Reoviruslike particles were visualized by electron microscopy in stool filtrates prepared from stools of infants and young children with severe acute gastroenteritis. Patients who had such particles in their stools and whose paired acute and convalescent serums were tested developed an antibody response to the reoviruslike agent, which was measured by immune electron microscopy and by complement fixation. The reoviruslike agent was antigenically related to the epizootic diarrhea of infant mice virus and the Nebraska calf diarrhea virus.

Background. Acquired immunodeficiency syndrome‐related non‐Hodgkin's lymphomas are associated with the B‐cell chromosomal translocation t(8; 14)(q24; q32). The most common secondary chromosome aberrations in these patients involve 1q and are believed to be associated with tumor progression. A mechanism for the origin of these 1q aberrations has not been demonstrated. To their knowledge, the authors report the first human immunodeficiency virus (HIV)‐positive patient to have centromeric decondensation and multibranched chromosome aberrations of chromosomes 1 and 16 resulting in telomeric associations and “jumping translocations” of 1q. Methods. Tumor cells from peritoneal fluid of an HIV‐positive patient were cultured for 24, 48, and 72 hours and analyzed by both conventional G‐banding and fluorescence in situ hybridization. Results. G‐band analysis showed a stemline with t(8;14)(q24;q32), but also showed the progression from centromeric decondensation to multibranched chromosome configurations of chromosomes 1 and 16. The interchange and duplications of chromosome arms resulted in the gain of extra copies of 1q material on a number of different chromosomes, but also the loss of 16q in at least one sideline and the formation of micronuclei. Fluorescence in situ hybridization analysis demonstrated that micronuclei predominantly involved chromosome 1 and, to a lesser extent, chromosome 16. Conclusions. The cytogenetic findings in this unique case suggest that immunodeficiency may be a factor involved in centromeric instability, multibranching, and the progression to the subsequent formation of telomeric fusions and multiple unbalanced translocations of 1q (jumping translocations). The striking similarity of the centromeric instability in this patient to those with ICF syndrome (variable immunodeficiency, centromeric heterochromatin instability, and facial anomalies) suggests hypomethylation as the etiologic mechanism for the chromosome instability.

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The intravenous administration of dextran has previously been shown to produce a bleeding tendency in laboratory animals and in humans. Extensive studies concerning the hemostatic defect have yielded much useful information. Carbone, Furth, Scott and Crosby (1) found that the major abnormality consisted of a prolongation of the bleeding time. In seven of 11 patients given 1,500 to 6,500 ml. of dextran intravenously over a five day period the bleeding time was prolonged over 30 minutes. Since there is ample indication that the platelet is concerned with changes in the bleeding time, it seemed pertinent to procure more evidence concerning the effect of dextran on the platelet. Rothman, Adelson, Schwebel and Langdell (3) have shown that C14 labeled dextran is taken up by the platelet. In substantiation of this effect Ponder Jan. 20, 1957. noted that the electrophoretic mobility of the platelet in saline appeared to be modified by dextran (4). He pointed out, however, that the electrophoretic mobility may be influenced by factors that are difficult to control or appraise. In the determination of the isoelectric point these uncontrolled factors may be eliminated or reduced significantly in their importance.Microelectrophoresis has been used rather extensively to study the red cell and those changes in its environment that affect its surface charge (5, 6). Recently Creger, Tulley and Hansen (7) utilized this method to determine the effect of hydrocortisone on red cell-antibody union. Relatively few studies of the platelet have been carried out by microelectrophoresis. Abramson (8) found that the horse platelet migrated at a rate of 0.45 ,u per second per volt per cm. in oxalated plasma. The pH was not recorded. The true mobility was determined by correcting for the electroosmotic effect at the center of the electrophoresis cell. This determination of the true mobility is accomplished more simply by observing the mobility at one of the stationary levels of the cell. Our studies include observations on the electrophoretic mobility and isoelectric point of platelets suspended in various buffer and protein solutions and the effect of dextran on these measurements. METHODBlood was obtained from patients without hematologic disease and from normal humans. Multiple donors were used for the determination of each isoelectric point. Blood was drawn using nonwettable equipment. Platelet suspensions were prepared in the following manner: 1) A silicone-coated needle was inserted into an antecubital vein after a tourniquet had been applied for no more than one minute. The first few drops of blood were discarded. 2) Fifteen ml. of blood was then permitted to flow down the side of a silicone-coated tube containing 0.5 ml. of 5 per cent sequestrene. 3) Thirty ml. of blood was spun at 5 to 100 C. in a refrigerated (International 155