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W M Behan

Publications and source records attributed to W M Behan.

At least 37 records · Page 2Linked to original sources
PubMed1992

Search for retrovirus in the chronic fatigue syndrome.

AIM: To examine peripheral blood and skeletal muscle from patients with chronic fatigue syndrome for exogenous retrovirus. METHODS: Blood samples from 30 patients and muscle biopsy specimens of 15 patients were examined for retroviral sequences by DNA extraction, polymerase chain reaction (PCR), and Southern blotting hybridisation. Sera were examined for human foamy virus by western immunoblotting and indirect immunofluorescence techniques. RESULTS: No differences between the patient and control populations was found for any of the PCR primer sets used (gag, pol, env, and tax regions of HTLV I/II). An endogenous gag band was observed in both the patient and control groups. All sera were negative for antibody to human foamy virus. CONCLUSION: The results indicate that there is no evidence of retroviral involvement in the chronic fatigue syndrome.

Blotting, Southern↗
PubMed1991

Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome.

OBJECTIVE: To determine the presence of enteroviral sequences in muscle of patients with the postviral fatigue syndrome. DESIGN: Detection of sequences with the polymerase chain reaction in a well defined group of patients with the syndrome and controls over the same period. SETTING: Institute of Neurological Sciences, Glasgow. SUBJECTS: 60 consecutive patients admitted to the institute with the postviral fatigue syndrome who had undergone extensive investigation to exclude other conditions. 41 controls from the same catchment area without evidence of fatigue, all undergoing routine surgery. MAIN OUTCOME MEASURES: Routine investigations, serological screen for antibodies to a range of viruses, and presence of enteroviral RNA sequences in muscle biopsy specimens. RESULTS: 15 (25%) patients and 10 (24.4%) controls had important serological findings. 12 patients had neutralising antibody titres of greater than or equal to 256 to coxsackieviruses B1-5 (six positive for enteroviral RNA sequences, six negative); three were positive for Epstein-Barr virus specific IgM (two positive, one negative). Six controls had similar neutralising antibody titres to coxsackieviruses (all negative); one was positive for Epstein-Barr virus specific IgM (negative); and three had titres of complement fixing antibody greater than or equal to 256 to cytomegalovirus (all negative). Overall, significantly more patients than controls had enteroviral RNA sequences in muscle (32/60, 53% v 6/41, 15%; odds ratio 6.7, 95% confidence interval 2.4 to 18.2). This was not correlated with duration of disease, patient and age, or to raised titres of antibodies to coxsackieviruses B1-5. CONCLUSIONS: Persistent enteroviral infection of muscle may occur in some patients with postviral fatigue syndrome and may have an aetiological role.

Adolescent↗
PubMed1991

Mitochondrial abnormalities in the postviral fatigue syndrome.

We have examined the muscle biopsies of 50 patients who had postviral fatigue syndrome (PFS) for from 1 to 17 years. We found mild to severe atrophy of type II fibres in 39 biopsies, with a mild to moderate excess of lipid. On ultrastructural examination, 35 of these specimens showed branching and fusion of mitochondrial cristae. Mitochondrial degeneration was obvious in 40 of the biopsies with swelling, vacuolation, myelin figures and secondary lysosomes. These abnormalities were in obvious contrast to control biopsies, where even mild changes were rarely detected. The findings described here provide the first evidence that PFS may be due to a mitochondrial disorder precipitated by a virus infection.

Adolescent↗
PubMed1991

Amplification and identification of enteroviral sequences in the postviral fatigue syndrome.

Evidence from several sources has long suggested that enteroviruses might play a role in the postviral fatigue syndrome (PVFS). We used the most sensitive molecular virological method available at present, the polymerase chain reaction (PCR) amplification technique, to look for enteroviral copies in peripheral blood leucocytes and muscle from a well-defined group of patients. We demonstrated that our PCR method amplified a sequence common to a wide range of enteroviral serotypes. A highly significant number of the muscle biopsies (53%: P = less than 0.001) from the patients were positive for enteroviral sequences. With regard to the leucocyte samples, 16% in both patient and control were positive. The PCR results on the peripheral blood leucocytes were in keeping with serological findings, in showing that the level of exposure to enteroviruses seemed to be the same in patients and controls: it was therefore of the greatest interest that patients were 6.7 times more likely to have enteroviral genome in their muscle. We conclude that persistent enteroviral infection plays a role in the pathogenesis of PVFS, also providing preliminary evidence that severe mitochondrial injury is one of the mechanisms involved.

Adult↗
PubMed1991

The muscle findings in the neuroleptic malignant syndrome associated with lysergic acid diethylamide.

A detailed pathological description of the muscle findings in a case of the neuroleptic malignant syndrome (NMS) following ingestion of lysergic acid diethylamide (LSD) is given, including the first ultrastructural analysis. Focal necrosis, oedema, and hypercontraction of fibres with glycogen and lipid depletion, were identified, all of which had resolved completely a year later. The findings are compared with those in malignant hyperthermia. It is suggested that the results support the view that in NMS, the muscle rigidity is due to central mechanisms and, in both this disorder and malignant hyperthermia, it is responsible for the hyperpyrexia and its life-threatening complications.

Adult↗
PubMed1990

Assay of complement activation in mouse serum by ELISA.

We describe a simple, sensitive and reproducible ELISA assay for complement activation in mouse serum, based on measurement of the opsonization of purified, heat-aggregated mouse gamma-globulin bound to the solid phase. This assay measures mainly classical pathway activation, and we used it to show significant differences in complement activation in sera from mice of various autoimmune, immunodeficient and immunologically normal strains. This assay has the advantage over existing methods of requiring minimal volumes of serum, and of avoiding problems of species incompatibility.

Animals↗
PubMed1990

Effect of high doses of essential fatty acids on the postviral fatigue syndrome.

Sixty-three adults with the diagnosis of the postviral fatigue syndrome were enrolled in a double-blind, placebo-controlled study of essential fatty acid therapy. The patients had been ill for from one to three years after an apparently viral infection, suffering from severe fatigue, myalgia and a variety of psychiatric symptoms. The preparation given contained linoleic, gamma-linolenic, eicosapentaenoic and docosahexaenoic acids and either it, or the placebo, was given as 8 x 500 mg capsules per day over a 3-month period. The trial was parallel in design and patients were evaluated at entry, one month and three months. In consultation with the patient the doctors assessed overall condition, fatigue, myalgia, dizziness, poor concentration and depression on a 3-point scale. The essential fatty acid composition of their red cell membrane phospholipids was analysed at the first and last visits. At 1 month, 74% of patients on active treatment and 23% of those on placebo assessed themselves as improved over the baseline, with the improvement being much greater in the former. At 3 months the corresponding figures were 85% and 17% (p less than 0.0001) since the placebo group had reverted towards the baseline state while those in the active group showed continued improvement. The essential fatty acid levels were abnormal at the baseline and corrected by active treatment. There were no adverse events. We conclude that essential fatty acids provide a rational, safe and effective treatment for patients with the post-viral fatigue syndrome.

Adult↗
PubMed1990

Immunological abnormalities in BXSB mice at the onset of SLE development.

Male BXSB mice develop murine lupus spontaneously at about 3 months of age. Polyclonal B-cell activation is thought to play a major role in the development of the syndrome in these mice, but the immunological events which lead to this activation are not known. We therefore examined the immune characteristics of mice aged 10-16 weeks, at the onset of disease. We found several immunological markers, indicating polyclonal B-cell activation leading to early, preclinical, disease activity in both male and female BXSB mice, but consistent abnormalities in the percentages and function of lymphocyte subpopulations were found only in male BXSB mice. In particular, the ratio of helper to suppressor/cytotoxic T cells was found to be significantly lower in male BXSB, than in either females of this strain, or normal control DBA2 mice. We conclude that defective immunoregulation is likely to be significant in the initiation of murine lupus, since it is detectable at the onset of disease in male BXSB mice.

Animals↗
PubMed1989

Family studies of congenital heart block associated with Ro antibody.

Complete congenital heart block is associated with the presence of maternal autoantibodies to small ribosomal nucleoproteins (such as anti-Ro) which cross the placenta and may be deposited at the site of cardiac damage. Ten such cases of congenital heart block, their mothers, and their siblings were studied. The seropositive mother of one case had a similar conduction defect (bifascicular block) to that in her affected child. None of the siblings examined had cardiac lesions. Six mothers had Ro or La antibody five to 17 years after the birth of the affected child. Four mothers examined 11-32 years after the birth of an affected child were seronegative. Three of these mothers had evidence of a connective tissue disorder. This evidence is consistent with a hypothesis that a maternal viral infection, associated with autoantibody production, leads to virus crossing the placenta, damaging the fetal heart, and eliciting local deposition of maternal antibody.

Adolescent↗
PubMed1989

A search for common immunological abnormalities at the onset of murine lupus in two genetically different strains.

Mice of the genetically different BXSB and MRL/lpr strains develop murine lupus spontaneously at about three months of age. Polyclonal B-cell activation is thought to play a major role in the development of the syndrome in each strains, but the immunological events which lead to this activation are not known. We therefore examined the immune characteristics of mice aged 10-16 weeks, at the onset of the disease. We found consistent abnormalities in the percentages of lymphocyte sub-populations in both male BXSB, and male and female MRL/lpr mice. In particular, the ratio of helper to suppressor/cytotoxic T cells was found to be significantly lower in male BXSB, and in male and female MRL/lpr mice than in normal, control, DBA2 mice. Significant increases in serum IgG and IgA concentrations, indicative of polyclonal B cell activation, were present in each strain. The histological appearance of the lymphoid organs and the functional responses to mitogen stimulation were, however, distinctly different. We conclude that defective immunoregulation is likely to be significant in the initiation of murine lupus, since it is detectable at the onset of disease in two genetically distinct strains. It may be associated, however, with different immunological phenomena in strains of different genetic backgrounds.

Animals↗
PubMed1988

Postviral fatigue syndrome.

Myalgic Encephalomyelitis or post-viral fatigue syndrome is a common disorder, which has been known previously under a variety of different names, i.e., Iceland disease or Royal Free disease. It may occur in epidemics or sporadically. The cause is unknown, with patients complaining of exhaustion, fatigue, muscle aches and pains, and invariable psychiatric symptoms such as emotional lability, poor memory/concentration, and depression. Present-day research points to the cause as a metabolic disorder secondary to persistent viral infection.

Adolescent↗
PubMed1987

A new model for multiple sclerosis: chronic experimental allergic encephalomyelitis induced by immunization with cerebral endothelial cell membrane.

Multiple sclerosis is considered to be an autoimmune demyelinating disease of the central nervous system. Damage to the blood-brain barrier, of which endothelial cells are the main constituent, occurs in multiple sclerosis, probably due to immunological mechanisms. We report here the results of immune-mediated damage to these cells, produced by immunizing guinea pigs with an endothelial cell membrane fraction. The fraction was obtained from cerebral endothelial cells grown in vitro and was free from myelin basic protein. The immunized animals developed a chronic neurological illness with evidence of delayed hypersensitivity to the cell membrane fraction but not to myelin antigens. Histological examination of the brain in the acute stage showed mononuclear cell infiltrates around blood vessels, while in the chronic phase large areas of demyelination, especially in the periventricular region, were present. This bore a striking similarity to the brain in multiple sclerosis. This may prove to be a useful new animal model for the investigation of the human demyelinating disease.

Animals↗
PubMed1987

Cardiac damage in polymyositis associated with antibodies to tissue ribonucleoproteins.

Cardiac damage, consisting of mild diffuse myocarditis or severe inflammation and fibrosis of the conduction system or both, occurs in more than 70% of patients with idiopathic polymyositis. The lesions are strikingly similar to those detected in the infants of mothers with connective tissue diseases. In these infants the damage is associated with the transplacental passage of a maternal antibody to tissue ribonucleoproteins (anti-Ro). The same antibody was identified in 60% of 55 patients with polymyositis and in 69% (23/33) of those with associated cardiac damage including four with complete heart block. Forty five per cent of those patients who were anti-Ro seropositive had no clinical or electrocardiographic evidence of cardiac lesions. They were in the acute phase of illness, however, and no other more detailed heart investigations had been done. It is postulated that cardiac damage in polymyositis is caused by the antibody and that its presence may serve as a marker for heart involvement.

Adolescent↗