Biomedical subjects
Publications and source records attributed to B Watson.
We studied lymphocyte subsets in the blood of twenty-four patients with alopecia areata of various degrees of severity. There was an increase in the ratio of helper to suppressor cells that correlated with the extent of the disease, providing further evidence that the immune system may be involved in its pathogenesis.
We present bacteriological and virological findings together with salient clinical features from a prospective study of 447 children aged under 2 years admitted to hospital with infectious gastroenteritis. Putative pathogenic micro-organisms were identified in the stools of 75% of these children. Eight identifiably distinct groups of viruses, found on electron microscopy and tissue culture were present in 67% of patients--rotavirus was detected most frequently. Pathogenic bacteria (salmonellas, shigellas, Escherichia coli, and Campylobacter jejuni--but excluding Clostridium difficile) were found in 16% only. Altogether 4 X 9% of 390 patients had gastroenteritis associated with Cl difficile toxin. The mean duration of diarrhoea was shortest in patients with identifiable virus, with rotavirus having a mean of 5 X 01 days, and was longest in patients with pathogenic bacteria in the stools (11 X 14 days). The finding of more than one type of virus did not seem to be associated with a significantly increased duration of diarrhoea. There are few clinical features which can be associated specifically with any particular micro-organism or groups of these. Multiple organism isolation was common, but the severity of the illness in those patients with at least two types of organism was not greater. Certain viruses, including the norwalk-like virus, known to be associated with outbreaks of gastroenteritis were found as frequently in a group of patients who did not have diarrhoea studied for comparison. Virus was still detectable in the stools of up to 40% of asymptomatic children on the day of discharge.
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The turnover and metabolism of the individual C apolipoproteins (C-II, C-III1, and C-III2) were studied following the injection of 125I-labeled VLDL into 15 normal and hyperlipoproteinemic subjects. The C apolipoproteins from very low density lipoprotein (VLDL) and high density lipoprotein (HDL) were separated by analytical isoelectric focusing, and subsequent densitometric scanning and radioassay of the stained bands yielded values for specific activity. In 13 of 15 subjects, kinetics of C-II, C-III1, and C-III2 were best described by a one-pool model, whereas two subjects showed biexponential kinetics. The specific activity-time curves for VLDL and HDL were super-imposable, indicating rapid exchange of all C apolipoproteins in hyperlipidemic as well as in normal subjects. In each subject the half-life was similar for C-II, C-III1, and C-III2, which suggests similar synthesis and catabolic mechanisms for each C apolipoprotein. The mass of exchangeable C-II (range 1.0-5.8 mg/kg), C-III1 (2.6-20 mg/kg), and C-III2 (2.0-13 mg/kg) increased with plasma triglyceride concentrations. Values for flux of C-II were 1.0-2.8 mg/d per kg, for C-III1 1.6-5.6 mg/d per kg, and for C-III2 1.2-3.1 mg/d per kg, but they were not related to levels of plasma triglyceride. However the irreversible fractional catabolic rates were inversely related to C apolipoprotein (and triglyceride) mass, suggesting that expansion in C apolipoprotein pool size is related to slower removal, due to the longer residence time of triglyceride-rich VLDL particles in plasma. This was confirmed by similar findings for B apolipoprotein kinetics in VLDL carried out simultaneously.
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Seventy-two families, selected for having at least two children affected with leprosy, were HLA typed for 57 A, B and C locus antigens recognized by the WHO Nomenclature Committee. In addition, 20 possible new "splits" were investigated. The distribution of A, B and C locus antigens in affected and unaffected family members was similar, irrespective of the type of leprosy in the family. Gene frequencies (derived by direct gene counting from 253 haplotypes), haplotype frequencies and delta values were calculated. There is evidence for heterogeneity of B5, B15, B17, Bw16 and Bw35 and for the existence of at least one A locus and one B locus antigen not previously detected. The value of the HLA system for detecting expaternal children in a highly inbred population and the effect of inbreeding on the HLA system is discussed.
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The evidence for a genetic determination of susceptibility to leprosy is reviewed. To test the hypothesis that an HLA (histocompatibility leukocyte antigen)-linked gene is associated with such susceptibility, the association between the distribution of leprosy within a family and the segregation of HLA haplotypes was investigated among 72 families who lived in Karigiri, Tamil Nadu State, South India. A statistically significant association was found for families in which siblings had tuberculoid leprosy and in which neither parent had leprosy. The findings from the data of this study agree with those of two previous studies carried out among smaller populations is Surinam and Wardha, Maharashtra State, India. Such an agreement suggests that a genetic determinant which is linked to the major HLA locus on chromosome 6 and which is probably recessive affects susceptibility to tuberculoid leprosy in humans.
Seven corticosteroids were tested for their effect on the release of beta-glucuronidase when human white cells were challenged with zymosan. Stabilization was noted in two areas of dilution with every steroid but destabilization occurred at high concentrations. However, those steroids that stabilized effectively at low concentrations were also those which were the most potent vasoconstrictors.
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Paraquat, a herbicide which is known to increase intracellular levels of superoxide anion (O2-), stimulated guanylate cyclase [GTP pyrophosphate-lyase (cyclizing), EC 4.6.1.2.] activity. This stimulation by paraquat was seen at concentrations as low as 0.005 mM. The activation of guanylate cyclase by paraquat was not blocked by KCN, an inhibitor of superoxide dismutase [EC 1.15.1.1.], suggesting that the activation process probably does not involve superoxide dismutase which converts superoxide anion to hydrogen peroxide and ultimately to hydroxyl radical. Catalase [EC 1.11.1.6.] did not block the paraquat activation of guanylate cyclase indicating that hydrogen peroxide was probably not involved in the activation process. Butylated hydroxytoluene, a hydroxyl radical scavenger, also had no effect on the paraquat activation of guanylate cyclase activity. Superoxide dismutase inhibited the paraquat activation of guanylate cyclase. Thus, it would appear that superoxide ion itself can activate guanylate cyclase circumventing any requirement for hydroxyl radical formation.
In seven out of 16 patients with drug rashes, the leucocytes selectively released beta glucuronidase when incubated in autologous plasma, indicating the possible presence of immune complexes. When the white cells were incubated with the suspected drug in vitro, they tended to react in three different ways. In four out of 16 cases additional beta glucuronidase was released, perhaps due to the formation of immune complexes, in two out of the 16, beta glucuronidase release was suppressed, perhaps due to antigen excess, and in two cases LDH release was decreased while beta glucuronidase remained unaltered.