Observation of tau -lepton decay to five charged particles.
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Biomedical subjects
Publications and source records attributed to D Rubin.
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A group of eight adult patients with congenital cyanotic heart disease (CCHD) with PaO2 values of less than 32 mm Hg at rest and/or exercise were studied. Four of the patients were re-studied after heart-lung transplantation and restoration of PaO2 to normal values. All eight patients showed increased red cell counts (polycythemia), whereas frankly elevated hemoglobin concentrations were found in only one patient. There was no impressive change in the affinity of hemoglobin for O2 as compared to normal subjects. Blood lactate concentrations were normal at rest before transplantation, rose very modestly during moderate exercise, and were normal following transplantation indicating that the concept of anaerobic threshold is not valid in the present group of patients. Cardiac index was not elevated in the pretransplantation period, indicating that an elevated cardiac output is not an essential adaptive mechanism for dealing with hypoxia. In the pre-transplant period, O2 consumption was elevated as compared to normal values and almost doubled during exercise despite a further decline in PaO2 and SaO2; this establishes that the rate of mitochondrial O2 utilization is maintained despite profound reduction in PaO2. These patients are capable of moderate exercise and normal brain function despite severe hypoxia and the absence or attenuation of various adaptive mechanisms for dealing with hypoxia. Further study of the specifics of O2 transport and utilization in similar patients should prove rewarding.
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Experiments were conducted to determine (1) whether glucocorticoids directly protected endothelial cells (EC) from radiation and (2) if angiotensin converting enzyme (ACE) activity, known to be increased by glucocorticoid, played a role in the EC response to radiation. Confluent monolayers of EC cultured from bovine aorta EC were treated with dexamethasone (10(-6) M); after irradiation (5.0 Gy, 60Co gamma), ACE and lactate dehydrogenase (LDH) activities, DNA and protein contents, and nuclei number were measured. Twenty-four hours after 5 Gy, there was increased cell loss (-40%, P less than 0.001), greater LDH release (greater than 100%, P less than 0.001), more LDH activity per cell (+40%, P less than 0.001), and unchanged ACE activity compared to sham-irradiated control EC. However, 48 hr after 5 Gy, ACE activity per cell was decreased (-24%, P less than 0.005). A 48-hr exposure to dexamethasone alone was accompanied by a slight cell loss (-10%, P less than 0.001) and increased cellular ACE activity (+40-140%, P less than 0.001), but a 24-hr dexamethasone exposure was not cytotoxic and did not change ACE activity. Dexamethasone exposure for 48 hr before and after irradiation did not attenuate cell loss or LDH release. However, combined dexamethasone treatment and radiation increased cellular ACE activity at a time when neither agent alone had an effect (24-hr dexamethasone exposure before 5 Gy and assayed 24 hr after 5 Gy). This interaction between radiation and dexamethasone treatment suggests that the glucocorticoid modifies the cell's response to injury. Although this interaction does not ameliorate radiation cytotoxicity, maintenance of ACE levels in injured vessels by hormones may have physiological significance in the hemodynamics of irradiated tissues.
A patient with aortic stenosis and ventricular pacemaker had clinical findings suggesting tricuspid regurgitation. Her presentation was actually caused by regular and constant cannon waves resulting from ventriculoatrial conduction of paced beats. The correct diagnosis was confirmed by abolition of hepatic pulsations during atrial pacing at the time of cardiac catheterization. Therapy consisted of restoring antegrade atrioventricular conduction.
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Five patients with recurrent syncope or pre-syncope due to rapid supraventricular tachycardias underwent electrophysiological study. In each patient, an AV nodal re-entrant tachycardia could be induced. By leaving a coronary sinus catheter in place, the effects of drugs on the ability to induce tachycardia could be tested on sequential days. Drug effects were highly variable, but in each patient it was possible to determine a drug which prevented induction of tachycardia. Patients treated with this drug have had no recurrent symptoms or tachycardias with a followup of 4-21 months. Although AV nodal re-entry is highly dependent on autonomic tone, electrophysiological study appears to be a useful means of selecting therapy in patients with severe, symptomatic tachycardias.
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The treatment of myofascial trigger point (TP) pain syndromes is not difficult once the source of the problem has been determined. Whereas many modalities may be used, two of the most effective are spray-and-stretch and TP injection. These can be followed by deep massage, specific, manual resistive exercises, and an exercise program which the patient can follow at home. The goal of management is to inactivate the TPs and to restore shortened and stretch resistant muscles to their full range of motion. A number of such syndromes are discussed in terms of recognition and management.
We have demonstrated that reovirus type 1, but not type 3, generates serotype-specific immunologic tolerance for DTH responses following oral administration of UV-inactivated virus. As shown by adoptive transfer experiments, the tolerance is secondary to the generation of viral-specific suppressor T cells that are present in spleen and mesenteric lymph nodes. No tolerance was generated when live virus was administered orally. Using recombinant viral clones, it was found that 2 viral gene products were required for tolerance induction; serotype specificity is a property of the viral hemagglutinin (the product of the S1 dsRNA segment). The inability of type 3 reovirus to induce suppression following oral administration is a property of the mu 1C polypeptide (the product of the M2 dsRNA genome segment).
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The effect of sleep state on arterial oxygen tension was determined in ten healthy term infants by means of continuous transcutaneous PO2 monitoring. In all ten infants, PaO2 was significantly lower and more variable during active as compared to quiet sleep. This fall in PaO2 during active sleep was accompanied by asynchronous (or paradoxical) chest wall movement. These findings may be important in our understanding of the higher incidence of apnea during active sleep in both preterm and term infants.
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To determine the optimal position for the preterm infant, arterial oxygen tension (Pao2) was monitored in 16 preterm infants by the transcutaneous method with the infants in both supine and prone positions. When the infants were prone, Pao2 rose by a mean of 7.4 mm Hg (P less than .001), an increase of 15%. In those infants with residual cardiopulmonary disease a 25% increase was noted. The higher Pao2 in the prone position was accompanied by a significant decrease in the amount of time the chest wall moved asynchronously. This improved oxygenation in the prone position appears to be the result of enhanced ventilation/perfusion ratios and not merely secondary to an alteration in sleep state with positioning of the infant. These findings may have important implications in the management of preterm infants, requiring neonatal intensive care.
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