The impact of public transport on the health of work commuters: a systematic review.

Although the public transport (PT) commute can form a substantial part of the working day, there is a significant gap in our understanding of how it influences health of those who engage in it. The purpose of this systematic review was to therefore generate evidence from 1972 about the extent to which the PT commute (involving train, bus, subway, tram, or metro) impacts on the mental health, physical health and well-being of the working people. We identified 47 studies in English worldwide involving an empirical quantitative focus which met the inclusion criteria. Of these, 23 studies involved over 500 participants. Although initial multi-modal comparisons showed impact on sickness rate, self-rated health complaints, perceived stress level and reduction in sleep, a more homogeneous analysis of rail commuters showed elevation in salivary cortisol, perceived stress, and affective reactions to crowding. Findings also revealed a bias towards use of endogenous self-report measures. On this basis, we argue that it would be of benefit to test theoretical models to account for more objective measures of job and commuting stress. Recommendations were made for flexible working agendas.

Dose-dependent effects of angiotensin converting enzyme (ACE) inhibitors on glomerular prostanoid production by normotensive rats.

1. This study was designed to investigate whether the angiotensin converting enzyme (ACE) inhibitors, captopril, enalapril and fosinopril have a dose-dependent effect on the production of prostaglandin E2 (PGE2), prostaglandin I2 (prostacyclin, PGI2) and thromboxane A2 (TxA2) by glomeruli isolated from normotensive Wistar-Kyoto rats. 2. Measurements of glomerular prostanoid production were made under basal conditions and in the presence of excess exogenous arachidonic acid. 3. All three ACE inhibitors demonstrated dose-dependent effects upon glomerular prostanoid production which varied with the individual ACE inhibitor. 4. Enalapril induced a dose-dependent increase in the ratio of (PGE2 + PGI2)/TxA2, from 2.17 +/- 0.20 to 5.35 +/- 0.84 and to 10.0 +/- 1.16 with the low and high doses of enalapril respectively. In contrast, the high dose of captopril tended to reduce the ratio when compared to the low dose. 5. The results obtained in this study suggest that although all three ACE inhibitors appear to induce prostacyclin synthetase and/or modulate phospholipase A2 (PLA2) activity, these effects differ with the ACE inhibitor studied and the dose employed. 6. This study has demonstrated dose-dependent effects of three ACE inhibitors on glomerular prostanoid production which may be significant in modulating glomerular haemodynamics and growth characteristics of glomerular cells.

Oestradiol-induced hypotension in spontaneously hypertensive rats: putative role for intracellular cations, sodium-potassium flux and prostanoids.

1. The effect of oestradiol alone and in combination with indomethacin on blood pressure, erythrocyte cation concentration and Na(+)-K+ flux has been studied in adult female normotensive and spontaneously hypertensive rats. 2. Oestradiol alone resulted in a significant decrease in blood pressure in spontaneously hypertensive rats (from 165.3 +/- 3.9 to 146.4 +/- 2.7 mmHg, P less than 0.001), whereas it induced a significant increase in normotensive rats (from 111.8 +/- 1.8 to 124.1 +/- 3.6 mmHg, P less than 0.001). When indomethacin and oestradiol were administered simultaneously or when indomethacin was given alone, no change in blood pressure occurred in spontaneously hypertensive rats (158.6 +/- 6.9 and 159.8 +/- 6.2 mmHg, respectively). 3. The fall in blood pressure induced by oestradiol in spontaneously hypertensive rats was associated with significant reductions in erythrocyte K+ concentration (from 127.4 +/- 1.2 to 116.9 +/- 1.7 mmol/l of cells, P less than 0.001), in erythrocyte Na+ concentration (from 14.3 +/- 0.8 to 13.0 +/- 0.6 mmol/l of cells, P less than 0.02), in ouabain-sensitive erythrocyte Na+ flux (from 17.8 +/- 0.3 to 16.0 +/- 0.4 mmol h-1 (l of cells)-1, P less than 0.01) and in ouabain-sensitive erythrocyte K+ flux (from 11.4 +/- 0.2 to 10.4 +/- 0.2 mmol h-1 (l of cells)-1, P less than 0.01). No change in blood pressure, erythrocyte cation concentration or Na(+)-K+ flux occurred when oestradiol and indomethacin were given together or when indomethacin was administered alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of angiotensin-converting enzyme inhibitors on glomerular eicosanoid production in normotensive and spontaneously hypertensive rats.

1. This study was designed to examine the production of certain eicosanoids (prostaglandin E2), prostacyclin (as 6-keto-prostaglandin F1 alpha) and thromboxane A2 (as thromboxane B2) by glomeruli isolated from normotensive Wistar-Kyoto and spontaneously hypertensive rats both before and after the administration of one of three angiotensin-converting enzyme inhibitors, captopril, enalapril or fosinopril, for 10 days. 2. Measurements of glomerular eicosanoid production were made under basal conditions and in the presence of excess exogenous arachidonic acid. 3. The production of prostaglandin E2, 6-keto-prostaglandin F1 alpha and thromboxane B2 was greater by glomeruli from untreated spontaneous hypertensive rats (prostaglandin E2 2.24 +/- 0.41, 6-keto-prostaglandin F1 alpha 1.20 +/- 0.13 and thromboxane B2 2.75 +/- 0.43 ng 10 min-1 mg-1 of protein) than by those from Wistar-Kyoto rats (prostaglandin E2 1.41 +/- 0.28, 6-keto-prostaglandin F1 alpha 0.98 +/- 0.11 and thromboxane B2 1.29 +/- 0.24 ng 10 min-1 mg-1 of protein) under basal conditions. However, these differences only achieved statistical significance for thromboxane B2 (P less than 0.01). Similar strain-related differences were noted in the presence of arachidonic acid. 4. The ratio of glomerular (prostaglandin E2 + prostacyclin)/thromboxane A2 production was significantly lower in spontaneously hypertensive rats than in their normotensive counterparts under basal conditions with values of 1.3 +/- 0.18 and 2.2 +/- 0.20, respectively (P less than 0.01). 5. Angiotensin-converting enzyme inhibitors induced significant changes in the glomerular production of some eicosanoids, which differed both between strains and with the nature of the inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of angiotensin converting enzyme inhibitors on isolated glomeruli.

The following study was designed to examine the effect of the angiotensin converting enzyme (ACE) inhibitors captopril and enalapril on certain biological and physiological activities of isolated preparations of glomeruli from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive SHR rats. The results suggest that the contractile response of glomeruli from SHR to exogenous angiotensin II (Ang II) is significantly enhanced by captopril whereas it has a different effect on those from normotensive (WKY) rats. These effects are unrelated to changes in glomerular Ang II binding or the level of plasma renin activity (PRA), but they do depend partially on the sodium status of the animal. Whereas captopril induced a modest increase in the basal rate of prostaglandin E2 (PGE2) synthesis by glomeruli from normotensive (WKY) but not by those from SHR, the reverse occurred in the presence of Ang II. Prostaglandin E2 synthesis was increased in both strains of rats in the presence of excess arachidonic acid. Further increases occurred with the addition of captopril, these increases being significantly greater by glomeruli from WKY rats than by those from SHR, while enalaprilat had no effect on PGE2 production. The glomerular synthesis of PGE2 was not influenced in either strain of rats by in vitro administration of captopril.

Influence of age on glomerular binding of angiotensin II in normotensive and spontaneously hypertensive rats.

1. Glomerular angiotensin II (ANG II) binding has been studied in normotensive (NTR) and spontaneously hypertensive (SHR) rats at 5, 10, 15 and 20 weeks of age. 2. Binding of 125I-labelled ANG II by glomeruli from NTR and SHR was similar at 5 and 10 weeks of age, with 5 week values of 426.4 (range 384-469) and 400.2 +/- 245 fmol/mg of protein; however, at 15 and 20 weeks ANG II binding by SHR glomeruli was significantly greater than by NTR, with 20 week values of 614.7 +/- 245 and 308.3 +/- 31.8 fmol/mg of protein, respectively (P less than 0.01). 3. The ANG II binding affinity constant (Ka) of glomeruli from NTR and SHR was comparable at 5, 10 and 15 weeks of age, with values of 1.5 (range 1.1-1.9) and 1.08 +/- 0.35 nmol/l, respectively, at 5 weeks; whereas at 20 weeks the Ka for SHR glomeruli was significantly greater than for NTR, with values of 1.85 +/- 0.45 and 0.66 +/- 0.22 nmol/l, respectively (P less than 0.001). 4. Age-related changes in glomerular binding of ANG II in SHR were not found to be related to changes in either plasma renin activity or systolic blood pressure.

Differences in glomerular binding and response to angiotensin II between normotensive and spontaneously hypertensive rats.

1. Angiotensin II (ANG II) binding and the physiological response to exogenous ANG II have been studied in isolated glomerular preparations from normotensive (NTR) and spontaneously hypertensive (SHR) rats. 2. The binding of 125I-labelled ANG II by glomeruli from SHR was significantly greater than that by glomeruli from NTR, whereas the binding affinity constant (Ka) showed that the SHR ANG II glomerular receptor had a lower affinity for the hormone than the NTR glomerular receptor. 3. Glomeruli from SHR were significantly less responsive to exogenous ANG II than those from NTR. 4. Sodium loading resulted in a significant increase in ANG II binding by glomeruli from NTR, whereas a decrease in binding occurred in glomeruli from SHR. 5. Although a high sodium intake caused a reduction in the response of glomeruli from both NTR and SHR to exogenous ANG II, these changes were not statistically significant. In NTR this was associated with a decrease in the concentration of agonist required to cause half-maximal response (EC50), whereas an increase in EC50 was shown by glomeruli from SHR.

Studies of phenylalanine hydroxylase activity in patients with chronic renal failure: the effect of haemodialysis.

The effect of serum from patients with renal failure on phenylalanine hydroxylase activity has been measured in normal individuals, patients with steady-state chronic renal failure and patients undergoing haemodialysis. Significant inhibition of enzyme activity was induced by serum from patients with steady-state chronic renal failure but not from patients undergoing haemodialysis. Inhibitor(s) was readily diffusible in vitro and appeared to have an approximate molecular mass of 800. The results suggest that the low-plasma tyrosine levels observed in patients with chronic renal failure are due, at least in part, to the inhibition of phenylalanine hydroxylase.

Cerebrospinal fluid amino acid concentrations in patients with viral and tuberculous meningitis.

Serial measurements have been made of the cerebrospinal fluid and plasma amino acid concentrations in 11 patients with viral meningitis and in four with tuberculous meningitis. A small increase in the concentrations of a few amino acids in cerebrospinal fluid has been found in a viral meningitis in contrast to a marked increase in most amino acids in tuberculous meningitis. The findings are compared with those found in patients with purulent meningitis and the possible causes and the diagnostic significance of these findings are discussed.

Abnormalities of cerebrospinal fluid amino acids in patients with the Guillain-Barré syndrome.

Measurements of cerebrospinal fluid (CSF) and plasma amino acid concentrations have been made in 12 patients with the Guillain-Barré syndrome. The CSF protein concentration was normal in seven specimens and raised in 13. Abnormalities of the CSF amino acid profile were found in all specimens but were more marked in those with a raised CSF protein concentration. The possible causes and diagnostic significance of these changes are discussed.

Abnormalities of cerebrospinal fluid amino-acids in purulent meningitis.

Serial measurements were made of the cerebrospinal fluid and plasma amino-acid concentrations in 12 patients with purulent meningitis. Marked increases in the concentrations of most CSF amino-acids were found, possibly caused by altered transport mechanisms in the inflamed meninges and choroid plexuses.

Studies of cerebrospinal fluid and plasma amino acids in patients with steady-state chronic renal failure.

The concentration of free amino acids in the plasma and lumbar CSF of 11 patients with steady-state chronic renal failure has been measured and the CSF: plasma concentration ratios calculated. The results have been compared with the corresponding data from 37 control subjects. In renal failure, elevation of the mean plasma concentration of total amino acids and a reduction in the ratio of essential to total amino acids have been found. Whereas some individual plasma amino acid concentrations in renal failure were higher than normal, others were lower. Striking abnormalities of the CSF amino acid concentration have been observed. Some amino acids have shown similar patterns of abnormality in both CSF and plasma, whereas in the case of others, the changes have been restricted to either CSF or plasma. Significant variations from normal of the CSF: plasma concentration ratios were observed for four amino acids.

The effect of haemodialysis on cerebrospinal fluid and plasma amino acids.

The concentration of free amino acids in CSF and plasma has been measured in 19 patients with renal disease undergoing haemodialysis therapy. The values obtained have been compared with those measured in non-haemodialysed patients. At the end of a 10-h dialysis period, the total CSF amino acid concentration had fallen by only 23.3% compared with a 57.7% fall in plasma. Examination of the results for individual amino acid concentrations showed 3 different patterns of inter-relationship between plasma and CSF.