Evidence that the Receptor for Soluble CD14:LPS Complexes may not be the Putative Signal-Transducing Molecule Associated with Membrane-Bound CD14

Membrane-bound CD14 acts as a receptor for lipopolysaccharide (LPS) on monocytes/macrophages and neutrophils. Studies have suggested that the activation of monocytes/macrophages by the binding of LPS to membrane-bound CD14 may require the association of a signal-transducing molecule with membrane-bound CD14. The observation that non-CD14 expressing cells, such as endothelial cells, can nevertheless be activated by a complex of LPS and a soluble form of CD14 (sCD14) suggests that the receptor for this complex may be identical to the signal transducing molecule associated with membrane-bound CD14. The studies described show that two CD14-specific MoAb are able to block the LPS-induced activation of endothelial cells but do not affect the response of monocytes to LPS. This suggests that the interaction of the sCD14:LPS complex with endothelial cells is distinct from the interaction of membrane-bound CD14 with its putative signal-transducing molecule.     

Effect of low glycogen on glycogen synthase in human muscle during and after exercise

Subjects cycled at a work load calculated to elicit 75% of maximal oxygen uptake on two occasions: the first to fatigue (34.5 ± 5.3 min; mean ± SE), and the second at the same workload and for the same duration as the first. Biopsies were obtained from the quadriceps femoris muscle before and immediately after exercise, and 5 min post-exercise. Before the first experiment, muscle glycogen was lowered by a combination of exercise and diet, and before the second, experiment muscle glycogen was elevated. In the low glycogen condition (LG), muscle glycogen decreased from 169 ± 15 mmol glucosyl units kg^-1dry wt at to rest to 13 ± 6 after exercise. In the high glycogen condition (HG) glycogen decreased from 706 ± 52 at rest to 405 ± 68 after exercise. Glycogen synthase fractional activity (GSF) was always higher during the LG treatment. During exercise in the HG condition, those subjects who cycled for < 35 min (n= 3) had GSF values in muscle which were lower than at rest, whereas those subjects who cycled for > 35 min (n= 4) had values which were similar to or higher than at rest. Thus the change in GSF in muscle during HG was positively related to the exercise duration (r= 0.94; y = 254–17x + 0.3x²; P < 0.001) and negatively related to the glycogen content at the end of exercise (r=–0.82; y= 516–2x + 0.001x²; P < 0.05). During LG exercise GSF remained constant. GSF increased markedly after 5 min post-exercise in both HG and LG conditions. cAMP dependent protein kinase activity increased similarly during both LG and HG exercise and reverted to the preexercise values 5 min post-exercise. It is concluded that muscle contraction decreases GSF, but low glycogen levels can attenuate or abolish the decrease in GSF. The rapid increase of GSF during recovery from exercise does not require glycogen depletion during the exercise.     

Neutrophil superoxide release and interleukin 8 in acute myocardial infarction: distinction between complicated and uncomplicated states

Superoxide release in neutrophils and sera levels of interleukin 8 (IL-8) were determined in 15 patients with complicated acute myocardial infarction (MI) and 15 patients with uncomplicated MI. All patients showed increased superoxide release in unstimulated and stimulated neutrophils compared with healthy control subjects, indicating priming of these cells. Superoxide release of unstimulated or stimulated neutrophils was found to be significantly higher in patients with complicated MI than in patients with uncomplicated MI. Thrombolytic therapy did not affect the rates of superoxide release. The neutrophil chemoattractant/activator IL-8 was detected in the sera of all patients, with significantly higher levels in those with complicated MI. The highest levels of IL-8 were detected at admission to the Coronary Care Unit and significantly decreased thereafter, suggesting its contribution to neutrophil-mediated tissue injury. The high levels of IL-8 may be one of the major contributors to the priming of neutrophils in these patients.     

ABSENCE OF "RECURARIZATION" IN PATIENTS WITH DEMONSTRATED PROLONGED NEUROMUSCULAR BLOCK

The possibility of "recurarization" after antagonism of thecompetitive neuromuscular block with anticholinesterases wasstudied. Observations were made on the time-course of the blockin five patients at risk from recurarization because of multipleorgan failure and who demonstrated unusually prolonged blockade.In none of these patients did the block recur. We conclude that,provided spontaneous recovery of neuromuscular transmissionhas made progress before the antagonism, and that the patientdoes not deteriorate or become exhausted afterwards, recurarizationis unlikely.     

Splenic Pseudocyst Associated with Hypersplenism

A patient with hypersplenism, who was found to have a splenic pseudocyst containing an organized hematoma, is described. There are only two patients with splenic pseudocyst and hypersplenism and an additional two patients with splenic cysts and hypersplenism reported in the world literature. The hypersplenism associated with splenic cysts and pseudocysts is explained on the basis of an expansion of the plasma volume and the total blood volume, an increased destruction of red blood cells and a pooling of blood in the enlarged spleen. The combined use of ultrasonography and computerized tomography has increased the accuracy of noninvasive diagnosis and made more invasive examinations unnecessary. When the ultrasound is technically unsuccessful or when it shows a mixed echo pattern, one should resort to computerized tomography with which it is possible, almost invariably, to differentiate between cysts and neoplasms.     

EFFECTS OF A FEMINIZING TESTICULAR LEYDIG CELL TUMOUR ON NONTUMOROUS TESTICULAR TISSUE: AN ULTRASTRUCTURAL STUDY

The ultrastructural effects of a Leydig cell tumour of the testis on nontumorous testicular tissue have not yet been reported. Described here are the electron microscopic findings in the nonneoplastic testicular tissue of a patient with a feminizing testicular Leydig cell neoplasm. Serial studies were carried out over a period of 3 1/2 years prior to removal of the tumour. The overall general picture was characterized by progressive degeneration of Leydig cells, cells of the germinal series and Sertoli cells. Concomitantly, there was increasing thickening and fibrosis of the tubular walls. Cytoplasmic focal accumulations of glycogen, increasing with the duration of the disease, were conspicuous in many spermatogonia. All of these alterations are nonspecific and are attributable to adverse endocrine effects introduced by the oestrogen-secreting tumour. They were present bilaterally and were more prominent on the tumour-bearing side. Attention is drawn to the role of artifacts, fixation technique and degenerative processes in the production and appearance of certain ultrastructural findings, such as ‘light’ and ‘dark’ cells, myelin figures, membranous whorls and focal glycogen accumulations.