What are health authorities doing about the health problems caused by unemployment?

Unemployment is over three million in Britain, and unemployment is known to be associated with poor health. It has been suggested that health authorities should produce a comprehensive response to the health problems caused by unemployment, and a survey was undertaken to find how many had done so. All the regional and district health authorities in England, the health boards of Wales, Scotland, and Northern Ireland, and the family practitioner committees of England and Wales were asked by letter what they were doing to respond to the health problems of unemployment. A list of suggestions of what they might be doing was enclosed. The overall response rate was 77% (255/331), and 50% (127/255) of the respondents were doing something--33.3% (3/9) of the regional health authorities, 64% (101/158) of the district health authorities and health boards, and 26% (23/88) of the family practitioner committees. The paper describes what they were doing. A relation was sought between the level of unemployment in an area and the extent of the response, and a significant association was found. Half of Britain's health authorities are now responding in some way to the health problems associated with unemployment.     

Paramyxovirus-like inclusions in two cases of pycnodysostosis

We describe the biochemical and histological features of two related patients with pycnodysostosis. Examination of bone biopsies taken from both patients showed the presence of large nonfunctional osteoclasts which contained paramyxovirus-like inclusions similar in size and arrangement to those found in Paget's disease of bone. No radiographic, histologic or biochemical evidence for Paget's disease was found in either patient. The presence of osteoclast inclusions may not be specific for Paget's disease, therefore, and could be the result rather than the cause of abnormal osteoclast metabolism.     

Clinical and genetic changes in a case of a Cushing''s carcinoma

A 30-year-old presented In 1984 with a clinically nonfunctional tumour which subsequently developed Into a metastatic corticotrophlnoma from which he died despite surgery In 1984,1986 and 1991 and external radiotherapy In 1986. Molecular genetic analysis of tumour and metastatic tissue revealed loss of heterozygosity at loci on the autosomes 1p, 3p, 10q26,11q13 and 22q12. Tissue taken at surgery In 1986 also revealed positive cytoplasmic Immunostalning for p53 protein. No such staining was evident in tissue taken at first surgery in 1984. Further analysis of Invasive pituitary adenomas may reveal loci associated with such behaviour, enabling better prediction of subsequent clinical outcome than is possible using standard histological techniques, and delivery of early, aggressive treatment to those tumours which show molecular markers associated with a poor prognosis.     

The electrophysiological properties of substantia nigra pars compacta neurones recorded from 6-hydroxydopamine lesioned guinea-pigs in vitro

Summary Intracellular recordings were made from substantia nigra pars compacta neurones in vitro from animals with partial unilateral 6-hydroxydopamine lesions of the nigrostriatal tract. Lesions were assessed and grouped according to the severity of the strital dopamine depletion. No differences were seen between neurones from control and lesioned side nigrae as regards their membrane properties, firing rates, burst activity or percentage of quiescent neurones in any of the lesioned categories. It is concluded that following partial lesioning, the remaining substantia nigra zona compacta neurones in vitro, are functioning normally.     

Carrier diagnosis of Duchenne muscular dystrophy using restriction fragment length polymorphisms

Molecular probes that are tightly linked to and flank the Duchenne muscular dystrophy (DMD) locus, have been used to characterize DMD mutations and diagnose female carriers. Deletions within the Xp21 region were identified for 8 of 71 families studied. Using both DNA and CK studies, accurate (96 to 98%) carrier or noncarrier diagnoses were made for 51 of 75 females at risk in 24 families with a single affected male. DNA studies resulted in an alteration of predicted risk in 40% of the cases. Recombinant diagnostic methods are useful for carrier detection in families with one or more affected males.     

APOE epsilon3 gene transfer attenuates brain damage after experimental stroke.

Apolipoprotein E (apoE, protein; APOE, gene) is the major lipid-transport protein in the brain and plays an important role in modulating the outcome and regenerative processes after acute brain injury. The aim of the present study was to determine if gene transfer of the epsilon3 form of APOE improves outcome in a murine model of transient focal cerebral ischaemia. Mice received an intrastriatal injection of vehicle, a second-generation adenoviral vector containing the green fluorescent protein gene (Ad-GFP) or a vector containing the APOE epsilon3 gene (Ad-APOE) 3 days before 60 mins focal ischaemia. Green fluorescent protein expression was observed in cells throughout the striatum and subcortical white matter indicating successful gene transfer and expression. ApoE levels in the brain were significantly increased after Ad-APOE compared with Ad-GFP or vehicle treatment. Ad-APOE treatment reduced the volume of ischaemic damage by 50% compared with Ad-GFP or vehicle treatment (13+/-3 versus 29+/-4 versus 27+/-5 mm(3)). The extent of postischaemic apoE immunoreactivity was enhanced in Ad-APOE compared with Ad-GFP or vehicle treated mice. These results show the ability of APOE gene transfer to markedly improve outcome after cerebral ischaemia and suggest that modulating apoE levels may be a potential strategy in human stroke therapy.