD2-linked families (mean age at ESRD: 56 versus 70, respectively). In this study, 11 Canadian families with ADPKD were screened for PKD2 mutations. In four families, linkage to PKD2 was previously documented. In the remaining seven smaller families, one or more affected members had late-onset ESRD at age 70 or older. Using single-stranded conformational polymorphism analysis, one affected member from each family was screened for mutations in all 15 exons of PKD2, which were PCR-amplified from genomic templates. A spectrum of mutations was found in approximately 73% (8 of 11) of the families screened, with no difference in the detection rate between the PKD2-linked families and the families with late-onset ESRD. In three unrelated families, insertion or deletion of an adenosine in a polyadenosine tract (i.e., (A)8 at nt 2152-2159) was found on exon 11, suggesting that this mononucleotide repeat tract is prone to mutations from "slipped strand mispairing." All mutations, scattered between exons 1 and 11, are predicted to result in a truncated polycystin 2 that lacks both the calcium-binding EF-hand domain and the two cytoplasmic domains required for the interaction of polycystin 2 with polycystin 1 and with itself. Furthermore, no correlation was found between the location of the mutations in the PKD2 coding sequence and disease severity. Thus, these findings are consistent with other recently published reports and suggest that most PKD2 mutations are inactivating.