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D Wallace

Publications and source records attributed to D Wallace.

At least 127 records · Page 7Linked to original sources
PubMed1989

Increased vascular contractile sensitivity to serotonin in spontaneously hypertensive rats is linked with increased turnover of phosphoinositide.

This study was conducted to determine if increased vascular contractile sensitivity to serotonin in spontaneously hypertensive (SHR) rats is linked with increased phosphoinositide turnover. Aortic and mesenteric artery rings from SHR exhibited 6.2- and 5.0-fold greater contractile sensitivity to serotonin than the aortic and mesenteric artery rings from normotensive Wistar-Kyoto (WKY) rats. Serotonin-induced turnover of phosphoinositide was measured by quantifying the accumulation of [3H] inositol labeled inositol monophosphate (IP), inositol bisphosphate (IP2) and inositol trisphosphate (IP3). Serotonin (3, 30, 200 microM) induced significantly greater accumulation of IP in SHR (279%, 590%, 895%) than in WKY (24%, 127%, 328%) aortic rings. Similarly, 3, 30 and 200 microM serotonin induced significantly greater accumulation of IP2 (118%, 241%, 451%) and IP3 (90%, 100%, 247%) in SHR than the accumulation of IP2 (15%, 58%, 122%) and IP3 (19%, 27%, 73%) in WKY aortic rings. Based on these data it is suggested that the greater vascular sensitivity to serotonin in SHR, at least in part, is attributable to increased turnover of phosphoinositide.

Animals↗
PubMed1989

Phospholipids containing polyunsaturated fatty acyl groups are mitogenic for normal mouse mammary epithelial cells in serum-free primary cell culture.

Epithelial cells obtained by collagenase digestion of mammary glands from virgin BALB/c mice were cultured in collagen gels in serum-free basal medium containing insulin (10 micrograms/ml), to which lipids or growth factors were added. Synthetic phospholipids were added as liposomes. Dilinoleoyl phosphatidic acid or phosphatidylserine or epidermal growth factor stimulated multifold growth. The optimum mitogenic effect of the phospholipids was dependent upon the presence of a polyunsaturated fatty acid esterified to the sn-2 position of the glycerol moiety. Dilinoleoyl phosphatidylcholine also stimulated growth but was generally less stimulatory than phosphatidylserine or phosphatidic acid, and phosphatidylethanolamine did not stimulate growth. Studies using phospholipids radiolabeled in either the sn-2 fatty acyl group or the glycerol backbone showed that the relative effect of phospholipids on growth did not correlate directly with the extent of their incorporation into cellular lipid, indicating that phospholipid turnover was the more important determinant for mitogenesis. Analysis of phosphatidic acid-stimulated growth suggested that both cAMP-dependent and cAMP-independent pathways were involved. Thus, mitogenic phospholipids stimulate proliferation by activating (directly or indirectly) multiple growth-regulatory pathways in mammary epithelial cells.

1-Methyl-3-isobutylxanthine↗
PubMed1989

The bifocal clinical nursing model: description and application to the patient receiving thrombolytic or anticoagulant therapy.

Carpenito's bifocal clinical nursing model enables the clinician to address the spectrum of clinical possibilities and problems associated with patients receiving thrombolytic and anticoagulant agents. Through correct application of nursing diagnoses, collaborative problems, and referrals, a global and multidisciplinary approach to patient care is achieved.

Adult↗
PubMed1989

Metabolism of [3H]equilin-[35S]sulfate and [3H]equilin sulfate after oral and intravenous administration in normal postmenopausal women and men.

The absorption of equilin sulfate and equilin from the gastrointestinal tract was determined in normal men after the ingestion of [3H]equilin-[35S]sulfate or a mixture of [3H]equilin and equilin-[35S]sulfate, while the metabolism of equilin sulfate was investigated after iv administration of [3H]equilin sulfate to postmenopausal women. After the oral administration of [3H]equilin-[35S]sulfate, equilin sulfate containing both 3H and 35S was isolated from plasma; however, only in the first sample taken at 10 min was the 3H/35S ratio the same as that of the [3H]equilin-[35S]sulfate ingested. The 3H/35S ratio then increased, and by 12 h only traces of equilin-[35S]sulfate were detectable. Similarly, after the ingestion of [3H]equilin and equilin-[35S]sulfate, [3H]equilin-[35S]sulfate was isolated from plasma. The 3H/35S ratio was at all time points greater than the 3H/35S ratio of the ingested mixture. Analysis of urine indicated that over 98% of 35S was not associated with any steroid and was most likely inorganic sulfate. After iv administration of [3H] equilin sulfate to postmenopausal women, equilin, equilenin, 17 beta-dihydroequilin, and 17 beta-dihydroequilenin were isolated from the urine. These results indicate that 1) some of the orally administered equilin sulfate was absorbed from the gut without prior hydrolysis, 2) some equilin sulfate was hydrolyzed in the gut before absorption; 3) equilin was absorbed more efficiently than equilin sulfate; 4) equilin absorbed was readily sulfated and circulated in this form; and 5) equilin sulfate was extensively metabolized, and the metabolites were excreted in the urine mainly conjugated with glucuronic acid.

17-Ketosteroids↗
PubMed1988

Prophylactic red-cell transfusions in pregnant patients with sickle cell disease. A randomized cooperative study.

Prophylactic blood transfusion has come to be regarded as necessary in the treatment of patients with sickle cell disease during pregnancy. Because of the risks associated with blood products and reports of successful outcomes without the use of blood transfusion, we conducted a prospective randomized controlled study of this issue. Seventy-two pregnant patients with sickle cell anemia were randomly assigned to one of two treatment groups: 36 received prophylactic transfusions of frozen red cells, and 36 received red-cell transfusions only for medical or obstetric emergencies. Twenty-eight patients with sickle cell anemia who did not qualify for randomization (mainly because they had other medical disorders), 66 with sickle cell-hemoglobin C disease, and 23 with sickle cell-beta-thalassemia were also followed and received transfusions only for emergencies. There was no significant difference in perinatal outcome between the offspring of mothers with sickle cell disease who were assigned to treatment with prophylactic transfusions and those who were not (15 vs. 5 percent). The occurrence of a perinatal death in a previous pregnancy and the presence of twins in the present pregnancy were two major risk factors for an unfavorable outcome; when they were present, perinatal mortality was 50 percent. Perinatal mortality was somewhat higher in the two groups that were randomized than in the three groups that were not. Prophylactic transfusion significantly reduced the incidence of painful crises of sickle cell disease (P less than 0.01) and substantially reduced the cumulative incidence of other complications of this disorder (P = 0.07). Other medical and obstetric complications occurred with nearly equal frequency in the two randomized groups. Increases in costs, the number of hospitalizations, and the risk of alloimmunization were disadvantages of prophylactic transfusion. We conclude that the omission of prophylactic red-cell transfusion will not harm pregnant patients with sickle cell disease or their offspring.

Adult↗
PubMed1988

Human platelet activation by bacterial phospholipase C: mechanism of inhibition by flurazepam.

We have shown earlier that phospholipase C (PLC) from Clostridium perfringens causes platelet activation possibly by inducing turnover of phosphoinositides and phosphorylation of a 47,000 Dalton protein (P47). Moreover, only 15 microM and 11 microM flurazepam inhibits PLC-induced platelet aggregation and serotonin secretion by 50% respectively. This study was conducted to better understand the mechanism of platelet activation by PLC and its inhibition by flurazepam. Incubation of (14C)-arachidonic acid labelled platelets with PLC produced diacylglycerol in a time- and concentration-dependent manner. Flurazepam did not inhibit diacylglycerol production by PLC. Paranitrophenolphosphorylcholine and prostaglandin E1 inhibited diacylglycerol production by 75% and 20% respectively. In a platelet-free system PLC hydrolyzed 14C-choline-phosphatidylcholine (14C-PC) in a time- and calcium ions-dependent manner. Flurazepam had no effect on PLC-induced hydrolysis of 14C-PC. Platelet cytosolic fraction (PCF), containing phosphatidylinositol-specific PLC (PI-PLC), hydrolyzed (3H-inositol)-phosphatidylinositol (3H-PI) in a platelet-free system. Flurazepam did not inhibit hydrolysis of 3H-PI by PCF. Phospholipase C caused phosphorylation of P47 in 32P-labelled platelets. Flurazepam did not block phosphorylation of P47 in the first three minutes and had very little inhibitory effect by five minutes. However, flurazepam completely blocked phosphorylation of P47 by seven minutes. Platelet aggregation induced by ionomycin, a calcium ionophore, was completely inhibited by 100 microM flurazepam whereas platelet aggregation induced by 12-O-Tetradecanoylphorbol-13-acetate (TPA), which mimics the action of diacylglycerol, was partially inhibited by 300 microM flurazepam. These findings suggest that PLC induced platelet activation depends, at least in part, on diacylglycerol production and phosphorylation of P47. These data also suggest that flurazepam does not inhibit PLC-induced platelet activation by inhibiting: (a) the production of diacylglycerol from phosphatidylcholine; and (b) the action of PI-PLC on phosphatidylinositol. The ability of flurazepam to inhibit ionomycin-induced platelet aggregation indicates that flurazepam is able to block platelet activation by inhibiting the increase in free cytosolic calcium ions in platelets or by inhibiting a step subsequent to the rise in intraplatelet calcium ions.

Alprostadil↗
PubMed1988

Growth stimulation by PGE2 and EGF activates cyclic AMP-dependent and -independent pathways in primary cultures of mouse mammary epithelial cells.

Mammary epithelial cells from virgin Balb/c mice were isolated by collagenase digestion and cultured within collagen gels in serum-free basal medium containing insulin (10 micrograms/ml). Previous work has shown that linoleate or its metabolite, prostaglandin E2 (PGE2), stimulate the growth of these cells only in the presence of a growth stimulant such as epidermal growth factor (EGF). Since PGE2 can stimulate cyclic AMP (cAMP) production, the role of cAMP in linoleate and EGF-stimulated growth was examined. The cAMP phosphodiesterase inhibitor, IBMX (0.1 mM), was found to augment growth when cells were cultured in the presence of both EGF and linoleate or PGE2, but not either factor alone. These results indicated that EGF does not stimulate proliferation via cyclic AMP mediated events but could synergize with cAMP events if cAMP levels were elevated by PGE2. When assayed in cells plated on top of collagen-coated culture dishes, cellular cyclic AMP levels were stimulated by PGE2, but only marginally by EGF. Although the stimulation of endogenous cAMP by PGE2 and IBMX was insufficient to stimulate growth in the absence of EGF, exogenous dibutyryl-cAMP (greater than 100 micrograms/ml) was able to do so showing that a sustained, and high level of cAMP (greater than 100 micrograms/ml) could stimulate growth in insulin-containing basal medium. EGF was capable of enhancing the cellular sensitivity to dibutyryl-cAMP but the converse was not observed. cAMP stimulation of growth was dependent upon a superphysiological concentration of insulin (10 micrograms/ml) or a physiological concentration of somatomedin-C. These results indicate that the proliferation of mouse mammary epithelial cells can be stimulated separately or in synergism by cAMP-dependent or -independent events.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Maternal diabetes and its effect on biochemical and functional development of rabbit fetal lung.

The effect of maternal diabetes on functional and biochemical maturation of the fetal lung was studied in a rabbit model. Pregnancy was initiated only after diabetes had been established. Both the pregnant doe and its fetuses were hyperglycemic. For comparison, the fetal heart and liver were also studied. In the diabetic group, the DNA content was lower in the fetal heart and lung while the protein content was higher in all three tissues. The glycogen levels were higher only in the fetal lung. Glycogen synthase was higher in the fetal lung and heart while phosphorylase activity was higher in all three tissues from the diabetic group. The activities of key enzymes involved in glycolysis were not affected. No difference was observed in the concentration of total phospholipids or in the ability of the airway fluid to reduce surface tension. In contrast, fetal lungs from diabetic does did not expand as well as the controls and retained less air on deflation. These findings suggest that the utilization of glycogen in fetal lungs from the diabetic does was not complete and that the increased incidence of respiratory distress in infants of diabetic mothers may not be due to a lack of surfactant.

Animals↗
PubMed1988

Effect of reconstituted pulmonary surfactant containing the 6000-dalton hydrophobic protein on lung compliance of prematurely delivered rabbit fetuses.

Chloroform:methanol extracts of bovine pulmonary surfactant contain small hydrophobic proteins, designated surfactant-associated apoproteins 6,000 (SAP-6), but do not contain the major surfactant-associated 35,000-dalton glycoprotein, designated SAP-35. Examination of lipid extract surfactant on sodium dodecylsulfate-polyacrylamide gel electrophoresis revealed hydrophobic proteins with apparent molecular masses of 15,000, 7,000, and 3,5000 daltons prior to reduction. After reduction, the 15,000-dalton species largely disappeared and was replaced by a 5,000-dalton species. In addition, the 7000- and 3500-dalton species exhibited a slightly enhanced mobility. Amino acid analysis demonstrated that SAP-6 possesses a more highly hydrophobic profile than SAP-35. Combining the protein-containing fractions from silicic acid chromatography of lipid extract with synthetic dipalmitoylphosphatidylcholine produced a reconstituted surfactant preparation which was just as active as lipid extract surfactant on a pulsating bubble surfactometer. The reconstituted surfactant contained SAP-6 but not SAP-35. Pressure-volume studies revealed that, at the optimal dose, reconstituted surfactant containing half the SAP-6 concentration of lipid extract exhibited similar effectiveness to lipid extract surfactant in promoting lung expansion with prematurely delivered rabbit fetuses of 27 days gestation. Reconstituted surfactant with an identical SAP-6 protein concentration as lipid extract possessed the same biological properties as the preparation with 1% SAP-6 protein. These studies support the view that an artificial surfactant composed of synthetic or semisynthetic lipids plus human SAP-6 produced via biotechnology could be useful for prevention and/or treatment of the neonatal respiratory distress syndrome.

Animals↗
PubMed1988

Umbilical arterial systolic/diastolic values in normal twin gestation.

Linear regression analysis was used to describe the relationship of umbilical arterial systolic/diastolic values to gestational age in 65 twin gestations. This relationship (y = 6.18 - 0.11x) was then compared with a previously described regression for singleton pregnancies using a multiple regression model. This comparison revealed that the relationship between the systolic/diastolic ratio and gestational age is the same in singleton and twin gestations.

Diastole↗
PubMed1987

Linoleate metabolites enhance the in vitro proliferative response of mouse mammary epithelial cells to epidermal growth factor.

Linoleic acid, arachidonic acid, prostaglandin E1, and prostaglandin E2 stimulated the proliferation of mammary epithelial cells in serum-free primary cultures only in the presence of epidermal growth factor. Linoleate-stimulated growth was manifest later in culture when proliferation, initiated by epidermal growth factor only, reached a plateau while linoleate-supplemented epidermal growth factor cultures continued to proliferate. The cultures in the plateau phase of growth could be restimulated to grow by adding either linoleic acid or prostaglandin E2 to the media. While the linoleate response could be abolished by the cyclooxygenase inhibitor, indomethacin, prostaglandin E2-stimulated growth remained unaffected. Linoleic acid was metabolized to arachidonic acid and prostaglandin E2, both in the growing and resting cultures. Proliferating cells metabolized linoleate and prostaglandin E2 extensively so that neither the fatty acid nor prostaglandin E2 accumulated in large quantities in the proliferating cultures. The concentrations of prostaglandin E2 in growing cultures supplemented with linoleic acid were much higher than in cultures without it. These results suggest that the metabolism of linoleic acid leading to prostaglandin production, not its contribution to membrane polyunsaturation, is necessary for sustained growth of mammary epithelial cells in the presence of epidermal growth factor.

Alprostadil↗
PubMed1987

Percutaneous nephrostomy: current indications and potential uses in obstetrics and gynecology. Literature review and report of a case.

Percutaneous nephrostomy offers a rapid and relatively safe means of short- or long-term management of urinary obstruction, irrespective of the underlying cause. It is particularly useful in patients who cannot undergo general anesthesia or surgery because of potential major risks. At present, the most common indication for percutaneous nephrostomy in OB/GYN is probably urinary tract obstruction secondary to pelvic malignancy. It is not indicated in terminal patients, but can be used to temporize renal function to allow palliative therapy and to assess the residual functional capacity of the obstructed kidney. Percutaneous nephrostomy will most likely be used even more frequently in the future as current roles are expanded particularly in areas such as perinatology.

Adult↗
PubMed1986

X linked hydrocephalus: a survey of a 20 year period in Victoria, Australia.

This study ascertained 164 males with non-communicating hydrocephalus in live or stillborn patients in Victoria. Australia in 1962 to 1982, after excluding those cases secondary to brain malformations other than aqueduct stenosis. Ascertainment was considered near complete, especially for the period since 1974, but details of the aqueduct pathology were inadequate in half the cases. A total of 91 families was seen to record detailed family information. The overall incidence of primary non-communicating hydrocephalus was estimated to be 0.6 +/- 0.2 per 1000 live and stillbirths, with three-fifths of the cases male. Twelve patients were classified as having definite X linked hydrocephalus and 13 others as probable cases of this condition. Deformities of the thumbs (generally adduction deformity) were present in nearly half of these cases. The pyramids were absent from sections of the medulla whenever these were available. Four of five survivors had signs suggesting pyramidal tract lesions, compared to four of 25 surviving non-X linked cases. The intellectual outcome was notably poorer in the X linked cases. Poor school performance was also described in five of 19 mothers of X linked cases but in only one of 64 mothers of the remaining cases. Familial recurrence in the whole group of patients was almost confined to the X linked families. The exceptions were two families in whom autosomal recessive inheritance is possible. It is important to remember X linked hydrocephalus in genetic counselling. Examination of the thumbs, search for clinical signs of pyramidal tract lesions, and anatomical examination of the pyramids in medullary sections are all important, along with careful questioning for a history of affected maternal relatives. The presence of any of these features is grounds for counseling on the basis of X linked inheritance. An empirical figure was derived to use when counseling about a male with non-communicating hydrocephalus in whom there is no adequate information about the thumbs or the pyramids: a 4% recurrence risk in male sibs and 2% in females.

Australia↗
PubMed1985

Physiology of IgD. VI. Transfer of the immunoaugmenting effect of IgD with T delta-containing helper cell populations.

We show that the IgD-induced augmentation of the immune response to trinitrophenylated keyhole limpet hemocyanin can be transferred to syngeneic mice with spleen cells from IgD-injected donors. The augmenting activity is present in the Lyt-1+2-, L3T4+ T cell population and is absent from B cells. The ability of transferred T cells to augment the immune response correlates with the presence of a high frequency of Lyt-1+2- T cells that form rosettes with IgD-coated sheep erythrocytes (T delta cells). Such rosette-forming cells can also be induced by incubation of spleen cells from normal donors in IgD-coated petri dishes. Injection of normal spleen cells exposed to IgD-coated petri dishes together with antigen also augments the immune response of recipients. The existence of a regulatory circuit based upon interactions between T delta cells, antigen, B cell surface IgD, and serum IgD, is proposed.

Adjuvants, Immunologic↗
PubMed1985

Tumor promoter phorbol esters induce unresponsiveness to antigen and expression of interleukin 2 receptor on T cells.

The tumor promoter 12-O-tetradecanoylphorbol 13-acetate induces the expression of the interleukin 2 receptor and the disappearance of the T3 complex in a T cell hybridoma, T cell clones, thymic and peripheral T cells and T cell tumors. These changes are accompanied by an increased sensitivity to interleukin 2 and antigen-specific unresponsiveness in T cell clones.

Antibodies, Monoclonal↗