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Biomedical subjects

E Rubin

Publications and source records attributed to E Rubin.

At least 199 records · Page 11Linked to original sources
PubMed1984

Ethanol increases calcium permeability of heavy sarcoplasmic reticulum of skeletal muscle.

The effects of ethanol on both Ca2+ pump activity and Ca2+-induced Ca2+ release in sarcoplasmic reticulum (SR) of rabbit skeletal muscle were studied. In concentrations of 0.1-1.0%, ethanol conspicuously enhanced Ca2+ release from the heavy fraction of SR, whereas a much smaller effect was noted in the light fraction. When Ca2+-induced Ca2+ release was inhibited by 10 mM Mg2+, the Ca2+ pump activities of both the heavy and light SR were the same; the activities were not significantly influenced by 1% ethanol. Ethanol itself did not release Ca2+ from the heavy SR. However, it appeared to render the heavy SR more permeable to Ca2+, thereby decreasing the amount of storable Ca2+. This action of ethanol may be related to the mechanism of its negative inotropic effect.

Animals↗
PubMed1984

Computerized tomography in evaluation of hepatic neoplasms.

We reviewed our experience with computerized tomography (CT) of the abdomen in 212 patients with histologically documented liver neoplasms seen during a 30-month period. The CT findings in cavernous hemangioma and focal nodular hyperplasia were specific, and permitted accurate diagnosis of this lesion before biopsy. The CT appearance of all other lesions was variable. We consider CT useful in providing an accurate evaluation of the intrahepatic and extrahepatic extent of the neoplasm.

Adenocarcinoma↗
PubMed1984

Thrombophlebitis of the internal jugular vein: noninvasive imaging.

Internal jugular thrombophlebitis usually results from contiguous infection or central catheterization. Ultrasonography and CT allow rapid, noninvasive methods of confirming the diagnosis of this condition. Although the choice of modality has not been systematically examined, where local expertise exists for both, ultrasonography is less expensive and should provide adequate images.

Adult↗
PubMed1984

Pneumonia in bone marrow transplant patients.

The radiographic, pathologic, and clinical features of 22 episodes of pneumonia in 18 bone marrow transplant recipients were analyzed retrospectively. These pneumonias could be divided into three diagnostic categories: (1) a transient form of nonspecific interstitial pneumonia resembling pulmonary edema in radiographic appearance occurred in five patients during the first 2 weeks after transplantation; (2) a fatal, progressive form of interstitial pneumonia began from 2 weeks to several months after bone marrow transplantation in seven patients; and (3) airspace pneumonias occurred in nine patients within 2 months of transplantation and were uniformly fatal. While the temporal and radiographic presentation of transient early interstitial pneumonia is often characteristic and may not require biopsy for diagnosis, the airspace and progressive interstitial pneumonias affecting bone marrow transplant recipients present variable patterns that are often radiographically indistinguishable. The direct pulmonary toxicity of high-dose total-body irradiation and chemotherapy may be contributory in producing both the early transient and later progressive forms of nonspecific interstitial pneumonia.

Bone Marrow Transplantation↗
PubMed1984

Pleural and extrapleural disease in Nocardia infections.

Pulmonary nocardiosis occurs most commonly in immunocompromised patients. Pleural involvement may be seen on a chest radiograph and may provide a clue as to the etiology of the infection, particularly if subcutaneous nodules or bone or joint symptoms are also present.

Adult↗
PubMed1984

Effects of chronic ethanol consumption on the partition of lipophilic compounds into erythrocyte membranes.

We have previously reported that chronic ethanol intoxication decreases the binding of various lipophilic substances to membranes of synaptosome and hepatic mitochondria. To determine whether this is a widespread effect, we used the quenching of the steady state fluorescence of membrane-bound diphenylhexatriene by halothane and the partitioning spin probe, 5-doxyl decane, to estimate the concentration of these compounds in erythrocyte plasma membranes. Membranes from ethanol-fed rats were resistant to the quenching of fluorescence by halothane or halothane plus 5-doxyl decane, compared with those from control animals, indicating lower quencher concentrations in the membranes of treated rats. These findings were confirmed by direct measurement of the partition of radiolabeled halothane into the membranes and by direct determination of the partition parameter of 5-doxyl decane by electron paramagnetic resonance spectroscopy. Halothane decreased the fluorescence lifetime to a larger extent in control membranes than in those from ethanol-fed rats. When various effects of halothane were expressed as a function of the concentration of halothane in the membrane, rather than the external buffer, no differences between membranes from control and treated rats were found. These data demonstrate that chronic ethanol intoxication decreases the partition of certain lipophilic compounds into the plasma membranes of erythrocytes, but that, at equivalent concentrations within the membrane, the interactions of halothane and the dye are comparable in both types of membranes. We suggest that the decreased partition of lipophilic compounds into biologic membranes is a widespread adaptive response to chronic ethanol intoxication and may play an important role in the resistance of such membranes to disordering after chronic ethanol ingestion.

Animals↗
PubMed1983

Ethanol and biological membranes: injury and adaptation.

Ethanol intoxication affects the protein and lipid constituents of biological membranes. Mitochondria exhibit specific decreases in components of the electron transport chain and in protein synthesis. In vitro ethanol reduces the transition temperatures of membrane-bound enzyme activities and decreases the order parameter. On the other hand, both are increased after chronic ethanol administration. After chronic ethanol treatment membranes are resistant to disordering by ethanol, possibly owing to an increased saturation of mitochondrial phospholipids, particularly cardiolipin. The increased rigidity of mitochondrial and synaptosomal membranes is associated with reduced binding of ethanol and of the general anesthetic halothane. The data suggest that initially ethanol increases the fluidity of all biological membranes. If continued chronically, this effect is balanced by a change in the lipid composition of the membranes, which increases their rigidity and makes them resistant to disordering by ethanol (homeoviscous adaptation). The change in molecular order reduces the binding of ethanol and other compounds, but also impairs a variety of membrane-bound functions. These changes may play a role in tolerance to ethanol and cross-tolerance to anesthetics, and in the pathogenesis of maladies associated with alcohol abuse.

Adenosine Triphosphatases↗
PubMed1983

Smoke inhalation: radiologic manifestations.

The medical records and radiographs of 62 patients admitted for smoke inhalation were reviewed to determine the value of the plain chest radiograph in the early detection of inhalation injury. Pulmonary edema resulting from the inhalation injury often leads to pulmonary insufficiency, and its early diagnosis is crucial to the management of patients with this condition. In addition to the usual presentation of pulmonary edema, subtle radiographic findings of interstitial edema such as perivascular fuzziness and peribronchial "cuffing" were observed. Of 56 patients with significant inhalation injury, 35 (62.5%) had radiographic findings attributed only to smoke inhalation. These abnormalities often had a characteristic distribution in the lungs, and in the majority of patients they appeared in the first 24 hours after the injury. The radiologic diagnosis of inhalation injury may be made at a time when findings of other diagnostic tests are still equivocal or mildly abnormal, thus alerting the clinician to impending pulmonary failure.

Adolescent↗
PubMed1983

Pulmonary complications in burn patients.

In recent years, pulmonary complications have become a major cause of death in burn victims. Familiarity with the spectrum of these complications leads to an earlier and more specific diagnosis based on chest radiographs. We reviewed the medical records and chest radiographs of 239 patients admitted to our burn unit over a one-year period. Pulmonary complications were categorized on the basis of their anatomic location in the respiratory tract and on whether they were the result of direct chemical injury from smoke inhalation, or were secondary to inhalation injury with or without cutaneous burns. Tracheobronchitis, chemical pulmonary edema, and adult respiratory distress syndrome (ARDS) resulted from direct injury. Pneumonia, ARDS, pulmonary congestion, atelectasis and pulmonary emboli were the main complications secondary to the injury. Pulmonary complications developed in 76 patients (31.8%) and, of these, 57 died (75%). Patients involved in a closed space fire and those who had a burn involving 50% or more of their surface area seem to be at the greatest risk of developing pulmonary complications.

Adolescent↗
PubMed1983

Ethanol, hepatocellular organelles, and microtubules. A morphometric study in vivo and in vitro.

The effects of chronic ethanol intoxication on hepatic microtubules are controversial. We, therefore, designed a morphometric study to examine ethanol-induced alterations in microtubules in vivo and in vitro. Using a computer-assisted point-counting system we determined the volume, surface, and length densities of hepatic microtubules, in addition to those of other hepatic organelles. Consistent with previous qualitative descriptions, chronic ethanol feeding caused increases in the volume and surface densities of mitochondria and microsomes. These changes account, in part, for the increased protein content of hepatocytes after chronic ethanol consumption. However, there was no effect on the volume, surface, or length densities of hepatic microtubules, nor on their calculated radii. The structure of isolated bovine brain microtubules after polymerization in vitro was not changed by ethanol or its metabolites, acetaldehyde and acetate. These data indicate that neither chronic ethanol intoxication nor the presence of ethanol, or its metabolites, affects the number or structure of microtubules.

Animals↗
PubMed1982

Antimycin inhibition as a probe of mitochondrial function in isolated rat hepatocytes. Effects of chronic ethanol consumption.

Previous studies have established that hepatic mitochondria and submitochondrial particles from rats, fed ethanol chronically, display diminished respiratory activities and alterations in the contents of specific electron transfer chain components. The latter include a decrease of about 50% in cytochrome b content. Titrations of respiratory activity in submitochondrial particles with antimycin, a stoichiometric inhibitor of electron flow through the cytochrome b-c1 region of the respiratory chain, indicated a comparable decrease (35%) in the amount of antimycin required to elicit maximal inhibition ('titer') after chronic ethanol treatment. Measurements of antimycin binding to submitochondrial particles by fluorescence quenching demonstrated a similar diminution in the number of tight binding sites per mg protein. By contrast, hepatocytes isolated from control and ethanol-fed rats exhibited nearly identical rates of oxygen utilization under a variety of conditions. However, antimycin titrations of respiratory activity in isolated hepatocytes revealed a 60% decrease in the antimycin titer, but no change in the maximal extent of inhibition after chronic ethanol treatment. Direct measurements of cytochrome b which could be reduced in the presence of antimycin in hepatocytes confirmed a comparable decrease (42%) after chronic ethanol treatment. The results demonstrate that molecular alterations in the cytochrome b region of the respiratory chain caused by ethanol feeding are present in intact liver cells, but suggest that substrate accessibility, rather than the respiratory chain, limits the rate of oxygen utilization in isolated hepatocytes. The data also suggest that mitochondria account for at least 80% of total oxygen utilization by liver cells from both control and ethanol-fed rats.

Alcoholism↗