The “Toxic Dose” of System Problems: Why Some Injured Workers Don’t Return to Work as Expected

Introduction Most workers who incur an injury on the job follow a relatively straightforward path through a workers’ compensation claim, recovery and return to work. However, a minority of compensation claims is prolonged and can be disproportionately costly. We conducted this qualitative study in order to gain an understanding of systemic, process-related problems affecting injured workers who had failed to return to work as expected. Method A total of 69 in-depth interviews were conducted with injured workers with complex and extended workers’ compensation claims and with return-to-work (RTW) providers such as health care providers, insurers, legal advisors, and workplaces. The study was based in Ontario, Canada. A modified grounded theory analysis led to the identification of common mechanisms in RTW problems. Results We identify problems with return to work and extended workers’ compensation claims in dysfunctions in organizational dynamics across RTW systems including the workplace, healthcare, vocational rehabilitation and workers’ compensation. These system problems are difficult to identify because they appear as relatively mundane and bureaucratic. These appeared to have damaging effects on workers in the form of a ‘toxic dose’ affecting the worker beyond the initial injury. Conclusions Worker’s problems with extended claims were linked to RTW policies that did not easily accommodate conflict or power imbalances among RTW parties and by social relations and processes that impeded communication about RTW situations and problems. Avenues for intervention are located in a shift to a critical lens to RTW process that addresses differences of knowledge, resources, and interests among different parties.     

Neonatal maternal deprivation promotes Nippostrongylus brasiliensis infection in adult rats

Neonatal stress is known to alter immune responses in adults and parasitic infection is modulated by the immune status of the host. The present study aimed to establish whether neonatal maternal deprivation affects the time course of Nippostrongylus brasiliensis infection and associated intestinal alterations in adult rats. Rat pups were separated from their dam 3h daily during postnatal days 2-14, or left undisturbed. At 12 weeks of age, N. brasiliensis infection was induced by subcutaneous administration of 3000 L3 larvae. At 7 and 12 days after primary infection, the number of intestinal adult worms, fecal egg output, jejunal paracellular permeability, and myeloperoxidase (MPO) activity were measured. On days 7 and 12 after a secondary infection, numbers of adult worms and egg production were determined. Maternal deprivation increased the number of jejunal adult worms and fecal eggs and larvae on day 7 after primary infection, and exacerbated the increase in jejunal MPO activity induced by the infection. On day 12, adult worms were only observed in deprived rats. N. brasiliensis infection did not potentiate the increase in jejunal paracellular permeability induced by maternal deprivation. After the second infection, no egg was detected in both control and deprived rats. In conclusion, maternal deprivation in rats facilitates primary infection by N. brasiliensis and enhances the inflammatory response of the jejunum, but does not induce severe breakdown of immunity to N. brasiliensis.     

The dex/CRH test-Is it better than the DST?

The dexamethasone suppression test (DST), frequently abnormal in mood disorder patients, is considered to measure glucocorticoid receptor-mediated negative feedback. We examined the hypothesis that the, apparently more sensitive, dexamethasone/corticotrophin-releasing-hormone (dex/CRH) test unveils subtle hypothalamic-pituitary-adrenal axis disturbance not detected by the DST in 82 patients with mood disorders and 28 controls. There was a close correlation between the cortisol responses on the two tests (r(s)=0.73, p<0.0005). However, ROC analysis revealed that the dex/CRH test had better diagnostic performance than the DST (p=0.031). The sensitivity of delta cortisol (from the dex/CRH) was 61.9% and the specificity 71.4%. The sensitivity of 1500 h cortisol (the DST) was 66.6% and the specificity was 47.6%. This suggests that the two tests measure common pathology but that the dex/CRH test has better diagnostic utility.     

The cariostatic potential of cheese: cooked cheese-containing meals increase plaque calcium concentration

OBJECTIVE: Eating cheese by itself increases plaque calcium concentration - which is probably one mechanism of the well-established action of cheese in reducing experimental caries. The objective of the present study was to determine whether consumption of cheese as part of a cooked, mixed meal (ie as it is habitually consumed) is able to increase plaque calcium concentration. DESIGN: Plaque samples were obtained from 16 adult volunteers before and 5 minutes after consumption of either a 15 g cube of cheese, one of two cheese-containing test meals, or one of two control meals. Each subject tested each of the four meals on a separate occasion. Plaque calcium concentration was measured using atomic absorption spectrophotometry. RESULTS: The test meals increased plaque calcium concentrations to a significantly greater magnitude than the control meals (P < 0.05). A non-significant trend was observed towards a larger magnitude of change in plaque calcium concentration in the 8 subjects with the lowest, compared with the 8 subjects with the highest baseline concentration. CONCLUSION: The findings suggest that cheese-containing meals increase plaque calcium concentration and thus probably protect against dental caries.     

Inhibition of nitric oxide synthase reverses changes in peritoneal permeability in a rat model of acute peritonitis.

BACKGROUND: Acute peritonitis is the most frequent complication of peritoneal dialysis (PD), and nitric oxide (NO) is thought to play a role in the structural and permeability changes observed in this condition. We have used a combination of expression, enzymatic and pharmacological studies to substantiate the potential role(s) played by NO during peritonitis. METHODS: The peritoneal equilibration test was performed in control rats and rats with acute peritonitis (originating from skin flora), using standard dialysate supplemented or not with the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). In parallel, peritoneal NOS enzymatic activities were measured and expression studies for NOS isoforms and S-nitrosocysteine reactivity performed in the peritoneum. RESULTS: In comparison with controls, rats with acute peritonitis were characterized by inflammatory changes, increased S-nitrosocysteine immunoreactivity, and increased NOS activities in the peritoneum, due to the up-regulation of endothelial and inducible NOS. In parallel, rats with acute peritonitis showed increased permeability for small solutes; decreased sodium sieving; loss of ultrafiltration (UF); and increased protein loss in the dialysate. Addition of L-NAME to the dialysate did not induce permeability changes in control rats, but significantly improved UF and reversed permeability modifications in rats with peritonitis. The effect of L-NAME was reflected by a mild but consistent increase in blood pressure during PD exchange. CONCLUSIONS: Our results demonstrate that local generation of NO, secondary to up-regulation of NOS isoforms, plays an important role in the regulation of peritoneal permeability during acute peritonitis in rats. By itself, NOS inhibition improves UF and reverses permeability changes, which might offer new therapeutic perspectives in acute peritonitis.     

Cognitive impairment in depression is not associated with neuropathologic evidence of increased vascular or Alzheimer-type pathology.

BACKGROUND: Cognitive impairment is common in depression, but underlying mechanisms remain unknown. We examined whether increases in Alzheimer-type or vascular pathology are associated with cognitive impairments in elderly depressed subjects. METHODS: Eleven subjects who had died during a well-documented episode of DSM-IV major depression were included. Neuropathologic assessments, blind to group membership, included standardized assessment of neuritic plaques, neurofibrillary tangles, and Lewy Bodies in frontal, temporal, parietal, and occipital cortices. Braak staging of Alzheimer pathology was also performed. Cerebral microvascular disease was scored according to a previously validated scale, and a score for cerebral and systemic atheroma of large and medium sized arteries was obtained. RESULTS: No subject had Lewy bodies. Plaque and tangle counts for all subjects were well within published norms for age-matched control subjects. There were no significant differences in plaque or tangle counts between subjects who were cognitively impaired (n = 5) and those who were nonimpaired (n = 6) during their depressive illness. Similarly, neither total microvascular pathology nor deep frontal microvascular pathology differed between the two groups. CONCLUSIONS: Our results indicate that the liability for some patients to develop cognitive impairment during a depressive episode is not related to an increase in Alzheimer-type or vascular neuropathologic change. This indicates that other mechanisms must underlie both the cognitive impairment associated with depression and the observation that depression is a risk factor for dementia.