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A Koestner

Publications and source records attributed to A Koestner.

157 records · Page 9Linked to original sources

Intubation quality assurance thresholds.

INTRODUCTION: Quality assurance (QA) and continuous quality improvement (CQI) are valued activities within health-care organizations. Quality assurance indicators as guidelines for quality practice usually are established intuitively. The purpose of this study was to determine an appropriate threshold for successful intubation in patients transported by air and to examine factors impacting this success rate. SETTING: Fifteen rotor-wing programs from across the United States participated. METHOD: The study was a prospective descriptive design. A total of 369 flight crew members agreed to participate, and intubations were attempted on 862 patients during the 12-month study. RESULTS: Intubations were attempted on 862 patients and were successful in 788 (91.4%) of the patients. Of the patients not successfully intubated, 14 received supplemental oxygen only, 25 were supported with bag-valve-mask, 26 received a surgical cricothyroidotomy and for nine patients it was unknown what form of airway support was provided. CONCLUSION: Factors impacting successful intubation include cardiac arrest, use of neuromuscular blockade, use of sedatives and facial trauma. Data from the study support a threshold for successful intubation of between 90% and 95%.

Air Ambulances↗

Case report: a nursing challenge, the unstable pelvic fracture.

A case report is presented that describes the initial care of a severely injured patient who was hemodynamically unstable. The discussion highlights the process used to recognize life-threatening injuries, to differentiate internal sources of hemorrhage, to provide damage-control surgery, and to stop further bleeding with an interventional radiologic examination. The emergency nursing care of a patient with unstable pelvic trauma is included.

Accidents, Traffic↗

Growth inhibition of anaplastic glioma cells by nerve growth factor.

Nerve growth factor (NGF) inhibited cellular DNA synthesis of rat T9 anaplastic glioma cells in a dose-dependent manner in the range of 0.5-5 micrograms/ml. Oxidation of 2 to 3 tryptophan residues of NGF, which had been known to destroy biological and immunological activity, greatly diminished its inhibitory effect on DNA synthesis. The inhibition was also abolished by anti-NGF IgG. Flow cytometric analyses and immunocytochemical assays of DNA synthesis using bromodeoxyuridine incorporation at various times during cell exposure to NGF revealed that the growth inhibition was attributable to gradual accumulation of growth-arrested cells at the G1 phase. Synthesis of nuclear regulatory proteins JUN and p53 was inhibited preferentially and progressively by NGF as inhibition of DNA synthesis increased.

Animals↗

ENU-induced in vitro neoplastic transformation of rat mammary epithelial cells.

Normal mammary epithelial cells, originating from female Sprague-Dawley rats, were grown in Dulbecco's Modified Eagles Medium containing 25% horse serum and hormone supplements. Once established as an epithelial cell culture, the cells were treated with N-ethyl-N-nitrosourea (ENU) in various doses (25-500 ug/ml) to study the process of in vitro mammary epithelial cell neoplastic transformation. The ENU-treatment of primary mammary epithelial cell culture resulted in a sequence of phenotypic changes, termed stages I-V. The rat mammary epithelial cells, after a period of approximately 30 days post-ENU exposure, showed a marked proliferation of morphologically altered cells which formed multi-layered colonies. Subsequently, these cells acquired the capacity to form colonies in soft agar and eventually produced a high yield of palpable tumors when inoculated into newborn female isologous hosts or female athymic nude mice. The immediate effect of ENU on these cells was monitored by measurement of cellular DNA content, unscheduled DNA synthesis, cell proliferation and chromosomal aberrations. The ENU effect on cell proliferation and DNA synthesis was dose dependent; doses greater than 100 ug/ml reduced the cell number and DNA synthesis. Cytofluorometric histograms of non-ENU-treated rat mammary epithelial cells showed a near diploid population of cells. The ENU exposed cells subsequently became hyperdiploid (24-72 hours after ENU) and then regained their near diploid pattern at 120 hours after ENU exposure. The ENU-treated cells also showed a second peak of cells with DNA content in the tetraploid and octaploid range at 24-72 hours after ENU exposure. Single chromatid breaks, isochromatid breaks, chromosomal exchanges, multiple chromosomal breaks and double minutes were among the chromosomal aberrations seen in ENU-treated cells. Most of the chromosomal aberrations peaked at 6 hours post-ENU exposure. The ENU-induced model of in vitro meplastic transformation of rat mammary epithelium as described in this communication appears to provide a good model for the systematic study of the early critical cellular events prerequisite to this carcinogenic process.

Animals↗

Characteristics of normal rat mammary epithelial cells and N-ethyl-N-nitrosourea-induced mammary adenocarcinoma cells grown in culture.

The characteristics of normal mammary epithelial cells derived from Lewis and Sprague-Dawley rats and N-Ethyl-N-Nitrosourea (ENU)-induced mammary gland adenocarcinoma cells derived from Sprague-Dawley (CD) and Fisher (CDF) rats and grown in culture were compared. After collagenase treatment, the rat mammary epithelial cell aggregates were placed in a hormone-supplemented medium. The normal mammary epithelial cells (NE) attached to the surface of the dish within 50 hours, whereas the mammary adenocarcinoma cells (MA) attached within 24 hours and grew as cell multilayers. After the colonies of NE and MA cells became confluent, the culture system entered a steady state in which the cells from the upper layer were shed into the medium. The rate of proliferation and squame detachment in confluent cultures was increased by the presence of epidermal growth factor (EGF). Rhodanile blue staining and transmission electron microscopy showed that the shed cells were partially keratinized. In addition, cultured MA (but not normal) cells were able to grow in soft agar and form tumors when inoculated into appropriate hosts. The opposite was true in each case for the mammary adenocarcinoma cells. Karyotypes of normal and neoplastic rat epithelial cells revealed a hypodiploid modal number of chromosomes.

Adenocarcinoma↗

Chemical control of growth and morphological characteristics of anaplastic glioma cells.

Nerve growth factor (NGF) and glia maturation factor (GMF) reverse some of the transformed characteristics of T9 glioma cells (Marushige et al., Cancer Res 47: 4109-4115, 1987). As an attempt to define the mechanisms of such actions, various chemical agents which modulate second messenger systems were examined for their effects on growth and morphological characteristics of these cells. Administration of bromo-cAMP, forskolin and methylisobutylxanthine retarded cell growth and induced formation of long, branching processes which were similar to those induced by GMF. Perturbation of Ca2(+)-mediated processes by a Ca2+ ionophore, ionomycin, and by calmodulin antagonists, chlorpromazine and W-7, on the other hand, arrested cell growth, and caused clustering of cells, spreading of the cytoplasm and development of lamellipodium-like protrusions which were reminiscent of the effects of NGF. Administration of bromo-cAMP in combination with chlorpromazine, W-7 or ionomycin prevented spreading of the cytoplasm and produced compact cell bodies with well-developed processes. The results of this study demonstrate that modulation of specific second messenger systems by chemical agents are capable of simulating selective morphological changes inducible by NGF and GMF.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Neuropathology of canine epilepsy.

Canine epilepsy can be classified into primary (idiopathic) and secondary (symptomatic) epilepsy, which is similar to human epilepsy. Primary epilepsy in both species is inherited and characterized by the absence of recognizable causative lesions. Secondary epilepsy is linked to a variety of lesions such as brain tumors, trauma, encephalitis, lysosomal storage diseases, congenital malformations, and metabolic-toxic injury. Correspondingly, various subtypes of secondary epilepsy have been recognized. The pathogenesis of secondary epilepsy is basically associated with selective loss of inhibitory neurons that disturbs the balance between excitation and inhibition.

Animals↗

Cytoskeletal reorganization induced by nerve growth factor and glia maturation factor in anaplastic glioma cells.

Changes in cytoskeletal organization in T9 anaplastic glioma cells have been examined during morphological changes induced by nerve growth factor (NGF) and by glia maturation factor (GMF). Indirect immunofluorescent labeling of cytoskeletal proteins has revealed that while neither GMF nor NGF induces expression of glial fibrillary acidic protein in this cell line, changes in cytoskeletal organization induced by these factors show some features similar to those observable during maturation of normal glial cells. Changing cell shapes induced by these factors are clearly outlined by the prominent distribution of microfilaments along cellular margins. Microtubules and intermediate filaments gradually extend during morphological changes and fill the characteristic cytoplasmic processes induced by NGF and GMF.

Actins↗

DNA damage, repair, replication, and tumor incidence in the BDIV rat strain following administration of N-ethyl-N-nitrosourea.

Berlin-Druckrey (BD-IV) rats were used to evaluate the level of neoplastic transformation, initiation of DNA damage and repair following treatment with N-ethyl-N-nitrosourea (ENU). ENU, a potent neurocarcinogen in the Sprague-Dawley (CD) and BDIX rat strains, was a less potent neurocarcinogen when administered to 30 day old BDIV rats. ENU induced significantly higher levels of tumors of the nervous system, kidney, and liver in CD rats than in BDIV rats. Initial DNA damage was determined by quantitating and comparing the number of alkaline labile sites (ALS) and alkylation of [14C]ENU to deoxyguanosine in the brain, kidney, and liver of BDIV rats. A smaller percentage of ALS were lost from the DNA of the brain (10-15%) than from the kidney (19-27%) and liver (30%). Similarly, loss of 0(6)-ethylguanine was greatest in liver (100%), next in kidney (73%), and least in brain (23%) DNA during a seven-day period. Loss of N7-ethylguanine ranged between 23-44%. These levels of repair are similar to those previously observed in the more sensitive Sprague-Dawley rat. Cellular replication was highest in the liver and lowest in the brain of BDIV rats at 30 days of age and was inhibited to varying extents in all three tissues by ENU. These data indicate, that while there is a good correlation between organ sensitivity to ENU induced carcinogenesis and the persistence of DNA lesions and levels of DNA replication in the same strain of rat, there is no correlation across strains with different carcinogenic potential.

Animals↗

Neoplasms induced with high single doses of N-ethyl-N-nitrosourea in 30-day-old Sprague-Dawley rats, with special emphasis on mammary neoplasia.

Intraperitoneal administration of high doses (45, 90, and 180 mg/kg of ENU (N-ethyl-N-nitrosourea) to 30-day-old female Sprague-Dawley (CD) rats resulted in a high incidence (greater than 100%) of mammary tumors (MT), of which 95% were malignant. The mean induction time was 92 days for the high dose group. There was a definite dose-effect relationship. As the dose of ENU decreased the number of rats affected and number of tumors per rat decreased, but the survival time and mean induction time increased. At the time of death 7.5% of mammary tumors had metastasized to the lung. A variety of histological MT types were produced simulating breast tumors in women. In addition to MT, a number of rats developed primary tumors in other organs (brain, ovary, kidney, and hemic-lymphatic system). The high MT incidence, high rate of malignancy, short latent period, and the simulation of human breast tumor types suggest this experimental design to be a valuable animal model to study initiation, hormone dependency, and pathogenesis of mammary neoplasia.

Age Factors↗

Growth inhibition of synchronized trigeminal neurinoma cells by nerve growth factor.

Nerve growth factor (NGF) reduces the development of trigeminal neurinomas in vivo. To characterize the action of NGF on these tumors, clonal cells (476-16) isolated from a rat trigeminal neurinoma cell line were synchronized at early S phase by aphidicolin, a reversible inhibitor of DNA polymerase alpha, and effects of NGF on DNA replication were examined in vitro. While NGF did not inhibit DNA replication in the ongoing S phase, it reduced the level of DNA synthesis in the succeeding S phase without altering its timing and duration. The inhibitory action was elicited by a brief exposure to NGF during progression through the preceding S to G1 phases with decreasing effectiveness in the later stage of G1.

Animals↗