SummaryCytotoxicity mediated by natural killer (NK) and lymphokine-activated killer (LAK) cells may be of significance in host defense against viral infections. This study included 347 patients infected with human immunodeficiency syndrome virus (HIV) type 1 and 110 controls. The NK cell activity, either unstimulated or stimulated with interferon-tx (IFN-tx) or interleukin-2 (IL2), and the LAK cell activity were suppressed in patients, but the NK/LAK cell activity did not differ between patients with AIDS and patients without AIDS. However, the IFN-ol-stimulated NK cell activity and LAK cell activity were reduced in patients with symptoms of HIV disease (CDCIV) when compared with asymptomatic patients (CDCII + III). When the data were analyzed by multiple linear regression, the percentage of CD4 + cells had a positive effect on these two parameters in patients without AIDS, whereas the percentage of CD4 + cells had no significant effect on unstimulated and IL-2-stimulated NK cell activity in these patients. In controis and AIDS patients, the percentage of CD4 + cells had no effect on NK/LAK cell activity in multiple linear models. The total number of CD16 § cells was low in patients compared to controls, whereas the percentages of CD16 +, CD56 +, and CD16 + CD56 + were either normal or elevated. Therefore, the decrease in NK cell subpopulations did not contribute to the observed depression in NK/LAK cell activity in vitro. It is concluded that natural immunity is suppressed in HIV-seropositive patients primarily because of a qualitative defect of the NK/LAK cells. This qualitative defect includes a reduced responsiveness to IFN-c~, which is progressive until the onset of symptoms, and possibly related to the loss of CD4 + cells.
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Fourty-four multiple publications of 31 comparative trials of nonsteroidal anti-inflammatory drugs in rheumatoid arthritis were examined for mutual agreement. Thirty-two of the papers were published in the same language as the primary version. Important discrepancies were seen in 14 trials, involving description of the study design in two, exclusion of protocol violators in two, inconsistency in the number of effect variables in five, in the number of side-effects in five, and in the significance level in one. In three articles the conclusion became more favourable for the new drug with time. Only half of the trials had the same first author and number of authors. For six trials, multiple publication was difficult to detect. Adherence to the manuscript guidelines published by the International Committee of Medical Journal Editors should diminish the risk of inflated meta-analyses, reference lists and curricula vitae, and inexplicable discrepancies in articles based on the same data.
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