Electron microscopy of the bean and cowpea strains of southern bean mosaic virus within leaf cells.
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Biomedical subjects
Publications and source records attributed to M Weintraub.
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The composition of crystalline inclusions and dense bands in cells of broad bean leaves infected with bean yellow mosaic virus was studied by differential enzymatic digestion. Frozen thick sections were prefixed in glutaraldehyde and exposed to proteinases and nucleases, after which ultrathin sections were prepared for electron microscopy. Examination revealed that the crystals were completely digested by pepsin in 30 min, whereas the dense bands remained intact for the first 20 min, and could not be found after longer periods of digestion. When ultrathin sections of tissues embedded in glycol methacrylate were incubated with the enzymes, pepsin digested the crystals; this left only a filamentous residue which did not disappear after further exposure to pepsin or to RNase. Trypsin had the same effect, but was slower and less consistent. The dense bands were entirely digested in thin sections by pepsin and trypsin. Neither inclusion was affected by RNase or DNase in thick or thin sections. These results demonstrate that the crystals and dense bands are composed entirely or primarily of protein, but there is no evidence that they contain nucleic acid.
Tobacco mosaic virus particles were found in small packets and in small numbers, with the electron microscope, in necrotic leaf cells of Nicotiana glutinosa when the samples were fixed in glutaraldehyde and postfixed in OsO(4), and the sections were stained with heavy metals. The numbers and size of the virus packets were increased greatly when the leaves were detached from the plant after inoculation Assay of concentration showed that detachment resulted in a 30-fold increase of virus. A similar increase in the number of virus particles detected by electron microscopy was produced by keeping inoculated plants at an air temperature of 26 degrees C. A still greater increase in concentration was effected by incubating detached inoculated leaves at 26 degrees C. Moreover the arrangement of virus particles in these cells resembled that of a systemic virus infection. Cells in local lesions of Chenopodium amaranticolor contained large numbers of virus particles both as packets and in the loose arrangement characteristic of systemic infection. Neither the number of particles nor their arrangement was affected in this host by detaching the leaf or by changing the air temperature. It is suggested that there may be two types of localized virus infections, one of which produces virus in low concentration and is amenable to changes in virus concentration and arrangement as a result of environmental manipulation.
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PURPOSE: Langerhans cell histiocytosis (LCH) is a disorder of unknown etiology involving the proliferation and accumulation of cells with the phenotype of a bone marrow-derived antigen-presenting cell of the skin, the Langerhans cell. We have studied p53 expression, an element in the control of cell proliferation, to determine whether it plays a role in the pathogenesis of LCH. PATIENTS AND METHODS: LCH lesions from 10 patients with either localized (n = 5) or multisystem disease (n = 5) were studied. p53 protein expression was assessed by immunohistochemistry, and p53 gene mutation by the single strand conformation polymorphism (SSCP) technique. RESULTS: p53 protein expression was detected in all 10 LCH biopsy specimens examined. It was restricted to Langerhans cells (LCH cells), absent from adjacent cells, and localized to the cell nuclei. No mutations of the p53 gene were detected, nor was there abnormal expression of the p53 binding protein, mdm2. CONCLUSIONS: p53 is readily detectable in LCH cells but not in normal cells. This is either caused by an unusual mechanism (given the absence of mutations in the p53 gene and of mdm2 expression in LCH cells) or by overexpression or posttranslational changes of normal p53 in response to an as yet unidentified cellular stress. Stabilization and inactivation of p53 could lead to the uncontrolled proliferation of LCH cells, or the abnormality could lead to the induction of programmed cell death.
BACKGROUND: Constipation and lower urinary tract symptoms (LUTS) very frequently occur in the elderly, and several reports have suggested that dysfunction in either one of these systems may affect the other. Most studies correlating rectal and bladder dysfunction, however, have been carried out in children or young women. OBJECTIVE: To examine the effect of alleviating constipation on LUTS in the elderly. METHODS: Fifty-two patients aged 65-89 (mean 72 +/- 13) years with chronic constipation and LUTS participated in this prospective cohort study. Before treatment of constipation was initiated and on their monthly visits, patients completed a questionnaire regarding their constipation pattern, urinary symptoms, sexual function and mood, and underwent urinalysis. Urinary tract anatomy and residual urine were evaluated by abdominal ultrasound at the commencement and completion of the study. Patients were followed up for 4 months. RESULTS: Treatment of constipation increased the number of weekly defecations from 1.5 +/- 0.9 to 4.7 +/- 1.2 (p < 0.001). Patients spent less time on the toilet (25 +/- 2.1 versus 63 +/- 1.9 min, p < 0.0001). Fewer patients reported urgency (16 versus 34, p < 0.001), frequency (25 versus 47, p < 0.001) and burning sensation during urination (6 versus 17, p < 0.05). There was improvement in the scoring of urgency, frequency and burning sensation (from a baseline of 52 to 126, 131 and 95, respectively, p < 0.001). Urinary stream disturbances improved in 32 of the 52 patients (p < 0.001). Residual urine volume decreased from 85 +/- 39.5 to 30 +/- 22.56 ml (p < 0.001). There was also a significant decrease in the number of patients with bacteriurial events (5 versus 17, p < 0.001), and an improvement in sexual activity and mood (p < 0.05). CONCLUSIONS: Our data demonstrated that medical relief of constipation significantly improves LUTS in the elderly which, in turn, improves the patient's mood, sexual activity and quality of life.
Significant problems exist in the interpretation of serum digoxin concentration data. Failure to distinguish between results that do not require precise clinical correlation (proof of absorption, presence of drug, etc) and those which depend upon clinical correlation for their meaning ('toxicity' or 'effectiveness') can result in interpretive errors. Problems relating to the source of the serum digoxin concentration can also confound interpretation. Such difficulty may be controllable (obtaining the sample at the proper time, haemolysis, etc) or related to the laboratory technique (cross-reactivity with digoxin metabolites or other medications, technical errors, or lack of precision). Variation within the same patient over time or between patients related to disease (alterations in electrolytes, adrenergic or parasympathomimetic tone, or other medications) may prevent the direct attribution of an observed phenomenon to a particular digoxin concentration. Techniques for determining the effect of digoxin do exist and can be used to gather data for clinical correlations. Ways of improving the interpretaion of serum digoxin concentrations also exist and should be used to improve their value in patient management. The serum digoxin concentration seems to have an important future role. However, we need to know how better to interpret and exploit serum digoxin concentration data.
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