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Biomedical subjects

J B Smith

Publications and source records attributed to J B Smith.

At least 361 records · Page 20Linked to original sources
PubMed1982

Independent segregation of NZB immune abnormalities in NZB x C58 recombinant inbred mice.

The study of NZB x C58 recombinant inbred mouse strains has revealed independent segregation of naturally occurring thymocytotoxic antibody and Coombs' anti-erythrocyte autoantibody. The lack of concordance of either of these autoantibodies with known heavy and light chain markers suggests that the autoantibodies are produced as a result of regulatory gene defects rather than alterations of antibody structural genes. Further, lack of concordance of the various autoimmune traits with each other or with H-2 or virus expression suggests that the autoimmune phenotype is not the result of a single "autoimmunity' gene but rather the outcome of faulty regulation of a number of independently segregating genes.

Aging↗
PubMed1982

Anti-thromboxane A2 actions of pinane thromboxane A2 derivatives.

Six pinane-thromboxane A2 analogs have been synthesized and tested for their ability to antagonize carbocyclic thromboxane A2 (CTA2) induced coronary vasoconstriction and prostaglandin endoperoxide analog induced platelet aggregation. Two of the derivatives, 5C-15S BPTA2 and 5T-15S BPTA2 and 5T-15S BPTA2 (1 microM) showed 76 +/- 3 and 72 +/- 9 percent inhibition of CTA2 (15 nM) induced vasoconstriction of cat coronary arteries respectively, while the other compounds showed between 15 and 50 percent inhibition at 1.0 and 2.0 microM. 5C-15S BPTA2 also antagonized prostaglandin-endoperoxide analog induced human platelet aggregation, although the other compounds showed little or no antagonism of aggregation in this system.

Animals↗
PubMed1982

Angiotensin increases Na+ entry and Na+/K+ pump activity in cultures of smooth muscle from rat aorta.

Angiotensin markedly altered the Na+ permeability of smooth muscle cells cultured from explants of rat aorta. The rate of net Na+ uptake was followed in the presence of ouabain in order to block Na+ efflux via the Na+/K+ pump. Angiotensin II (AII) or angiotensin III (AIII) increased net Na+ uptake by about 3-fold. Maximal stimulation of Na+ uptake was produced by about 10 nM AII. Bradykinin and the angiotensin antagonist [Sar1, Ileu5, Ala8]AII had no significant effect on net Na+ uptake. Angiotensin also enhanced the activity of the Na+/K+ pump, which was assayed by following the rate of ouabain-sensitive 86Rb+ uptake by the cells. AII and AIII nearly doubled ouabain-sensitive 86Rb+ uptake, but bradykinin, norepinephrine, and [Sar1, Ileu5, Ala8]AII had no effect. In the presence of ouabain, 86Rb+ uptake was not significantly affected by AII or AIII, indicating that angiotensin did not alter passive permeability to Rb+. Loading the cells with Na+, either by incubation in K+-free medium or exposure to the Na+-selective ionophore monensin, markedly increased ouabain-sensitive 86RB+ uptake. This result indicates that the activity of the Na+/K+ pump is limited by the low level of Na+ that is normally in the cells. AII had no effect on the activity of the Na+/K+ pump in Na+-loaded cells. These results suggest that AII or AIII stimulates the Na+/K+ pump in cultured aortic muscle cells by increasing its Na+ supply.

Angiotensin II↗
PubMed1982

Onset of respiration in infants delivered by cesarean section.

We studied the ventilatory parameters and the pattern of breathing including the onset of respiration in 20 healthy infants immediately after cesarean-section delivery. In eight of the infants further measurements were obtained at 60 min of life. The pattern of breathing immediately after delivery is very irregular with a marked tendency to keep the lung inflated mainly through interruptions of expiration. After the first expiration some air remains in the lung representing the formation of functional residual capacity (FRC). FRC obtained with the first breath is proportional to the previous inspired volume and is the largest contribution towards the full establishment of FRC. Tidal volume and FRC of the first breath are similar to that reported in babies delivered vaginally, which suggests that the forces required for lung inflation are similar in the two groups of infants. The first breath tends to be deeper and slower and has a longer expiratory time than subsequent breaths. At 60 min of life the respiratory pattern becomes more regular, tidal volume is further decreased, and respiratory frequency is increased through a reduction of expiratory time.

Adult↗
PubMed1982

Respiration in newborns: development of the control of breathing.

The pattern of breathing has been studied in human infants at 10, 60, and 90 min, and at a few days after birth. The major characteristics of the pattern of breathing in the immediate period after birth is a marked variability that decreases progressively with time. Interruptions of expiration and peak expiratory flows occurring late in expiration are common findings at 10 to 90 min of age but are infrequent at a few days. From 10 to 90 min to a few days of life the tidal volume increases and respiratory rate decreases with no changes in minute ventilation. The decrease in respiratory rate is due to proportional increases in both inspiratory and expiratory time. Infants born vaginally behave similarly to those delivered by cesarean section except with regard to tidal volume, which at 10 min is closer to the value measured at a few days; this may be the result of the mechanics of the vaginal delivery, which results in less fluid to be absorbed from the lung at birth. Vagal respiratory reflexes are present at birth and the prolongation of inspiratory time during occlusion at end expiration appears to decrease from 10, 60, and 90 min to a few days of age. Values of mouth pressure at 0.1 s after an occlusion at end expiration are higher at 10 min after birth than at 60 and 90 min. Because mean inspiratory flow is similar in this time period it could indicate a progressive increase in the compliance of the respiratory system, possibly reflecting the absorption of pulmonary fluid.

Anesthesia, Epidural↗
PubMed1982

Deficient autologous mixed lymphocyte reactions correlate with disease activity in systemic lupus erythematosus and rheumatoid arthritis.

We have examined autologous mixed lymphocyte culture (AMLC) reactions in patients with systemic lupus erythematosus (SLE), classical rheumatoid arthritis (RA), and in normal age and sex matched healthy control individuals. AMLC responses were found to be lower than the median of all controls and patients in 30 of 31 individuals with SLE and RA and in only 2 of 15 healthy controls. In both SLE and RA there was a statistically significant correlation of decreased AMLC reaction with disease activity. On an individual basis, there was no direct correlation between decreased AMLC reactivity, concomitant steroid therapy, or the occurrence of clinical or laboratory parameters of autoimmunity.

Adrenal Cortex Hormones↗
PubMed1981

Formation of lysophosphatidylcholine by human platelets in response to thrombin. Support for the phospholipase A2 pathway for the liberation of arachidonic acid.

Significant increases in lysophosphatidylcholine from a basal level of 4.2 +/- 0.36 nmol/mg of platelet protein to 6.4 +/- 0.46 nmol/mg of protein occur within 20 s after the addition of thrombin (5 units/ml) to washed human platelets. The increases are essentially complete by 1 min, at which time levels of 8.5 +/- 0.53 nmol of lysophosphatidylcholine/mg of platelet protein are reached. Decreases in phosphatidylcholine and also phosphatidylethanolamine occur within 20 s after stimulation of platelets by thrombin. These changes were detected by quantitative measurements of endogenous phospholipid phosphorus after extraction and thin layer chromatography of the platelet lipids. The concomitant increases in lysophosphatidylcholine and decreases in phosphatidylcholine, as well as the decreases in phosphatidylethanolamine, can only be explained by the stimulation of phospholipase A2 activity in platelets by thrombin.

Animals↗
PubMed1981

Autologous mixed lymphocyte reactions in NZB mice: analysis in recombinant inbred lines shows a T cell defect unrelated to autoantibody production.

The autologous mixed lymphocyte reaction (AMLR) has been examined in the AMLR-deficient strain, NZB, in C58 mice, which have normal AMLR responses, and in the (NZB x C58) recombinant inbred (NX8 RI) lines. Half of the NX8 RI lines had deficient AMLR and half were comparable in reactivity to the C58 parent strain. AMLR unresponsiveness did not correlate in the NX8 RI lines with H-2 or any other marker known to affect immune recognition. Non-T cells from H-2k NX8 RI lines which had deficient AMLR were able to stimulate an MLR when cultured with T cells of C58 origin. AMLR-positive H-2d lines responded to NZB stimulators, whereas NZB T cells did not respond to any of the H-2d NX8 RI lines but did exhibit strong alloreactivity. Thus, the AMLR defect in NZB mice is due to a T cell lesion. Furthermore, since AMLR deficiency in the NX8 RI lines did not correlate with a positive Coombs test or the production of naturally occurring thymocytotoxic antibody, we conclude that autoimmunity in NZB mice is a complex disease resulting from the inheritance of multiple independently segregating genes.

Animals↗
PubMed1981

Thromboxane synthetase inhibitors differentially antagonize thromboxane receptors in vascular smooth muscle.

A number of thromboxane (Tx) synthetase inhibitors have been found to prevent thromboxane release in acute cardiopulmonary disorders. However, little is known about Tx receptor antagonism by these substances. Imidazole, UK-37,248 and pinane thromboxane A2 (PTA2) were tested in isolated perfused cat coronary arteries, spirally cut rabbit pulmonary artery strips, and in rabbit and cat platelets for their ability to antagonize vasoconstrictor and aggregatory effects of a stable Tx agonist, carbocyclic thromboxane A2 (CTA2). Imidazole, at concentrations that completely inhibit thromboxane synthesis, failed to antagonize the vasoconstrictor effects of CTA2 in both systems. UK-37,248, at 10 to 1000 micrograms/ml, failed to inhibit CTA2-induced coronary constriction but at 1 microgram/ml reduced rabbit pulmonary artery constriction by 80 +/- 8% (P less than 0.0005). In comparison, 1 micro M PTA2 completely prevented PTA2-induced constriction in both coronary and pulmonary arteries. PTA2 did not antagonize KCl and angiotensin II responses. In platelets, PTA2 but not UK-37,248 prevented arachidonate induced aggregation in rabbit and cat platelets. Some of the beneficial effects of thromboxane synthetase inhibitors may be associated with thromboxane receptor antagonism. Inhibitors structurally similar to TxA2 appear to have greater thromboxane receptor antagonistic activity. This additional activity may be of importance in therapeutics of coronary and pulmonary disorders.

Animals↗