Behavior of artificially produced holes in lung parenchyma

Spherical and cylindrical holes were cut in the parenchyma of isolated dog lung lobes. The holes were insufflated with tantalum dust and the hole diameters were measured along the deflation limb of the lobe pressure-volume curve from transpulmonary pressures of 20 to 0 cmH2O. Hole volume as a fraction of lobe volume was found to be independent of transpulmonary pressure. The hole volume relative to the amount of tissue removed was used to determine the displacement at the hole boundary. A comparison of this displacement with the displacement predicted by a continuum mechanics analysis provides evidence for the applicability of the methods of continuum mechanics and further evidence that the shear modulus of the parenchyma is relatively small.     

Lymphocytes and cells in malignant transformation: similarities and possible relationship between the two cell types

This paper points out some similarities between the behaviour and characteristics of lymphocytes and their transformation to lymphoblasts on one hand and malignant cells on the other. The areas of similarity are (1) anomalous communicating junction formation; (2) recruitment of neighbouring cells; (3) random antigen expression; (4) Fc synthesis; (5) stimulation by immune attack; (6) relation to a plasminogen activator, and (7) inhibition of stimulation by trypsin inhibitors. It is argued that, considering the anomalous membrane characteristics shown by lymphocytes and malignant cells and the list of similarities, carcinogenesis could represent a normal cell line infected with lymphocytic information. Two incidental ideas are presented based on the main idea. These concern lymphocytes but are related to malignant cells and their characteristics too. They are (1) a mechanism whereby generation of randomness in the variable region of Ig molecules could take place, and (2) a mechanism whereby the lymphocyte, in order to kill its target, could use the normal cell's propensity to form communicating intercellular junctions.     

Exit block of artificial pacemaker induced by carotid sinus massage

Failure of the pacemaker is a common complication of pacemaker therapy. Identification of the disorder responsible for the failure to pace is often difficult. An increase in myocardial threshold can result in nonconduction of the artificial impulse, particularly near the end of the life of the battery, when the output of current has started to decline. This report demonstrates such an increase in myocardial resistance which was apparent only upon massage of the carotid sinus.     

Small low-density lipoproteins and vascular cell adhesion molecule-1 are increased in association with hyperlipidemia in preeclampsia

The pregnancy disorder preeclampsia is characterized by endothelial cell dysfunction that may be promoted by abnormal increases in circulating lipids, particularly triglycerides and free fatty acids. Serum triglyceride concentration is a major regulatory determinant of low-density lipoprotein (LDL) size and density distribution. Smaller, denser LDL particles have several intrinsic properties capable of inducing endothelial dysfunction. The present nested, case-control study of gestationally matched preeclamptic and normal pregnant women tested the hypothesis that hypertriglyceridemia in preeclampsia is accompanied by decreases in LDL peak particle diameter (predominant LDL size). Plasma LDL peak particle diameter was determined by nondenaturing 2% to 16% polyacrylamide gel electrophoresis. Correlations of LDL diameter with the concentration of serum triglycerides, free fatty acids, total cholesterol, LDL-cholesterol, and apolipoprotein B (apo B) were determined. In the same individuals, we measured serum concentrations of a marker of vascular dysfunction previously reported to be increased in preeclampsia, soluble vascular cell adhesion molecule-1 (VCAM-1), and examined the association of VCAM-1 with LDL diameter and serum lipids. LDL peak particle diameter was decreased in preeclampsia relative to normal pregnancy (P < .01). The LDL-cholesterol:apo B ratio, which frequently decreases with decreasing LDL diameter, was also decreased (P < .04). Triglyceride concentrations were increased in preeclampsia (P < .0002), and there was a significant inverse relationship between LDL peak particle diameter and triglycerides (r = -.55, P < .02). Serum soluble VCAM-1 concentrations were markedly increased in preeclampsia (P < .0003). Apo B (P < .004), free fatty acids (P < .01), total cholesterol (P < .01), and LDL-cholesterol (P < .02) were also increased. VCAM-1 correlated with apo B (r = .50, P < .03) and LDL-cholesterol (r = .50, P < .03), but showed no relationship with the LDL diameter, LDL-cholesterol:apo B ratio, or other lipids. We conclude that the predominance of smaller, denser LDL, a potential contributor to endothelial cell dysfunction, is a feature of preeclampsia. However, the serum VCAM-1 level, one indicator of endothelial involvement, may be influenced more by quantitative lipoprotein changes (serum apo B or LDL-cholesterol) than by LDL particle size.