Odorant responses in taste neurons of the rat NTS

In the experiment reported in this paper, 22 of 35 neurons in the gustatory NTS were found to respond to odorant as well as taste stimuli. This odorant response was apparently mediated by the ethmoid nerve and at least one other odorant-responsive system, possibly other nasal trigeminal afferents. These gustatory neurons responded to odorants, as they did to taste stimuli, in a manner consistent with an encoding of stimulus quality information. Thus at least some of the neurons of the gustatory NTS carry information concerning several of the senses involved in ingestion.     

Orbital involvement in 'sinus' histiocytosis. A report of four cases

Sinus histiocytosis is a newly recognized benign disease affecting mainly children and young adults and usually having a protracted clinical course that is relatively unaffected by therapy. This paper describes four additional patients who had orbital involvement initially and reviews the salient clinical and histopathologic features of this entity. The outstanding clinical feature is cervical lymphadenopathy. Associated findings include low-grade fever, anemia, leukocytosis, and elevated IgG levels. A small percentage of patients develop proptosis with palpable orbital tumors. Such patients may not have appreciable lymphadenopathy. Progressive proptosis may lead to exposure keratitis, corneal ulceration, endophthalmitis, and loss of the eye. Histopathologically, the lymph nodes and orbital mass show a proliferation of large histiocytes intermixed with a variable proportion of lymphocytes and plasma cells. Lymphocytes and occasionally other cells derived from the hematopoietic system are commonly seen within the cytoplasm of the histiocytes.     

The application of rigid internal fixation to the treatment of non-union and delayed union using the AO technique

This paper describes our experience over a period of 10 years (1966-76) with fractures showing non-union and delayed union. All were treated by the AO technique. The source of our patients, the management of their fractures and the results are described. From this experience we have drawn conclusions on which future policy will be based.     

Cholesterol-dependent human complement activation resulting in damage to liposomal model membranes

Human (but not guinea pig) complement-mediated damage. It was concluded that human complement was activated spontaneously by liposomes containing a high concentration (71 mol %) of cholesterol. This occurred in the absence of any recognizable antigen or antibody, and did not occur at a low concentration (43 mol %) of cholesterol. Activation of complement resulted in membrane damage and release of trapped liposomal glucose. The complement activity was inhibited by preheating (56 degrees C, 30 min), 10 mM Mg2EDTA3 or EGTA, and by prior adsorption with insoluble immune complexes. Almost all human sera had some reactivity, but it ranged from very low levels (less than 7% liposomal glucose release) to very high levels (greater than 50% glucose release). Complement activation appeared to be mediated by a serum factor which could be removed by adsorption and which was partially heat labile. The factor was transferred by adding heated high reacting human serum to unheated low reacting human serum, or to guinea pig serum. The serum factor, although quantitatively diminished in potency due to heat lability, caused equal activation of each of these two latter complement sources in the presence of high cholesterol liposomes. It did not cause activation of C4-deficient guinea pig complement. These data suggested that the classical complement pathway was activated. The liposomal membrane composition had an influence on this phenomenon. Activities of about half of the human sera were enhanced when galactosyl ceramide, or ceramide alone, was present in the liposomes. Activity was enhanced by longer fatty acyl chain lengths of lecithin when dimyristoyl-, dipalmitoyl-, or distearoyllecithin was employed in the liposomes. Liposomes containing sphingomyelin as the only phospholipid were not sensitive to cholesterol-dependent complement-mediated damage. It was concluded that human complement was activated in the presence of high concentrations of membrane cholesterol and that this was caused by an uncharacterized serum factor and was influenced by the lipid composition of the membrane.