NOAH rescue AIDS orphans.
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Acquired Immunodeficiency Syndrome↗
Biomedical subjects
G Ash
Publications and source records attributed to G Ash.
The effects of dothiepin on subjects with rheumatoid arthritis and depression.
BACKGROUND: The relative importance of direct analgesic and antidepressant effects of antidepressant drugs in rheumatoid arthritis (RA) is not clear. METHOD: Forty-eight female out-patients with RA, with depression and/or anxiety, were entered into a double-blind, placebo-controlled study of dothiepin in doses up to 150 mg daily to assess the effects on mood [Hospital Anxiety and Depression (HAD) scale and Hamilton Rating Scale (HRS) for Depression], pain [visual analogue scale (VAS)] and disability [Health Assessment Questionnaire (HAQ)]. RESULTS: Repeated measures multivariate analysis of variance revealed that treatment had a significant effect on pain (F(d.f. 1,39) =5.7, P=0.02). There were further interaction effects between treatment and time on pain (F(d. f. 3,117) =3.3, P=0.03), disability (F(d.f. 3,117)=4.2, P=0.008) and duration of early morning stiffness (F(d.f. 3,117) =3.3, P=0.03). Depression (HRS) was considerably reduced in both the dothiepin and placebo groups, and there was no significant difference between groups. Post hoc analyses using analysis of covariance revealed that, in the dothiepin group, pain was significantly reduced by week 4 and remained so at week 12. Disability scores and duration of early morning stiffness were consistently lower in the dothiepin group, although differences failed to reach statistical significance at any follow-up assessment. In the group as a whole, reductions in pain were highly significantly correlated with reductions in HAD depression (r =0.63, P<0.0005), HAD anxiety (r=0.46, P=0.001) and HRS depression (r=0.37, P=0.01). CONCLUSION: Dothiepin is effective in relieving pain, disability and reducing the duration of early morning stiffness in out-patients with RA. Although there is a general association between pain reduction and improved anxiety and depression, the analgesic effect of dothiepin is independent of its antidepressant effect. Individual variation is considerable and further research should try to identify mechanisms of interaction between the antidepressant and analgesic effects of treatment in different patient groups.
Affect↗
HIV surveillance in South Africa.
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Data Collection↗
Study of sulphamethoxazole in rheumatoid arthritis.
Twenty-three patients with rheumatoid arthritis (RA) entered a single-blind cross-over study of sulphamethoxazole 2 g daily compared to placebo. Sulphamethoxazole was administered for 3 months during the 6-month study. Sulphamethoxazole exhibited properties commensurate with a second-line effect with a significant acute-phase reactant response and a parallel change in the clinical state. Adverse effects were common and resulted in nine drug-related withdrawals, mainly due to nausea and vomiting. There were also reversible abnormalities in liver function tests on the active drug. The role of sulphonamides in treatment of RA requires further exploration.
Adult↗
5-HT antagonists and blockade of neuronal (5-HT) receptors on ganglion cells.
Potential changes in superior cervical ganglion cells evoked by 5-HT or the nicotinic agonist, dimethyl-phenyl piperazinium (DMPP), were recorded using the sucrose-gap method and a number of putative 5-HT antagonists tested for potency and selectivity. Selective blockade of 5-HT responses was produced by 5-HT itself and, in increasing order of potency, by cocaine, metoclopramide and quipazine. A non-selective blockade was observed with bufotenine and d-tubocurarine. Substances which had no effect on 5-HT responses included methysergide and other compounds related to LSD, cinanserin, cyproheptadine, phenylbiguanide and morphine. The results provide further information about the 5-HT receptor on sympathetic ganglion cells and support the view that this receptor is distinct from neuronal receptors in the myenteric plexus and on cholinergic nerve terminals.
Acetamides↗
Three genes coding for subunits of the membrane sector (F0) of the Escherichia coli adenosine triphosphatase complex.
Two mutant unc alleles, unc-469 and unc-476, have been characterized as affecting a previously undescribed gene, designated uncF. The uncF gene is part of the unc operon (with the gene order being uncBFEAGDC), although some uncertainty remains as to the relative order of the uncF and uncE genes. Mutant strains carrying the uncF469 or uncF476 allele lack the 18,000-molecular-weight component of the F0 sector of the adenosine triphosphatase in the cell membrane but retain the dicyclohexylcarbodiimide-binding protein (molecular weight, 8,400). Conversely, strains carrying mutations in the uncE gene lack the dicyclohexylcarbodiimide-binding protein but retain the 18,000-molecular-weight protein in the cell membrane. Strains carrying mutations in the uncB gene have both the 18,000-molecular-weight protein and the dicyclohexylcarbodiimide-binding protein present in the cell membranes. The three proteins of the F0 portion of the adenosine triphosphatase, viz., 24,000, 18,000, and 8,400 molecular weights, became membrane associated after in vitro transcription-translation with plasmid pAN51 as template. Plasmids carrying deletions which affected the UncBFE region were isolated from plasmid pAN51 and characterized genetically. A comparison of the genes that were absent from the various deletion plasmids with the membrane-associated products formed after in vitro transcription-translation indicated that the uncB gene coded for the 24,000-molecular-weight protein and that the gene order was probably uncBFE. A correlation between length of deoxyribonucleic acid, genes present, and their products is presented in relation to plasmid pAN51.
Adenosine Triphosphatases↗
Assembly of the adenosine triphosphatase complex in Escherichia coli: assembly of F0 is dependent on the formation of specific F1 subunits.
A strain of Escherichia coli (AN1007) carrying the polar uncD436 allele which affects the operon coding for the F1-F0 adenosine triphosphatase (ATPase) complex was isolated and characterized. The uncD436 allele affected the two genes most distal to the operon promoter, i.e., uncD and uncC. Although the genes coding for the F0 portion of the ATPase complex were not affected in strains carrying this mutant allele, the lack of reconstitution of washed membranes by normal F1 ATPase suggested that a functional F0 might not be formed. This conclusion was supported by the observation that the 18,000-molecular-weight F0 subunit, coded for by the uncF gene, was absent from the membranes. Plasmid pAN36 (uncD+C+), when inserted into a strain carrying the uncD436 allele, resulted in the incorporation of the 18,000-molecular-weight F0 subunit into the membrane. A further series of experiments with Mu-induced polarity mutants, with and without plasmid pAN36, showed that the formation of both the alpha- and beta-subunits of F1 ATPase was an essential prerequisite to the incorporation into the membrane of the 18,000-molecular-weight F0 subunit and to the formation of a functional F0. Examination of the polypeptide composition of membranes from various unc mutants allowed a sequence for the normal assembly of the F1-F0 ATPase complex to be proposed.
Adenosine Triphosphatases↗
Viral antibody titres in HBs antigen-positive and -negative chronic active hepatitis.
A comparative study of antibody titres to nine common viruses has been carried out in hepatitis B surface (HBs) antigen-positive and -negative chronic active liver disease. The results show that increased titres of antibody to morbilli virus by complement fixation and to rubella by haemagglutination inhibition are found in HBs antigen-negative but not in HBs antigen-positive chronic active liver disease. There was a significant association of increased morbilli but not of rubella virus antibody titres with the presence of high-titre nuclear antibodies (ANA) but no association with smooth-muscle antibody or the presence of HLA-B8.
Adolescent↗
Reduction of dialyzer fibrin deposition with sulphinpyrazone.
To determine whether sulphinpyrazone reduces thrombus formation within artificial kidneys, dialyzer 125I-fibrinogen and platelet and fibrinogen levels during dialysis were compared during a non-treatment control period and while patients were receiving sulphinpyrazone. Mean fibrin deposition within the dialyzers, measured as gram X 10(-3) of clottable fibrinogen, was significantly less during sulphinpyrazone treatment (2.5) than during the control period (5.3). Arterial blood platelet counts and plasma fibrinogen levels during dialysis were higher on treatment despite similar predialysis values during control and treatment periods. The results indicate that sulphinpyrazone reduces fibrin formation within artificial kidneys and, since the reduction in deposition of fibrin alone is insufficient to explain the higher plasma fibrinogen levels during treatment with sulphinpyrazone, suggests that this therapy reduces fibrinogen consumption within the patient during hemodialysis.
Blood Platelets↗
Prostacyclin can replace heparin in haemodialysis in dogs.
Despite the use of heparin, activation of platelets on the artificial surface of dialyser membranes results in thrombus formation, microembolisation, and thrombocytopenia. To assess the effects on these events of prostacyclin, the most potent inhibitor of platelet aggregation yet discovered, three groups of healthy greyhounds were dialysed with heparin, heparin plus prostacyclin, or prostacyclin alone. Prostacyclin, either alone or with heparin, abolished microembolisation from the dialyser (as estimated by whole-blood screen filtration pressure) and prevented thrombocytopenia. With prostacyclin, dialysis could be carried out without heparin, and there was no clotting of blood within the extracorporeal circuit nor any change in tests of coagulation.
Animals↗
Coagulation factor concentrate in the treatment of the haemorrhagic diathesis of fulminant hepatic failure.
To assess the value of clotting factor concentrate infusions in fulminant hepatic failure, a controlled trial was performed in which nine patients were randomly allocated to treatment with either concentrate alone or concentrate plus heparin. The five patients receiving concentrate alone all died, with major bleeding as the direct cause of death in three, whereas in the four receiving heparin as well there was only one instance of bleeding and one patient survived. Clinical evidence of intravascular coagulation appeared in two patients treated with concentrate alone and the laboratory evidence of this progressed during the period of infusions in all patients in both treatment groups, although to a lesser extent in those receiving heparin. Additional evidence for intravascular coagulation came from the changes observed in factor VIII levels which, although initially high in all patients, fell subsequently, particularly in those given concentrate alone. There was some improvement in the prothrombin ratio in both groups of patients but not complete correction, and serial assays of clotting factors showed that although factor II rose to high levels during treatment, factors IX and X showed little response. Thus, the use of concentrate of factor IX in this trial, as well as potentiating intravascular coagulation, was inadequate as replacement for the clotting factor deficiencies.
Acute Disease↗