Somatic cell hybrid mapping of human chromosome band 5q31: a region important to hematopoiesis.

As a means of characterizing the distal long arm of chromosome 5, in particular, the region spanning 5q23-->q31, we analyzed somatic cell hybrids prepared from cells with overlapping chromosomal rearrangements. In one hybrid, the derivative chromosome 5 from a patient with acute myeloid leukemia (AML) de novo, whose bone marrow cells had a balanced translocation, t(5;7)(q31;q22), involving chromosome band 5q31, was isolated in a somatic cell hybrid (B294). In addition, we prepared somatic cell hybrids from a lymphoblastoid cell line (CC) derived from a patient who has a constitutional interstitial deletion of chromosome 5 spanning 5q23.1-->q31.1. By a combination of Southern hybridization analysis and fluorescent in situ hybridization, we constructed a map dividing 5q23-->q31 into four regions. We can assign genes to these regions and relate them to anonymous RFLP markers that have been genetically mapped.     

Role of free radicals in the pathogenesis of acute chest syndrome in sickle cell disease

Acute chest syndrome (ACS) of sickle cell disease (SCD) is characterized pathologically by vaso-occlusive processes that result from abnormal interactions between sickle red blood cells (RBCs), white blood cells (WBCs) and/or platelets, and the vascular endothelium. One potential mechanism of vascular damage in ACS is by generation of oxygen-related molecules, such as superoxide (O₂ ^-), hydrogen peroxide (H₂O₂), peroxynitrite (ONOO^-), and the hydroxyl (•OH) radical. The present review summarizes the evidence for alterations in oxidant stress during ACS of SCD, and the potential contributions of RBCs, WBCs and the vascular endothelium to this process.     

Neurophysiological mechanisms of recognition fragmented images by five- to six-year-old children

Behavioral indices and event-related potentials (ERP) were analyzed in five- to six-year-old children who were shown a set of previously unseen fragmented drawings of familiar images. These children recognized less fragmented images than seven- to eight-year-old children. At the age of five to six years, there was no increase in N350–400 prefrontal negativity and slow positive complex, which is characteristic of mature recognition that involves executive control. Comparison of ERP for recognized vs. unrecognized stimuli revealed a significant increase in the P300 and N400 amplitudes in the right occipital area. Note that, in children of this age, there were no significant differences between reactions to recognized and unrecognized images in the lateral extrastriate cortex (T₅/T₆), which is the key structure for recognition of familiar images via integration of their sensory features. Our data suggest that in five- to six-year-old children recognition of fragmented images has specific features determined by immaturity of the executive control and insufficient involvement of the ventral visual system.     

The effect of acid shock on the heat resistance of Listeria monocytogenes

The effect of acid shock on the heat resistance of Listeria monocytogenes was investigated. After growth for 24 h at 30°C in tryptic soy broth containing 0.6% yeast extract, cell culture suspensions of L. monocytogenes were acidified with HCl or acetic acid over various time periods before being heated in whole milk to a temperature of 58°C. When cells were acid-shocked immediately with HCl for 1, 2 or 4 h, those acid-shocked for 1 h demonstrated the largest increase in thermotolerance as compared to control cells, when heated at 58°C in whole milk. In fact, cells acid-shocked for longer than 1 h with HCl demonstrated in some instances a decreased recovery as compared to control cells. Other types of acid-shock treatments included lowering the pH gradually either over a 4 h or a 24 h period. However, regardless of the type of acid-shock treatment, cells acid-shocked with HCl (but not acetic acid) prior to heating had significantly greater heat resistance as compared to control (non-acid-shocked) cells. It appears that acidification with HCl prior to final heating can enhance the heat resistance of L. monocytogenes.     

Protease inhibitors do not prevent the killing of cultured hepatocytes by cystamine

A study was made of the conditions of the killing of cultured hepatocytes by the reactive disulfide cystamine. Six to 12 mM cystamine killed up to 60% of the hepatocytes within 3 hours. The cytosolic calcium ion concentration rose prior to the loss of viability. Treatment with EGTA in a Ca2+-free medium lowered the initial Ca2+ concentration and prevented the rise in response to cystamine. However, there was no change in the number of dead cells. Furthermore, the sensitivity of cultured hepatocytes to cystamine was unaffected by the concentration of calcium in the culture medium. Addition to the culture medium of 3 protease inhibitors, leupeptin, antipain, or chymostatin, did not reduce the extent of cell killing by cystamine despite an inhibition of protein degradation. These data do not support the hypothesis that the toxicity of cystamine is necessarily mediated by proteases activated by a rise in the cytosolic calcium ion concentration.     

Pulmonary hypertensive response to foreign body microemboli

Pulmonary hypertension and foreign body granulomas are recognized sequelae of chronic intravenous drug abuse. We have recently described the development of transient pulmonary hypertension and increased permeability pulmonary edema after the intravenous injection of crushed, suspended pentazocine tablets in both humans and dogs. To determine the role of vasoactive substances in the development of this transient pulmonary hypertension, we measured pulmonary hemodynamics and accumulation of arachidonic acid metabolites in dogs during the infusion of indomethacin, a cyclooxygenase inhibitor, diethylcarbamazine (DEC), a lipoxygenase inhibitor, and FPL 55712, a receptor antagonist for leukotriene C4/D4 (LTC4/D4). Following the intravenous administration of crushed, suspended pentazocine tablets (3-4 mg/kg of body weight), mean pulmonary artery pressure increased from 14 +/- 2 mmHg to 30 +/- 6 mmHg (p less than 0.05) at 60 secs with a concomitant increase in plasma concentrations of 6-keto-PGF1 alpha from 187 +/- 92 pg/ml to 732 +/- 104 pg/ml and thromboxane B2 from 206 +/- 83 pg/ml to 1362 +/- 117 pg/ml (both p less than 0.05). Indomethacin prevented the increase in both cyclooxygenase metabolites, but had no effect on the pulmonary hypertension. In contrast, DEC had no effect on the increase in cyclooxygenase products, but blocked the pulmonary hypertension. FPL 55712 did not effect either the increase in cyclooxygenase metabolites or the pulmonary hypertension. We conclude that the transient pulmonary hypertension, induced by the intravenous injection of crushed, suspended pentazocine tablets, is not mediated by cyclooxygenase products but may be mediated by lipoxygenase product(s) other than LTC4/D4.