The implementation of occupational health guidelines principles for reducing sickness absence due to musculoskeletal disorders

BACKGROUND: Occupational health guidelines recommend a biopsychosocial approach to manage sickness absence due to musculoskeletal disorders (MSDs), with a primary focus on early intervention through provision of a supportive network. AIMS: To investigate the implementation of a guidelines-based intervention (early contact of absentees; addressing psychosocial obstacles; offering temporary modified work; communicating among the players), and to determine whether this is effective for reducing return-to-work times and duration of future absence. METHODS: A non-randomized controlled trial was conducted within a UK company. Occupational health nurses at two experimental sites (1,435 workers) were trained to deliver the intervention to workers taking absence due to MSDs (low back and upper limb disorders), while usual care was delivered at three control sites (1,483 workers). Company-recorded absence data were collected over a 12-month follow-up period. RESULTS: The implementation of the experimental intervention was impeded by unforeseen organizational obstacles at one site (policies, procedures and individual approaches) which had a detrimental effect on uptake and delivery. At the site where the intervention was delivered per protocol, absence was significantly less compared with controls; 6.5 and 10.8 days, respectively. However, the duration of future absence was not significantly different (13.0 and 25.1 days, respectively). CONCLUSIONS: An early intervention addressing psychosocial obstacles to recovery can be effective for reducing absence due to MSDs. Successful implementation, where the key players are onside and organizational obstacles are overcome, is difficult to achieve.     

The regulation of renal ammoniagenesis in the rat by extracellular factors. III. Effects of various fuels on in vitro ammoniagenesis

The addition of many oxidizable substrates to the medium of incubating rat renal slices decreases ammoniagenesis from glutamine and glutamate. Interestingly, lactate and β-hydroxybutyrate depress ammoniagenesis less in renal slices from acidotic rats compared with normal-control rats. In this study, the effects of an expanded panel of substrates on ammoniagenesis in kidney slices from control and acidotic rats were followed to discern patterns of inhibition. In addition to lactate and β-hydroxybutyrate, acetate, pyruvate, and perhaps acetoacetate caused relatively less depression of ammoniagenesis in acidotic slices. Citrate, succinate, fumarate, octanoate, and α-ketoglutarate decreased ammoniagenesis to the same extent or more in acidotic slices compared with that in normal-control slices. Glycerol had little effect on ammoniagenesis under either condition. From the substrates tested, it can be generalized that those outside the TCA cycle (with exception of octanoate) depress ammoniagenesis less during acidosis, while those in the TCA cycle depress ammoniagenesis equally or even more during acidosis. We hypothesize from the pattern of our results that changes in renal intermediary metabolism at or before citrate formation occur during acidosis and are important regulatory mechanisms for ammoniagenesis.     

Ureteral fistula after renal transplantation: the significance of delayed images

Urinary leakage after renal transplantation is a serious complication that can lead to diagnostic difficulties. A case is reported of urinoma secondary to ureteral fistula characterized in the routine study by a photon-deficient area. Only the image obtained at 6 h allowed a correct diagnosis. The causes for this are discussed and the need to include a delayed study in the follow-up protocol of these patients is emphasized.     

Epidemiological investigation on epilepsy in children of school age (author's transl)

An epidemiological investigation was carried out in 1976-77 on all children attending the fourth year of primary education (9-10 years old) in Venice. The method of analysis was a questionnaire similar to that proposed by Rose (Epilepsy 1973) and by Meighan (Epilepsy 1976). Out of 1838, 1350 answered the questionnaire. The questionnaire synthesises various symptoms of epilepsy in 30 questions starting from the most severe ones. In a second phase the answers were divided into 8 groups: the hypothesis was that the percentage of children with epilepsy in groups 1-3 (high probability to have epilepsy) would be significantly higher than in groups 4-7. In order to test this hypothesis and to assess the discriminating quality of the questionnaire, a random sample of 114 children was submitted to clinical and EEG examination. The final classification in: A) epilepsy; B) febrile convulsions; C) minimal brain disfunction (M.B.D., according to Rose's definition); D) normal, was agreed upon including the heterogeneous information derived from history, neurological examination and EEG interpretation. A statistical elaboration of the findings has shown that the weighted average prevalence rate resulted to be 8.7%; the one relating to febrile convulsions was 27.93%; the one of M.B.D. was 5.2%. The high incidence of apparently positive cases may be explained because of difficulty in understanding some of the terminology used in the questionnaire; such cases, however, have been identified and discarded after a fuller history and neurological examination had been obtained. The problem of false negative cases seems however more important since it may also be caused by prejudice and by the reluctance of many people to accept the idea of epilepsy. For the appraisal of the incidence of this phenomenon we have examined all children (about 90) in two schools of the city indipendently from the answers in the questionnaire: no case of epilepsy was found. Further investigation is being carried out through an inquiry in EEG laboratories, hospitals and private phisicians in order to find out the real number of epileptic children. The incidence of epilepsy estimated with other methods appears similar to our data (Cooper 1965 - Huser and Kurland 1975). As a conclusion the questionnaire survey approach can be effectively used in studies on epilepsy together with epidemiological investigations in the assessment of cases of epilepsy not yet diagnosed as such.     

Probiotic bacteria Bifidobacterium animalis MB5 and Lactobacillus rhamnosus GG protect intestinal Caco-2 cells from the inflammation-associated response induced by enterotoxigenic Escherichia coli K88

Probiotic bacteria may provide protection against intestinal damage induced by pathogens, but the underlying mechanisms are still largely unknown. We investigated whether Bifidobacterium animalis MB5 and Lactobacillus rhamnosus GG (LGG) protected intestinal Caco-2 cells from the inflammation-associated response induced by enterotoxigenic Escherichia coli (ETEC) K88, by inhibiting pathogen attachment to the cells, which is the first step of ETEC pathogenicity, and regulating neutrophil recruitment, a crucial component of inflammation. A partial reduction of ETEC adhesion was exerted by probiotics and their culture supernatant fractions either undigested or digested with proteases. ETEC viability was unaffected by the presence of B. animalis, LGG or their supernatant fractions in the culture medium, indicating an absence of probiotic bactericidal activity. Probiotics and their supernatant fractions, either undigested or digested with proteases, strongly inhibited the neutrophil transmigration caused by ETEC. Both B. animalis and LGG counteracted the pathogen-induced up regulation of IL-8, growth-related oncogene-alpha and epithelial neutrophil-activating peptide-78 gene expression, which are chemokines essential for neutrophil migration. Moreover, the probiotics prevented the ETEC-induced increased expression of IL-1beta and TNF-alpha and decrease of transforming growth factor-alpha, which are regulators of chemokine expression. These results indicate that B. animalis MB5 and LGG protect intestinal cells from the inflammation-associated response caused by ETEC K88 by partly reducing pathogen adhesion and by counteracting neutrophil migration, probably through the regulation of chemokine and cytokine expression.