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Biomedical subjects

R W Yurt

Publications and source records attributed to R W Yurt.

At least 37 records · Page 2Linked to original sources
PubMed1989

Identification and characterization of macrophage inflammatory protein 2.

In response to endotoxin, macrophages secrete a protein with a molecular mass of approximately 6000 Da and with an affinity for heparin. This protein, which we term "macrophage inflammatory protein 2," is a potent chemotactic agent for human polymorphonuclear leukocytes. In addition, subcutaneous administration of the monokine causes a localized inflammatory reaction. Partial N-terminal sequence data reveal similarity to a family of proteins, the archetype of which is platelet factor 4. Although macrophage inflammatory protein 2 is a distinct member of the platelet factor 4 family, its sequence is most closely related to that of the gro/KC gene product, which is expressed in transformed or platelet-derived growth factor-treated cells.

Amino Acid Sequence↗
PubMed1989

Tracheostomies in burn patients.

The use of tracheostomies in burned patients with inhalation injuries is now reserved for specific indications rather than as prophylactic airway management. A 5-year burn center experience with tracheostomies used in this fashion is presented. Ninety-nine tracheostomies were performed in 3246 patients who had indications of prolonged respiratory failure or acute loss of airway. Although colonization of the sputum was universal, neither rates of pulmonary sepsis nor mortality were significantly increased in patients who underwent tracheostomies. Twenty-eight patients developed late upper airway sequelae, including tracheal stenosis (TS), tracheoesophageal fistula (TEF), and tracheoarterial fistula (TAF). Duration of intubation correlated only with development of TAF, whereas patients in whom TEF developed were significantly older and more likely to have evidence of tracheal necrosis at the time of tracheostomy. The pathogenesis of upper airway sequelae in these patients as divergent responses to the combined insults of inhalation injury, infection, and intubation is considered.

Burns↗
PubMed1989

Occult diaphragmatic injury from stab wounds to the lower chest and abdomen.

Ninety-five patients with stab wounds to the lower chest and abdomen underwent routine abdominal exploration. Eighteen of these patients had diaphragmatic injury and in five patients it was the only injury found. Isolated diaphragmatic injury in asymptomatic patients cannot be reliably delineated by either serial physical examination or peritoneal lavage. Delayed recognition of incarcerated diaphragmatic hernia after stab wounds to the lower left chest and upper abdomen has an associated mortality rate of 36%. The anatomic area of concern can be defined as stab wounds that penetrate the left side of the chest below the fourth intercostal space anteriorly, the sixth intercostal space laterally, and the tip of the scapula posteriorly. Exploratory laparotomy is necessary in these patients until a reliable nonoperative method is established that can exclude injuries to the diaphragm.

Abdominal Injuries↗
PubMed1989

Comparison of an occlusive and a semi-occlusive dressing and the effect of the wound exudate upon keratinocyte proliferation.

Three consecutive studies were performed in 58 patients evaluating the effect of occlusion on the healing of partial-thickness wounds. Mirror-image donor sites were covered with the occlusive hydrocolloid dressing (HCD) (DuoDerm) and compared to fine mesh gauze, and the HCD was subsequently compared to a semi-occlusive dressing of polyurethane film, (Op-site). In addition, partial-thickness burn wounds were covered with the HCD and the remaining burn wound was treated with silver sulfadiazine. The donor sites and burn wounds treated with HCD healed significantly faster than those covered with fine mesh gauze or silver sulfadiazine (p less than 0.001) and with less pain. The HCD and polyurethane film were equivalent. There were no clinical infections with the wounds that were occluded. The exudate collected beneath the DuoDerm and Op-site on donor sites was added to the tissue culture system and resulted in a modest increase in keratinocyte proliferation. However, the exudate from burn wounds under HCD resulted in a marked increase in cell proliferation (p less than 0.001).

Adolescent↗
PubMed1989

Emergency room visit time: changes over a 16-year period.

A one-week time and motion study was conducted at a large urban hospital replicating a study performed in 1969 in the same hospital, allowing a longitudinal study of emergency room utilization to be reported. Despite a 36% increase in the number of emergency room patients over the 16-year period, the findings from both studies replicate many of the patterns previously reported. Over time, both length of stay and wait times to see physicians have increased, although the values are still well within the ranges found in the literature. As competition increases, hospitals and their emergency room managers will have to determine what constitutes acceptable visit and waiting times in order to compete effectively for emergency room "clientele." Studies such as this one serve as a foundation for hospitals to implement policy changes that will improve health care delivery, and, in fact, this institution has already implemented changes based on this study.

Adult↗
PubMed1988

Effect of prostaglandin E on immune function in multiple animal models.

The immunosuppression seen following major trauma and burns has long been attributed in part to prostaglandin E (PGE). This has been due primarily to the demonstration that PGE levels are elevated following burns and that when PGE is added to leukocyte cultures, it impairs multiple types of leukocyte functions. We investigated the effect of a new long-acting PGE derivative, 16,16-dimethyl-PGE, on immune function in multiple animal models. The PGE derivative had no effect on mortality in burn sepsis models but improved mean survival times in an Escherichia coli peritonitis model. The PGE derivative impaired neutrophil migration into burn wounds at lower dosages. In a rat burn model, when PGE was administered parenterally, it failed to impair cell-mediated immunity at any dosage and improved lymphocyte function at certain dosages. These data indicate that PGE may not be as immunosuppressive in in vivo models as it has been shown to be in in vitro models.

Animals↗
PubMed1988

Tumor necrosis factor-enhanced leukotriene B4 generation and chemotaxis in human neutrophils.

In an in vivo study of five normal volunteers infused with endotoxin (20 U/kg of US reference endotoxin lot EC-5), increased neutrophil (PMN) generation of leukotriene B4 and chemotaxis to leukotriene B4 were found concomitantly with elevated plasma tumor necrosis factor (TNF) levels. To clarify the role of TNF in PMN activation, neutrophil responsiveness after in vitro treatment with TNF was examined. Neutrophils from seven normal subjects were incubated with TNF for 30 minutes and tested for chemotaxis to leukotriene B4, formyl-methionyl-leucyl-phenylalanine and zymosan-activated serum, or the calcium ionophore A23187 to assess leukotriene B4 generation. A range of 10(-13) to 10(-9) mol/L of TNF was used for these assays. When 10(-9) mol/L of TNF was used, the amount of leukotriene B4 that was produced was significantly greater than in control cells. The effect of TNF on PMN chemotaxis was uniformly inhibitory for the three stimuli at 10(-10) mol/L compared with untreated cells. At a picomolar range, PMN migration to leukotriene B4, but not to zymosan-activated serum or formyl-methionyl-leucyl-phenylalanine, was significantly increased over that of PMNs not exposed to TNF. This suggests that TNF has a specific facilitatory effect on PMN responsiveness for both leukotriene B4 production and chemotaxis to leukotriene B4 and may be the same signal for this phenomenon in endotoxemic patients.

Calcimycin↗
PubMed1988

Differential neutrophil activation before and after endotoxin infusion in enterally versus parenterally fed volunteers.

This study was done to determine whether or not increased susceptibility to infection seen in enterally versus parenterally fed patients was caused by altered neutrophil (PMN) responsiveness. To determine the differential effects of route of feeding on human PMN activation, plasma C3a levels, circulating PMN counts, PMN migration to leukotriene B4 (LTB4), the peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP) and zymosan activated serum (ZAS) and generation of LTB4 were assayed before and after and infusion of endotoxin. Nine normal volunteers were enterally (n=4) or parenterally (n=5) fed a diet sufficient to maintain body weight for seven days prior to a standard challenge of endotoxin. Samples were taken prior to the infusion and hourly thereafter for six hours. Prior to the injection of endotoxin, significant differences were seen in the two feeding groups. Plasma C3a levels, absolute circulating PMN counts and chemotaxis to LTB4 were all significantly (p less than 0.02) elevated in the enterally fed group. Generation of LTB4 was higher in the intravenously fed group at base line than the orally fed group (p less than 0.05). Plasma C3a levels rose in the enterally fed group, but not in the intravenously fed group, at two hours after infusion. Neutrophil counts rose in both feeding groups after endotoxin infusion; but the change in percentage was greater in the enterally fed group than in the intravenously fed group. Chemotaxis to FMLP and ZAS was not different during the study and did not differ between the two feeding can have significant impact on neutrophil function and that parenteral nutrition may impair host responsiveness.

Chemotaxis↗
PubMed1987

Increased susceptibility to infection due to infusion of exogenous chemotaxin.

Previous studies indicate that endogenous chemotaxins, such as the chemotactic factor C5a, may modulate the function of neutrophils (PMNs) and account for increased susceptibility to infection after injury. These effects were investigated by continuously infusing rats with saline or the chemotaxin formyl-methionyl-leucyl-phenylalanine (FMLP). Rats that sustained a full-thickness burn covering 30% of total body surface area and whose wounds were inoculated with Pseudomonas aeruginosa had a significantly shorter survival when FMLP was infused (6.5 +/- 0.91 days) than did saline-infused rats (9.9 +/- 0.83 days). Rats infused with FMLP had significantly more leukocytes in their burn wounds, significantly fewer PMNs in the circulating pool, and the same number of PMNs at the site of FMLP infusion compared with the saline-treated group. These findings support the hypothesis that chemotaxins generated by tissue injury or sepsis contribute to increased susceptibility to infection.

Animals↗
PubMed1986

Enterococcal burn sepsis. A highly lethal complication in severely burned patients.

A retrospective study was undertaken to examine the incidence and clinical significance of enterococcal bacteremia in burned patients with enterococcal burn-wound infections. During a 26-month period from 1983 to 1985, 38 patients were found to have enterococcal burn-wound infections. Twenty of these patients developed positive blood cultures for enterococcus with no other identifiable source for the bacteremia. Cases occurred sporadically during the study period without evidence of a specific epidemic. Ten patients died within ten days of the bacteremia, while nine others eventually died from other complications. Only one patient survived to discharge. Prior antibiotic therapy did not appear to increase the risk for enterococcal infection, and specific therapy against the enterococcus after the bacteremia was identified appeared to have no effect on mortality. Mortality was significantly greater for bacteremic patients than for patients with enterococcal wound infection alone or for burned patients without enterococcal infections. Although previously not considered pathogenic, enterococcal burn-wound infections should prompt aggressive therapy to prevent the development of enterococcal sepsis with its associated high mortality.

Bacterial Infections↗
PubMed1986

Base-line and postthermal injury plasma histamine in rats.

Although plasma histamine concentration has been reported to increase after thermal injury in the rat to as much as 100-fold over normal human plasma levels, the pathophysiological significance and relevance to human disease is questionable. Lack of confidence in the rat as a model of histamine-mediated disease is based on reports that normal rat base-line plasma histamine concentration exceeds that of human plasma by 20- to 70-fold. The present study confirms that high concentrations of histamine (20-68.9 ng/ml) are found in rat plasma obtained in an uncontrolled manner; but concentrations are lower (1.17 +/- 0.49 ng/ml) or undetectable in a sensitive radioenzymatic assay when sampling technique and plasma isolation are controlled. The primary cause for falsely elevated values for plasma histamine concentration appeared to be due to manipulation of the rat. Plasma histamine concentration increased within 1 min after thermal injury and the increase was proportional to extent of surface area injured. In contrast to the finding of a single time-related peak of plasma histamine concentration after partial-thickness burn, a biphasic elevation was found after full-thickness injury. Thus the data indicate that normal rat plasma histamine concentration is similar to that of the human and below the reported threshold for modulation of a variety of immune responses. Furthermore, the data support a role for histamine and other mast-cell mediators in the local and systemic responses to injury.

Animals↗
PubMed1985

Decreased wound neutrophils and indiscrete margination in the pathogenesis of wound infection.

To assess the pathogenesis of increased susceptibility to infection and septic death in a rat model, neutrophils (PMNs) in the wound, circulating PMNs, and their in vivo activity were evaluated after 30% and 60% burns. Eight hours after injury there were twice as many PMNs in the wounds of rats that sustained 30% compared with 60% burns. There was no difference between these two groups in the number of circulating PMNs at 2, 4, 6, and 8 hours after injury. In vivo evaluation of PMN response to infusion of F-Met-Leu-Phe revealed that circulating PMNs were more sensitive 4 hours after 60% burns compared with sham burns. At this time PMNs were found to be less sensitive to zymosan-activated serum infusion after 30% burns compared with sham burns. However, the PMNs in rats with 30% burns were more sensitive to this stimulus than were PMNs in rats with 60% injuries. Thus rats with greater injury, known to be more susceptible to wound infection, have fewer PMNs in their wounds 8 hours after injury. This is preceded by an increased sensitivity of PMNs in vivo to bacterial chemotactic factor and a relative increase in sensitivity to wound factors. This unusual finding implicates indiscrete margination as a factor in the pathogenesis of infection.

Animals↗
PubMed1984

Increased susceptibility to infection related to extent of burn injury.

A model of burn wound sepsis in which the mortality caused by infection was significantly greater after a 60% total body surface area (TBSA) burn than after a 30% TBSA burn was developed in the rat. In rats that sustained a 60% TBSA burn (30% partial plus 30% full thickness), the 30% TBSA partial-thickness burn that was inoculated with Pseudomonas aeruginosa strain 59-1244 developed invasive wound infection (greater 10(5) colony-forming units per gram of tissue). Infection did not develop in rats that had a 30% TBSA partial-thickness burn inoculated, without additional injury. The additional burn in the rats with a 60% TBSA burn seemed to affect the development of infection in the partial-thickness wound and the overall outcome by a mechanism other than by infection of the full-thickness wound itself. Autopsy confirmed that mortality was caused by sepsis.

Animals↗
PubMed1978

Modulation of the formation of the amplification convertase of complement, C3b, Bb, by native and commercial heparin.

Native rat mast cell macromolecular heparin proteoglycan and commercial hog heparin glycosaminoglycan chains inhibit generation of the amplification convertase, C3b, Bb. The inhibitory action of heparin is not due to chelation of magnesium. Heparin is most active in inhibiting convertase formation on cellular intermediates formed with the lowest C3b input and developed with the highest B concentration, thereby suggesting the receptor site for B on C3b as the point of heparin action. This interpretation is consistent with the demonstration that heparin prevents B utilization during the fluid phase interaction of C3b, B, and D. Inhibition is observed also when C3b,Bb generation takes place on cellular intermediates in the presence of P or C3NeF, which yield stabilized forms of the convertase. 50 times the concentration of heparin required to inhibit convertase generation does not accelerate the decay of the unstabilized or the C3NeF-stabilized convertases and has only a modest effect on the P-stabilized convertase. An additional effect of heparin is to impair beta1H-mediated decay-dissociation of C3b,Bb. The concentration of native or commercial heparin which prevents convertase formation is in the same range as that required for the demonstration of its anti-coagulant and anti-thrombin III cofactor activities. The additional finding that this inhibitory action of heparin can be expressed by the isolated mast cell granule suggests that native heparin may contribute to the modulation of the amplification pathway of complement.

Animals↗
PubMed1977

Native heparin from rat peritoneal mast cells.

[35S]Heparin was produced in vitro by incubation of rat peritoneal mast cells with [35S]sulfate and in vivo by injection of [35S]sulfate into rats. The [35S]heparin together with nonlabeled heparin in the mast cells was isolated in native form by mild methods that avoided the use of proteolytic enzymes or high alkali concentrations. The heparin had low anticoagulant activity. Incubations of mast cells with [35S]sulfate for less than several hours in vitro resulted in [35S]heparin of approximately Mr=200,000 to 400,000 based on gel filtration, while longer incubations yielded [35S]heparin of approximately Mr=750,000 that was similar to the nonlabeled heparin in the mast cells. When [3H]serine was included in the in vitro incubations, 3H-labeled material was found to co-chromatograph with the [35S]heparin. None of the heparin could be degraded by any of several proteolytic enzymes, but incubation for 14 h at 25 degrees with 0.5m NaOH degraded all samples to a size of approximately Mr=40,000. One-third of the [3H]serine label continued to co-chromatograph with the [35S]heparin after alkali treatment, while the remaining two-thirds appeared as smaller molecules completely separated from the [35S]heparin. Thus, native heparin of the mast cell may be an unusual proteoglycan that is resistant to proteolytic enzymes.

Animals↗
PubMed1977

Immunologic release of heparin from purified rat peritoneal mast cells.

High m.w. [35S]heparin, labeled in vivo or in vitro, was released from purified rat mast cells by challenge with rabbit anti-rat F(ab')2, guinea pig anti-rat IgE, or calcium ionophore. The released and the residual heparin were isolated by Dowex 1 chromatography and were of comparable size by Sepharose 4B gel filtration. The majority of the released heparin was found by differential centrifugation to be granule-associated. Net percentage of mast cell heparin release, quantitated by metachromasia after isolation on Dowex 1 chromatography, correlated in a linear fashion with net percentage of histamine release, with heparin exhibiting a threshold requirement for onset of release. The correlation of histamine and high m.w. heparin release provides chemical support for the conclusion of others from ultrastructural studies that mast cell activation by immunologic means or by the calcium ionophore results in secretion of the whole granule.

Animals↗
PubMed1970

Cardiac arrest among geriatric patients.

In a review of 292 hospital patients who had cardiac arrests over a period of two and a half years patients aged 60 and over were contrasted with those under 60, based on a 50-item clinical questionary completed at the time of the episode. Survival rates were identical (23%) in these two groups. On contrasting patients who survived with those who did not it was again found that age did not influence outcome. Patients with multiple arrests or without cardiographic evidence of ventricular standstill were much more likely to recover. Whether or not a doctor initiated therapy did not affect survival.

Age Factors↗