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S McCoy

Publications and source records attributed to S McCoy.

At least 37 records · Page 2Linked to original sources
PubMed1988

Periodontics.

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Defensive Medicine↗
PubMed1987

Sera from HTLV-III/LAV antibody-positive individuals mediate antibody-dependent cellular cytotoxicity against HTLV-III/LAV-infected T cells.

The causative agent of the acquired immunodeficiency syndrome (AIDS) has been shown to be a human retrovirus called human T lymphotropic virus (HTLV)-III or lymphadenopathy-associated virus (LAV). The nature of the protective immune response against this virus is currently unknown. We report here results using an antibody-dependent cellular cytotoxicity (ADCC) assay which has been developed for measuring a specific immune response against HTLV-III/LAV. Forty-four sera were examined for their ability to mediate ADCC against HTLV-III/LAV-infected T cells. Sera from healthy HTLV-III/LAV seropositive individuals in the presence of mononuclear cells from healthy HTLV-III/LAV seronegative donors exhibited significantly higher levels of ADCC activity compared to sera from patients with AIDS. Western blot analysis of serum samples indicated that antibody reactivity with the p24 protein of HTLV-III/LAV correlated with higher levels of ADCC activity than did reactivity with Gp120/160. The observation that sera from healthy HTLV-III/LAV seropositive individuals mediated higher levels of ADCC activity than did sera obtained from subjects with AIDS suggests that ADCC may represent a protective immune response to infection with HTLV-III/LAV.

Acquired Immunodeficiency Syndrome↗
PubMed1981

Insulin effectiveness in hypovolemic dogs.

The question addressed in this study was whether exogenous insulin can enhance the rate of assimilation of blood glucose after prolonged hypovolemia when homeostasis is waning. Twenty-three well-fed mongrel dogs were maintained at a mean arterial blood pressure of 50 mm Hg by bleeding. Periodic analyses were made of arterial and venous plasma concentration of glucose, femoral blood flow, arterial plasma concentration of insulin, and hematocrit. At the onset of physiologic deterioration signaled by the need to reinfuse 50 ml of shed blood to maintain 50 mm Hg blood pressure, dogs received either 10 ml saline (control; n=15) or 10 ml saline containing 2 units insulin (treated; n=8). Administration of 2 units of insulin to eight of the dogs caused a significantly faster decline of blood glucose than that observed in saline-treated animals. Despite the more rapid decline in plasma concentration of glucose in animals that received insulin, there was no significant difference in glucose uptake between the two groups of animals. The hemoconcentration reflected by a rising hematocrit that develops when hypovolemia persists was accentuated by the administration of insulin without supplementary fluids. The absence of any effect of insulin on glucose uptake in the hindlimb in the late phase of hypovolemic shock suggests that the accelerated decline in arterial glucose levels may be due to inhibitory effects of insulin on hepatic glucose release. These results are not consistent with the resistance of plasma glucose to insulin in the late phases of hypovolemic shock.

Animals↗
PubMed1981

Increased platelet prostaglandin and thromboxane synthesis in diabetes mellitus.

Platelets obtained from some diabetic patients show enhanced in vitro platelet aggregation. These studies were designed to determine if platelets obtained from diabetic subjects manifest increased metabolism of arachidonic acid to labile aggregating substances, such as thromboxane A2 (TXA2), and if they play a role in the enhanced platelet aggregation. Arachidonic acid stimulated TXA2 synthesis, as determined via radioimmunoassay of its stable metabolite TXB2, was significantly greater (p less than 0.01, n = 12) in platelet-rich plasma obtained from diabetic compared to matched controls. Arachidonic acid stimulated TXB2 synthesis in the diabetic platelet-rich plasma was positively correlated with the ambient fasting plasma glucose (r = 0.61, p less than 0.02, n = 15). Platelet aggregation induced by arachidonic acid (0.4-0.8 mM) was inhibited significantly less by 13-azaprostanoic acid (p less than 0.04, n = 14), an antagonist of the actions of prostaglandin H2 or TXA2 on platelets, compared to matched controls. We conclude that platelets obtained from some diabetic subjects manifest increased metabolism of arachidonic acid to labile aggregating substances which may contribute to the enhanced platelet aggregation.

Arachidonic Acids↗
PubMed1977

Porous acrylic cement.

The use of acrylic bone cement has a number of shortcomings, viz., high curing temperatures that can cause thermal necrosis, release of toxic monomer, and a less than perfect cement-to-bone bond. However, by modifying the cement composition through the addition of a soluble, nontoxic filler such as sucrose or tricalcium phosphate which does not impair the workability of the material during surgery, a significant improvement in the performance of the cement can be achieved. Because the filler replaces part of the acrylic components, less heat is generated during curing while the filler itself acts as a heat sink. Also, less monomer, proportional to the amount replaced by the filler, diffuses from the implant site. Upon elution of the filler, a porous cement will be obtained provided that a critical minimum percentage loading is exceeded so that the filler crystals will make physical contact with each other. The value of this percentage depends on both crystal modification and size. In the 125-175 micron sucrose crystal size range, the critical minimum percentage lies in the range of 20-28 wt% loading. Above 30%, the interconnecting pore size increases sharply to a value which allows good tissue ingrowth into the pores. The introduction of filler and pores causes a drop in strength, but the diametral tensile strength of modified cement containing up to 40% pores and sucrose lies between .7 and 1.5 kg/mm2, respectively, which is still in the same range as that of bone.

Acrylic Resins↗
PubMed1977

Determinants of blood amino acid concentration after hemorrhage.

Many mechanisms, including alterations in muscle metabolism, cellular damage, decreased blood volume, and hepatic disfunction, are influential in producing the observed progressive rise in the concentration of amino acids in arterial and venous blood during persisting hypovolemic shock. The rapid rise of venous and arterial concentrations of amino acids and the increase in venoarterial concentration difference suggest that hypovolemia causes a net release from muscle of a potential substrate for energy metabolism. The blood flow through peripheral tissues, however, is reduced to such an extent during hypovolemic shock that the net rate of release of amino acids is not greater than preshock release and may be less. Therefore, the homeostatic advantages served by the alteration in protein metabolism during the more chronic stresses of starvation or after injury may not obtain during acute hypovolemia.

Amino Acids↗
PubMed1977

Contribution of glucose to the hyperosmolality of prolonged hypovolemia.

Normal rats subjected to hypovolemic shock (Wiggers model) exhibited the characteristic rise in blood glucose as well as the initial fall in hematocrit indicative of plasma refill. Concurrently there was a rise in osmolality. Late in shock these animals became hypoglycemic and the hematocrit rose despite a persisting hyperosmolality. Rats which had been deprived of food for 24 hours in order to deplete the liver glycogen did not become hyperglycemic after hemorrhage and had a less marked fall in hematocrit. The plasma osmolality rose to the same high level as that of the fed rats but the rise was slower. From this we conclude that glucose may be largely responsibile for the rise in osmolality early in shock in fed animals but it is not responsible for the continuing hyperosmolality in fed or fasted animals. Nor is it responsible for the initial rise in fasted animals. Hyperosmolality may delay but does not prevent fluid loss from the capillaries late in shock.

Animals↗
PubMed1975

The influence of diet on response to hemorrhagic shock.

Prior nutrition is known to influence tolerance to hypovolemic shock. This study was undertaken to determine the influence of dietary composition on the response of animals subjected to hypovolemic shock. Particular attention was directed to the role of high and low protein diet content with a proportionate change in carbohydrate content to yield isocaloric diets. Rats were placed on one of three diets and were subsequently subjected to shock either by 1) hemorrhage to a pre-determined mean arterial blood pressure, or by 2) hemorrhage of a pre-determined volume of blood based on per cent of body weight. Serial measurements were made of blood pressure, blood volume removed, survival time,hematocrit, blood glucose, pH and blood gases. The results indicate that a high protein diet does not prolong tolerance to recurrent blood loss but there is a greatly reduced tolerance to hemorrhage shock in rats whose body weight was maintained on a low protein/high carbohydrate diet. The latter animals also exhibited impaired refill of plasma volume and a paradoxical, continuing hyperglycemic response during hypovolemia. This study suggests that although an abundant supply of blood glucose is available as an energy source, glucose uptake in the peripheral tissues is inhibited during hypovolemia by unknown mechanisms and thus homeostasis is curtailed. The protein content of the diet may be a critical factor in carbohydrate use during shock.

Animal Nutritional Physiological Phenomena↗
PubMed1975

Hemodynamic and metabolic alterations in peripheral tissue during hemorrhagic shock.

In dogs subjected to hypovolemic shock (modified Wiggers model) severe enough to decrease the arterial flow in an isolated hind limb by two-thirds, a marked hyperglycemia (three times control) and an increase in blood glucose AV difference (ten times control) occur. Despite the decreased arterial flow, glucose uptake by peripheral tissues increased by a factor of three within one-half hour of hemorrhage and remained elevated for several hours. Presumably, the increased glucose uptake reflects the need for more energy substrate during the hypoxic conditions of the decreased peripheral blood flow.

Animals↗