Ultrasound of the breast. What are the indications?
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Biomedical subjects
Publications and source records attributed to E Rubin.
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The enormous range of animal size raises a fundamental problem: How do larger animals maintain adequate control of peripheral structures that are many times more massive and extensive than the homologous structures in smaller animals? To explore this question, we have determined neuronal number, the number of axons that innervate each neuron (convergence) and the number of neurons innervated by each axon (divergence), in a peripheral sympathetic pathway of several mammals (mouse, hamster, rat, guinea pig, and rabbit). The average adult weights of these species vary over approximately a 65-fold range. However, the number of superior cervical ganglion cells increases by only a factor of 4 between the smallest of these animals (mice; about 25 gm) and the largest (rabbits; about 1700 gm); the number of spinal preganglionic neurons that innervate the ganglion increases by only a factor of 2. Thus, the number of nerve cells in the sympathetic system does not increase in proportion to animal size. On the other hand, our results indicate that there are systematic differences across these species in the number of axons that innervate each ganglion cell and in the number of ganglion cells innervated by each axon. We suggest that modulation of convergence and divergence in sympathetic ganglia allows this part of the nervous system to effectively activate homologous peripheral targets over a wide range of animal size.
Ethanol, in vitro, is known to perturb the molecular order of the phospholipids in biological membranes, while chronic ethanol exposure, in vivo, leads to resistance to disordering. Such changes have usually been measured by electron spin resonance, utilizing fatty acid spin probes. The use of such probes is controversial, since their orientation in the membrane may not accurately represent that of individual phospholipids. We, therefore, compared ethanol-induced structural perturbations in the membranes of rat hepatic microsomes measured with the spin probe 12-doxylstearic acid (SA 12) with those assayed with various phospholipid spin probes. With SA 12, the addition of increasing amounts of ethanol (50-250 mM) in vitro caused a progressive decrease in the membrane molecular order, as measured by electron spin resonance (ESR). By contrast, microsomes obtained from rats chronically fed ethanol were resistant to the disordering effect of ethanol. Microsomes labeled with the phospholipid spin probes 1-palmitoyl-2-(12-doxylstearoyl)phosphatidylcholine, -phosphatidylethanolamine, or -phosphatidic acid also exhibited increased disordering with the addition of increasing amounts of ethanol. However, the effect noted with phospholipid spin probes was less than that observed with the fatty acid probe. Microsomes obtained from the livers of chronically intoxicated animals labeled with the phospholipid probes were also resistant to the disordering effects of ethanol in vitro. These results suggest that fatty acid spin probes are qualitatively valid for measuring membrane perturbations in biological membranes, ethanol affects all microsomal phospholipids, regardless of chemical dissimilarities (e.g., head-group structure), in a qualitatively similar fashion, and the fluidization of fatty acyl chains in microsomal membranes is comparable in different membrane phospholipids.
The relationship between the proton electrochemical potential (delta mu H) and the maximal free energy of ATP hydrolysis (delta GP) in coupled respiring rat liver mitochondria was investigated as a function of temperature and chronic ethanol-feeding. The flow dialysis method was utilized to measure the temperature dependence of delta mu H from the uptake of 86Rb (in the presence of valinomycin) and [14C]DMO. delta GP in state 4 was determined by a null-point titration of the reversible, H+-coupled ATPase against the phosphate potential. delta mu H increases with temperature from 196 mV at 10 degrees C, to 217 mV at 40 degrees C. The maximal delta GP at state 4 decreases as a function of temperature from 67.8 kJ/mol at 10 degrees C, to 54.8 kJ/mol at 40 degrees C. As a result, the ratio delta GP/delta mu H decreases with temperature from 3.56 at 10 degrees C to 2.60 at 40 degrees C. Similar studies with mitochondria from rats which were chronically fed with ethanol show that, while delta GP at state 4 decreases in these rats from 61.2 to 56.0 (25 degrees C), the delta mu H is essentially unchanged at 212 mV. Thus the ratio delta GP/delta mu H in ethanol-fed rats at 25 degrees C is 2.77 as compared with 2.97 in control. Similar reduction of delta GP was observed in inverted inner membranes from ethanol-fed rats. Both the temperature dependence of delta GP/delta mu H and the effect of ethanol-feeding cannot be easily explained by the chemiosmotic hypothesis which postulates that delta mu H is the only driving force for ATP synthesis. In contrast, a parallel coupling model, which postulates that intramembrane proton transfer from redox pumps to ATPase is mediated by the formation of dynamic aggregates of the mitochondrial inner-membrane proteins, can easily accommodate these findings. Accordingly, the temperature effect is due to weakening of these fragile aggregates, while the ethanol-feeding effect is the result of reduced concentration of active pumps, which decrease the frequency of formation of functional aggregates.
The effects of ADP and ethanol on Ca2+ binding of troponin and the superprecipitation of actomyosin were studied. Ca2+ binding of troponin-tropomyosin complex bound to polystyrene particles (Lytron) was increased by ADP, and this increase was inhibited by ethanol. However, Ca2+ binding of the complex as measured by equilibrium dialysis and by the chelex resin method was not influenced by either ADP or ADP plus ethanol. Ca2+ binding of the thin filament, myosin-ghost myofibrils and myofibrils was also not inhibited. Superprecipitation of actomyosin was augmented in the presence of ADP, and the enhancement was inhibited by ethanol. However, this effect of ADP or ethanol was not observed in the presence of an inhibitor of myokinase, p1, p5-di (adenosine-5') pentaphosphate (Ap5A). In the presence of Ap5A, superprecipitation of actomyosin was enhanced when small amounts of ATP (10 microM) and ADP (100 microM) were added 5 min prior to the addition of 2 mM ATP to start the reaction. The enhancement of superprecipitation of actomyosin by ADP may be caused by nuclei produced by a low concentration of ATP which is produced from ADP by contaminating myokinase activity. These data suggest that ADP and ethanol influence Ca2+ binding of the troponin-tropomyosin complex bound to a solid phase, but their effects on superprecipitation may not necessarily reflect muscle contraction in vivo.
Pathologic and computed tomographic correlation of an obstructing common bile duct mass, found to be malignant melanoma, is presented. No tumour was demonstrated elsewhere. Such a pattern of presentation has not previously been described in this condition. Malignant melanoma, even in the absence of disease elsewhere, should be considered in the differential diagnosis of such lesions seen on computed tomography.
The transbilayer distribution of phospholipids in right-side-out and inside-out vesicles derived from human erythrocytes was studied by phospholipase A2 digestion assays and by staining with the fluorescent dye merocyanine 540. In both types of vesicles, the normal asymmetric distribution of phospholipids characteristic of intact cells was disrupted. Because both types of vesicles are deficient in spectrin, the major protein of the cytoskeletal network which normally underlies the membrane, these results support the contention that spectrin is involved in the maintenance of phospholipid asymmetry.
A phototimer technique chart for mammography is presented along with the methodology used to design it. The chart is based on accurate measurement of breast thickness and helps overcome the inability of the phototimer to track as breast thickness varies. In clinical practice, the chart results in the consistent attainment of optimally exposed films and decreased number of retakes.
The results of real-time hand-held sonographic breast examinations on 86 patients are presented. The technique is described in detail. Sonography was found to be a useful adjunct to the x-ray mammogram in three groups of patients: (1) patients with dense breasts and localized symptomatology or a suspicious area on x-ray mammogram; (2) patients with nonpalpable abnormalities discovered on x-ray mammogram; and (3) patients with palpable masses considered indeterminate on x-ray mammogram. The examination was also found useful for guiding needle aspiration biopsies, in patients with persistent nipple discharge, and in those with breast prostheses. Advantages of the hand-held real-time technique include supine positioning, the ability to flexibly orient the probe, improved resolution due to higher frequency transducers and the lack of compounding, and the ability to vary the amount of compression to assess tissue compliance and fixation. The disadvantage of decreased resolution in the near field can be overcome by attaching a detachable water-path step-off device to the transducer. Geometric distortion from the pressure of the transducer was not believed to be a problem. Hand-held sonographic technique is useful when attention can be directed to a specific area of the breast. The additional information provided results in fewer equivocal interpretations of the x-ray mammogram; however, it should not be used as a substitute for routine mammography.
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The development of superior cervical ganglion cells has been studied in the fetal rat. Sympathetic cells appear first in thoracic sites and, one day later, in cervical sites; localized proliferation among these cells gives rise to the superior cervical and stellate ganglia. The maturation of superior cervical ganglion cells was examined by staining these neurons with horseradish peroxidase in fetal preparations maintained in vitro. This method showed that cells begin to extend processes at widely different times, without regard to a given cell's position in the ganglion. Postganglionic axons appear as early as day 12 of gestation (E12), when only a small number of ganglion cells have emerged from the mitotic cycle. The axon generally originates from a point on the ganglion cell body that is oriented toward the route of subsequent axon extension. As the postganglionic axons grow, they do not branch within the superior cervical ganglion and branch only to a slight extent, if at all, within developing peripheral nerves. Axonal growth is rapid, and fibers reach relatively remote sympathetic targets as early as E15. Dendrites first appear on E14 and are elaborated by ganglion cells that have already extended their axons. By the end of gestation, the number of primary dendrites found on some cells already falls within the range found in maturity.
The growth of sympathetic preganglionic axons has been studied in the fetal rat. Preganglionic axons first emerge from the spinal cord and enter the paravertebral chain of ganglia between days 12 and 13 of gestation (E12 to E13). By E14, hundreds of preganglionic neurons have sent axons into the sympathetic chain. Even at this age, the arrangement of the preganglionic axons conforms to the adult organization in a number of ways. As in maturity, these axons leave the spinal cord only through the ventral root of the segment in which their cell bodies reside. Furthermore, axons grow into the superior cervical ganglion only from the same set of spinal segments as supply this ganglion in maturity, and in correct segmental proportions, although there is a slight rostral-to-caudal lag along the spinal cord in the full establishment of the projection. The development of appropriate projections in this system owes little to the growth of axons along stereotyped pathways. Rather, preganglionic organization apparently reflects a more general instruction that governs the relative number of axons from each spinal segment which course rostrally or caudally within the sympathetic chain. The appropriate distribution of preganglionic axons early in development suggests that a fiber's segmental level of origin biases the axon to grow in a particular direction.
Synapse formation in the rat superior cervical ganglion has been investigated electrophysiologically and at the ultrastructural level. Preganglionic axons first enter the superior cervical ganglion between days 12 and 13 of gestation (E12 to E13), and on E13 a postganglionic response can be evoked by preganglionic stimulation. The susceptibility of this response to fatigue and to blocking agents indicates that it is mediated by cholinergic synapses. On E14, the overall strength of ganglionic innervation arising from different spinal segments already varies in a pattern resembling that found in maturity. However, the distribution of synapses on individual target cells gradually changes in the prenatal period. Transmission begins prior to the elaboration of ganglion cell dendrites; therefore, the first contacts to form are largely axosomatic. As dendrites appear (beginning on E14), ultrastructural evidence shows that synaptogenesis becomes focused upon these processes. The significance of these findings is discussed in relation to possible mechanisms for the formation of appropriate synaptic connections.
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A case of hepatic myelolipoma is described, including the angiographic and computed tomographic appearance. Only three such cases have been reported previously.
Primary cultures of adult rat hepatocytes were used to study the effects of 100 mM ethanol on various neutral amino acid transport systems. Ethanol exposure for 24 h selectively decreased amino acid uptake by the A and N systems by 40-70%, but had no significant effect on the ASC and L systems. The decrease in the A system was significant after 3 h of ethanol exposure, and the activity was not affected by the presence or absence of ethanol during the uptake measurements. Kinetic analysis showed that ethanol treatment affected predominantly the high-affinity component of A system activity by decreasing the apparent Vmax without significantly changing the apparent Km. Ethanol treatment did not prevent the cells from increasing A system activity in response to insulin and glucagon, but the magnitude of hormone-stimulated uptake was reduced.