Blastic transformation associated with 5q- and 12p-.
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Biomedical subjects
Publications and source records attributed to J Dobbin.
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The prevalence of antibodies to HTLV-I and HIV-I in Brazil was determined by testing sera from: (a) 119 members of an isolated Amazonian community of African origin; (b) 100 voluntary blood donors in Rio de Janeiro; (c) 215 patients treated at the Hematology Service, National Cancer Institute, Rio de Janeiro, and (d) 44 Cebus apella New World monkeys, wild-caught in Amazonia. Anti-HTLV-I was detected in 1 (0.84%) of 119 Amazonians, in 8 (3.72%) of the 215 patients and in none of the blood donors or monkeys. The high prevalence found in patients included 4 (5.79%) of 69 with non-Hodgkin lymphoma, 2 (5.88%) of 34 with Hodgkin lymphoma, 1 (16.66%) of 6 patients with diagnosis of anemia and 1 (20%) of 5 with HIV-I infection. Anti-HIV-I was found in 7 (14.89%) of 47 patients and in none of the other groups. The high incidence of HTLV-I infection in the patient group suggests that this retrovirus is endemic in parts of Brazil.
The influence of reperfusion after profound incomplete forebrain ischaemia on blood-brain barrier (BBB) permeability to a small protein tracer was studied in male Sprague-Dawley rats. The mean cortical blood to brain transfer constant (Ki) for 14C-amino isobutyric acid (AIB) was significantly greater at 3 and 6 h of reperfusion, 2.5 times the mean values of controls (p less than 0.05) (2.5 microliter g-1 min-1 and 1.0 microliters g-1 min-1 respectively), but had returned to control values after reperfusion for 24 h. Analysis of distribution of Ki values showed that following 15 min and 30 min of profound ischaemia, there was a significant increase in transfer of AIB across the blood-brain barrier (BBB) after recirculation for up to 6 h, though there was no evidence of protein extravasation as assessed by Evans Blue (EB) dye. After 24 h of reperfusion, the BBB to AIB was restored, and Ki values had returned to control values. It is concluded that following transient global ischaemia, the BBB may recover rapidly.
A 75-year-old man with obstructive sleep apnea and secondary right heart failure was started on nasal CPAP therapy. Shortly thereafter he experienced massive life-threatening epistaxis requiring nasal packing and hospitalization. The epistaxis was thought to be due to the drying effect of nasal CPAP.
Fluorine (19F) nuclear magnetic resonance may be used to image cerebral perfusion in cats receiving perfluorocarbon blood substitutes. 19F relaxation times in these blood substitutes are dependent on oxygen tension (PO2) and may be used to calculate and spatially map cerebrovascular PO2 values in vivo. We have applied this noninvasive method to experimental middle cerebral artery (MCA) occlusion. Following MCA occlusion a perfusion defect is evident in the sylvian region, followed by the appearance of collaterals. Signal from the ipsilateral rete mirabilis is increased. Calculated cortical vascular PO2 values indicate a relative reduction in oxygenation in the ischaemic hemisphere. PO2 maps show a perfused hypoxaemic zone adjacent to the perfusion defect. These changes are partly reversed with reperfusion.
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The distribution of labelled cells through 5 different mouse tumours was measured after a single injection of [3H]-thymidine [( 3H]-TdR) or [3H]-deoxyuridine [( 3H]-UdR). All the tumours had areas where the percentage of labelled cells (the labelling index, LI) was high and areas where the LI was very low. The total area with a low LI was greater after [3H]-TdR than after [3H]-UdR injection in all 5 tumours. In one of the tumours, carcinoma NT, repeated injections of [3H]-UdR at 2 h intervals caused the areas of high LI to spread, eliminating all areas of low LI in many specimens. When 5-fluorodeoxyuridine (FUdR) was injected, to block de novo DNA synthesis in carcinoma NT, [3H]-TdR was incorporated by many more cells. The LI was increased throughout the tumour and no area had a LI below 20% after FUdR plus [3H]-TdR. After flash-labelling with [3H]-TdR alone, nearly half the tumour had a LI below 20%. We conclude that the labelling seen after FUdR plus [3H]-TdR represented the true distribution of S phase cells in carcinoma NT. Routine flash-labelling with [3H]-TdR or [3H]-UdR left nearly half the S phase cells unlabelled and gave an erroneously low value for the proportion of DNA synthesising cells in the tumour. The results suggest that many tumour cells have very large endogenous nucleotide pools which cannot be flooded by a single injection, even of [3H]-UdR.
Cell kinetic parameters measured by the percentage labelled mitoses (PLM) technique have been compared with those derived from continuous labelling and stathmokinetic data in the mouse tumour Carcinoma NT. In [3H]TdR labelled tumours, a PLM curve showed the length of DNA synthesis (TS) to be 9 hr. With continuous labelling, 2.5% of cells entered S phase per hour and TS was 16 hr. Six per cent of cells incorporated [3H]TdR between 1 and 3 hr after an injection of the label. The stathmokinetic technique showed that the rate of entry to mitosis was 2.0% hr. The turnover time (TT) of the population was found to be 16 hr with the PLM data and 35 and 37 hr with the continuous labelling and stathmokinetic data, respectively. The PLM technique therefore showed the mean cell cycle parameters to be about half the values obtained with other methods of measurement. We conclude that in Carcinoma NT there is a wide range of cell cycle times. The continuous labelling and stathmokinetic data represent the mean cell cycle parameters, while the PLM data give the minimum values. A cell loss factor calculated from the PLM data would, therefore, be too high by a factor of two.
Cell cycle parameters measured by the percentage labelled mitoses (PLM) technique have been compared with the results of grain counting and continuous labelling studies in the mouse tumour Carcinoma NT. In [3H]deoxyuridine( [3H]UdR)-labelled tumours a PLM curve showed that the mean length of DNA synthesis (TS) was 7 to 9 hr and the mean cell cycle time (TC) was 16 hr. The turnover time (TT) was between 13 and 17 hr. In contrast, the rate of grain count halving showed that mean TC was 40 hr and TS was at least 19 hr. Cells entered S phase at a rate of 2.3%/hr with continuous labelling, which gave values of 22 hr for TS and 39 to 44 hr for TT. The PLM data therefore gave mean kinetic parameters which were less than half the lengths shown by the other techniques. We conclude that in Carcinoma NT there is a wide range of cell cycle times. The grain count halving and continuous labelling data showed the true mean values of TS and TC or TT, while the PLM data showed only the fastest cycle times. Therefore in this tumour, calculating the cell loss factor from PLM data would give a value too high by at least a factor of two.
We have studied carcinoma NT, a transplantable mouse adenocarcinoma of spontaneous origin. Cells labeled with [3H]thymidine ([3H]TdR) were restricted to a narrow zone around the periphery of this tumour and were also found in rings up to 50 micrometers wide, around isolated blood vessels in the central necrotic area. Labelling with [3H]deoxyuridine ([3H]UdR), another DNA synthesis precursor, produced a very different pattern. The labelled zone around the periphery was much wider than with [3H]TdR, and [3H]UdR labelled cells were found up to 110 micrometers from isolated vessels. [3H]iododeoxyuridine ([3H]IUdR) gave the same pattern of labelling as [3H]UdR. In the heavily labelled zone, within 1 mm of the tumour periphery, the labelling index (LI) was 51% after [3H]UdR or [3H]IUdR injection, and only 36% with [3H]TdR. The data show that at least half of the DNA-synthesizing cells in this tumour did not incorporate [3H]TdR. Previous workers reported cell loss factors for carcinoma NT of 60% calculated from [3H]TdR labelling data and 30% from the rate of loss of [125I]UdR. The present work suggests that calculations based on [125I]UdR data are more likely to be accurate for carcinoma NT than those using [3H]TdR data.