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Biomedical subjects

J C Goldsmith

Publications and source records attributed to J C Goldsmith.

At least 73 records · Page 4Linked to original sources
PubMed1984

Endothelial cell cycle kinetics. Changes in culture and correlation with endothelial properties.

Endothelial cells in culture have emerged as a model system for evaluation of endothelial properties. Culture conditions may affect expression of these endothelial properties or growth characteristics. Therefore, we evaluated cell cycle kinetics, prostacyclin release, and angiotensin-converting enzyme activity in primary and subcultured cells from bovine pulmonary and systemic vessels. Prostacyclin release was highly variable during passage in culture. However, release following stimulation with ionophore A23187 declined with serial passage. Angiotensin-converting enzyme activity also declined with repeated subculturing. Greater than 10% of primary confluent bovine endothelial cells were cycling compared to 2 to 8% of human umbilical vein endothelial cells. With passage in culture, 25% of bovine endothelial cells were cycling at confluence. Occasional strains of subcultured bovine endothelium arrested in G2 but would reenter G1 upon subculturing. Exposure to trypsin did not appear to contribute to this phenomenon. These studies have demonstrated variability in endothelial cell properties and growth characteristics during in vitro propagation. The existence of this variability must be considered when studying properties or responses of subcultured endothelium.

Animals↗
PubMed1984

Immunologic injury to vascular endothelial cells: effects on release of prostacyclin.

Prostacyclin is released from cultured and ex vivo bovine vascular endothelium following sublethal immunologic injury by a heterologous antibody to endothelial cells developed in rabbits. This release was dependent on calcium and complement and was not enhanced by the presence of platelets. Prostacyclin release was diminished 1-2 hr after the injury, but recovered fully following reculture of the endothelial cells for 72 hr.

Animals↗
PubMed1983

T-lymphocyte subpopulation abnormalities in apparently healthy patients with hemophilia.

T-lymphocyte populations in 12 apparently healthy heterosexual adult patients with hemophilia have been examined to ascertain if these patients have abnormalities in their lymphocyte subpopulations similar to those in homosexual men, Haitian refugees, and narcotic addicts. A striking reduction in the helper to suppressor cell ratio ([0.86 +/- 0.14]:1) was found in 9 of the 12 patients. These abnormalities were similar to those previously described in two patients with hemophilia critically ill with Pneumocystis carinii pneumonia, and in homosexual men. The abnormality in the ratio of helper to suppressor T cells may be related to the continual exposure of patients with hemophilia to commercial clotting factor concentrates. However, these patients with abnormal T-lymphocyte subpopulations remain healthy. At present there is insufficient evidence to advocate a change in therapeutic practices in patients with hemophilia.

Adolescent↗
PubMed1983

Capital planning strategies in an era of changing ground rules.

Changes in federal reimbursement policies and in the private health insurance system will affect boards' capital planning strategies. Actions recommended here include increased attention to debt service costs, return on investments, new capital sources, the efficient use of existing capital, and the substitution of capital for labor.

Capital Financing↗
PubMed1983

MDs and hospitals: conflict or partnership.

Hospitals and their medical staffs face separate and significant economic pressures. In working out their respective responses to these pressures, both will have to work hard to avert a collision of economic interests that could damage our health care system.

Economic Competition↗
PubMed1982

A comparative study of thromboxane and prostacyclin release from ex vivo and cultured bovine vascular endothelium.

Thromboxane B2, 6-keto-Prostaglandin F1 alpha, and Prostaglandin E2 release have been quantitated from cultured adult bovine endothelial cell monolayers and from ex Vivo vascular segments employing specific radioimmunoassays and thin layer chromatography. Release of all three prostaglandins was demonstrable from both endothelial cell systems under basal conditions and following exposure to the ionophore A23187 and arachidonic acid. In culture, the quantity of 6-keto-PGF1 alpha released was diminished compared to amounts released from the vessel segments while thromboxane B2 and prostaglandin E2 release were similar in the two endothelial model systems. However, the amount of thromboxane B2 assayed was small and the quantity of thromboxane A2 it represents is probably of little in vivo significance compared to prostacyclin.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Interactions of multiplication-stimulating activity with bovine endothelium: comparative studies in primary, passaged, and cloned cultures from the pulmonary and systemic circulations.

Endothelial cells were prepared from adult bovine pulmonary and systemic vessels and maintained as primary cultures, passaged cultures, and cloned cell strains. All cultures were shown to contain endothelial cells on the basis of several endothelial-specific and endothelial-associated traits. Both primary and passaged cells demonstrated specific receptors for the insulin-like growth factor, multiplication-stimulating activity (MSA). [125I]Iodo-MSA binding was greatest in cells derived from aortas, least in pulmonary venous cells, and intermediate in pulmonary arterial cells. When compared to MSA receptors on primary endothelial cell cultures derived from human umbilical veins or arteries, the bovine cells bound 4-10 times more MSA per cell. In all bovine cells, insulin competed weakly or not at all with [125I]iodo-MSA binding. The presence of MSA receptors on primary and passaged cells from five different vascular sources (three bovine and two human) suggests that receptors for the insulin-like growth factors may be an intrinsic component of the vascular endothelium.

Animals↗
PubMed1982

Strategies for surviving the capital shortage.

With traditional sources of capital threatened, hospitals are going to have to turn to new sources of capital and new methods of raising capital if they are to meet their facilities and equipment needs during the 1980s. New capital will come primarily from two sources: net income from new health services and health-related ventures operating in less regulated markets, and equity offerings.

Capital Financing↗
PubMed1982

Use of endothelium cultured on microcarriers as a model for the microcirculation.

The geometry of the vascular system is such that the surface area to volume ratio changes dramatically as a unit volume of blood circulates. Thus, it faces a surface area that is some 1000 times larger in the capillaries than in larger vessels. To approach the in vivo situation an in vitro model for the microcirculation was developed that uses endothelium cultured on microcarrier beads. Details of the culture method are presented. The cultures form confluent monolayers around the beads and resist removal by vigorous vortex mixing. Viability of the cells on the microcarrier is 100 per cent. The microcarrier cultures are packed into small columns (0.3 to 1.0 ml.) forming a perfusion system and used for studies of the binding of thrombin and platelet factor 4, for the demonstration of anticoagulant properties of the cells, for studies of the interaction between endothelium and platelets, and for the demonstration of prostacyclin release.

Animals↗
PubMed1982

Contribution of the subendothelium to prostacyclin release after vascular injury.

PGI2 release from intact and de-endothelialized vascular segments has been evaluated in a template device to determine the early response of the vessel wall to physical injury. The luminal surfaces of mechanically denuded areas of vascular segments released high concentrations (450 nM) of 6-keto-PGF1 alpha, the stable hydrolysis product of PGI2, in the initial hours after injury. Later the denuded regions of vessels had blunted 6-keto-PGF1 alpha release under basal and stimulated conditions equal to 5% to 25% of that obtained from adjacent intact regions. The recovery of 6-keto-PGF1 alpha from de-endothelialized segments suggests that subendothelial components of the vessel wall contribute to the PGI2 released at the luminal surface. These observations on intact and damaged vessels may have important implications with respect to vascular function after injury and the resultant platelet-vessel wall interactions.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Massive fatal pulmonary emboli with fibrinolytic therapy.

A case is described in which massive fatal pulmonary emboli followed the initiation of thrombolytic therapy. Several important issues regarding anticoagulation and fibrinolytic therapy are addressed, including the possibility of anticoagulant failure and the risks of using fibrinolytic therapy in the setting of recent and remote thrombotic disease.

Adult↗
PubMed1981

Prostacyclin release from cultured and ex vivo bovine vascular endothelium. Studies with thrombin, arachidonic acid, and ionophore A23187.

Prostacyclin release from systemic and pulmonary endothelium has been evaluated in cultured cell monolayers and in an ex vivo vascular segment model in which the endothelium remains in contact with subendothelial structures. The effect of exposure to arachidonic acid, ionophore A23187, and thrombin on prostacyclin release has been assessed. Arachidonic acid elicited prostacyclin release in a dose-dependent fashion. Ionophore also stimulated bovine systemic endothelium to release prostacyclin. Thrombin-endothelial cell interactions have been examined extensively. Unlike umbilical venous endothelium, systemic and pulmonary bovine endothelium did not release prostacyclin following exposure to thrombin. Exposure to thrombin also failed to evoke the release of tritiated arachidonate metabolites from the bovine endothelial cell preparations. The presence of high affinity binding sites for thrombin (KD = 9.5 X 10(-9) M) on the bovine endothelium suggests that either thrombin binding is causally unrelated to prostacyclin release or that the bovine cells lack mediators required for thrombin to exert its effect.

Animals↗
PubMed1980

Successful prostatectomy in patients with inherited abnormalities of the factor VIII molecule.

Urological procedures pose specific medical and surgical problems in the patient with a hemorrhagic disorder. Three men, each with a different inherited deficiency involving the factor VIII molecule, underwent prostatectomy. Prolonged postoperative genitourinary hemorrhage was encountered and treated with replacement therapy and the use of inhibitors of fibrinolysis. Successful management of these patients with inherited coagulopathies depends on a thorough understanding of the hemostatic defect, adequate laboratory support and sufficient supplies of blood products.

Aged↗