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Biomedical subjects

A Koestner

Publications and source records attributed to A Koestner.

At least 19 recordsLinked to original sources
PubMed2000

A subependymal giant cell astrocytoma in a cat.

A 6-year-old spayed female Domestic Shorthair cat presented with a 1 to 2-month history of blindness and altered behavior. At necropsy, a 1-cm-diameter, firm white mass was found arising from the subependymal region of the right lateral ventricular wall that protruded into and partially filled the lumen. Histologically, there was a well-demarcated, expansile paraventricular neoplasm composed of moderately pleomorphic cells within a richly fibrillar matrix arranged in interlacing streams and perivascular pseudorosette-like patterns. Neoplastic cells varied in morphology from small spindloid cells to larger polygonal cells with eccentric vesicular nuclei to neuronlike cells with vesicular nuclei and prominent nucleoli. The mitotic index was low. Immunohistochemically, neoplastic cells were positive for S-100 protein, glial fibrillary acidic protein, and neuron-specific enolase and negative for neurofilament protein. Ultrastructurally, the cells contained few to abundant bundles of intermediate filaments with variable numbers of mitochondria, endoplasmic reticulum, and ribosomes. These features are characteristic of subependymal giant cell astrocytoma (SEGA) in humans. To our knowledge, this is the first reported case of SEGA in domestic animals.

Animals↗
PubMed1998

Variation among trauma centers' calculation of Glasgow Coma Scale score: results of a national survey.

BACKGROUND: Glasgow Coma Scale (GCS) scoring is enigmatic in intubated patients. To determine if there is consensus among Level I trauma centers, a national telephone survey was conducted. METHODS: Trauma registrars at state-verified or American College of Surgeons-verified Level I trauma centers were questioned about GCS scoring, recording, and reporting in patients who are intubated or intubated and pharmacologically paralyzed. RESULTS: Seventy-three centers were contacted. Seventy-one use initial GCS scores for registry recording. Intubated patients are given 1 point for verbal component plus eye and motor scores at 26% of centers and a total GCS score of 3 at 23%; GCS score is estimated with "T" given for verbal component at 16%, scored as unknown at 10%, always scored as 15 at 10%, and the method of scoring is unknown at 15%. Pharmacologically paralyzed intubated patients are given a total GCS score of 3 at 34%, GCS score is estimated with "T" given for verbal component at 18%, patients are given 1 point for verbal component plus eye and motor scores at 12%, scored as unknown at 11%, always scored as 15 at 8%, and the method of scoring is unknown at 16%. CONCLUSION: Wide variation in GCS scoring among Level I trauma centers was identified. Because GCS scores are used in treatment algorithms, trauma scoring, and outcome prediction (Trauma and Injury Severity Score), uniform scoring is essential and should be pursued. Use of state and national databases and outcome research may be adversely affected by the lack of consistent GCS scoring.

Adult↗
PubMed1998

Primitive neuroectodermal tumor in a two-month-old black and white Colobus monkey.

A 2-month-old male black and white Colobus monkey (Colobus guereza kikuyuensis) was euthanatized because of progressive physical deterioration, rear limb paralysis, lymphadenopathy, and the presence of facial and retroperitoneal lumbar masses. At necropsy, soft white masses were present in and around lumbar vertebrae, the subcutis of the face, multiple lymph nodes, and the fourth ventricle of the brain. Histologic and immunohistochemical analysis of these masses revealed a primitive neoplasm with both neuronal and glial differentiation, consistent with a primitive neuroectodermal tumor (PNET) with bipotential differentiation. The extracranial tumors were synaptophysin (SYN)-positive, glial fibrillary acidic protein (GFAP)-negative, and neurofilament protein (NFP)-negative, while the intracranial tumor was SYN-positive, GFAP-positive, and NFP-negative.

Animals↗
PubMed1997

Esophageal tracheal Combitube in the emergency department.

The Combitube is currently being used in some prehospital cardiac arrest situations and in flight programs for management of airways in trauma patients, as well as in inpatient departments with limited availability to personnel experienced in intubation. The Combitube allows for quick intubation and for continuing airway access while the patient is in the emergency department.

Contraindications↗
PubMed1994

Radiation effects of boron neutron capture therapy on brain, skin, and eye of rats.

PURPOSE: The present study was carried out to evaluate the radiation effects of boron neutron capture therapy (BNCT) on the brain, skin, and eyes of nude rats following systemic administration of boronophenylalanine (BPA) and neutron irradiation to the head. METHODS AND MATERIALS: A solution containing 120 mg of 10B-enriched-L-BPA complexed with fructose was administered IP to nude rats. Boron concentrations were approximately 8.4, 9.4, 10.0, and 11.0 micrograms/g in the brain, blood, skin, and eyes, respectively, at 6 h when the animals were irradiated at the Brookhaven Medical Research Reactor (BMRR). As determined in a study carried out in parallel with this one, the BNCT radiation doses were sufficient to cause tumor regression in nude rats carrying intracerebral implants of the human melanoma cell line MRA 27. RESULTS: Mild to moderate increases in loose fibrous tissue were observed in the choroid plexus at estimated physical doses to the brain and blood that ranged from 4.3-7.1 Gy and 4.6-7.7 Gy, respectively, and these appeared to be dose and time dependent. Other changes in the choroid plexus included occasional infiltrates of macrophages and polymorphonuclear leukocytes and vacuolation of epithelial cells. Dose-dependent moist desquamation of the skin was observed in all rats, but this had healed by 28 days following irradiation. Cataracts and keratitis developed in the eyes of most animals, and these were dose dependent. CONCLUSION: The minimal histopathological changes seen in the brain at doses that were sufficient to eradicate intracerebral melanoma indicates that BNCT has the potential to cure a tumor bearing host without producing the normal brain injury usually associated with conventional external beam radiation therapy. Studies in canines, which currently are in progress, should further define the dose-effect relationships of BNCT on critical neuroanatomic structures within the brain.

Animals↗
PubMed1992

The use of nerve growth factor as a reverse transforming agent for the treatment of neurogenic tumors: in vivo results.

The rationale behind the evaluation of natural differentiating agents, such as nerve growth factor (NGF), for reverse transforming potential is based on the theory that such compounds may represent a nontoxic means of controlling tumor growth. Previous in vitro experiments have shown that NGF is capable of retarding growth and of inducing persistent differentiation of neurogenic tumor cell lines. In vivo, NGF is capable of causing a persistent reduction in the number of ethylnitrosourea-induced neurinomas and of increasing survival time following intracerebral implantation of F98 anaplastic glioma cells. In this study, anaplastic glioma and neurinoma implants were treated with NGF to evaluate the reverse transforming potential of NGF in vivo. Results indicate that NGF is capable of causing a significant decrease in the growth rate of subcutaneous T9 (anaplastic glioma) and clone 16 (anaplastic neurinoma) implants. Significantly, NGF treatment was accompanied by adverse effects that were minimal and transient. Continued tumor growth (although greatly retarded) following NGF treatment is an aspect that requires further investigation. However, the results of this study suggest that NGF may prove useful, alone or in combination with other types of therapy, for the treatment of tumors of neurogenic origin.

Animals↗
PubMed1991

The reverse transforming effects of nerve growth factor on five human neurogenic tumor cell lines: in vitro results.

The role of nerve growth factor (NGF) in the development, maintenance and regeneration of the mammalian sensory and sympathetic nervous systems has been well characterized, as has the ability of NGF to induce a variety of neoplastic cell lines of neuroecto-dermal (neurogenic) origin to differentiate. The ability to stimulate neoplastic cells of neurogenic origin to differentiate suggests that NGF may prove useful as a reverse transforming agent for the treatment of neurogenic tumors. Five human neurogenic tumor cell lines were evaluated for their response to NGF in vitro to determine whether the NGF is capable of inducing changes consistent with a reverse transforming response. Results indicate that NGF was able to reverse some of the transformed properties of these tumor cell lines, as NGF treatment stimulated neoplastic cells to develop a more differentiated phenotype, diminished or arrested growth, and induced changes that were persistent.

Cell Transformation, Neoplastic↗
PubMed1991

Chronic toxicity and oncogenicity of inhaled methyl acrylate and n-butyl acrylate in Sprague-Dawley rats.

No exposure-related clinical signs or lesions of systemic toxicity and no oncogenic responses were observed in male and female Sprague-Dawley rats exposed by inhalation to methyl acrylate (MA) or n-butyl acrylate (BA) vapours, at concentrations of 0, 15, 45 and 135 ppm. The rats were whole-body-exposed 6 hr/day, 5 days/wk, for 24 consecutive months. There was a 6-month post-exposure observation period for subgroups of BA-exposed rats. Atrophy of the neurogenic epithelial cells and hyperplasia of reserve cells were observed in the nasal mucosa of all MA- and BA-exposed groups. These changes were dose related and mainly affected the anterior part of the olfactory epithelium. Opacity and neovascularization of the cornea were seen in all MA-exposed groups and in the group exposed to 135 ppm BA. These toxic effects of the olfactory epithelium and cornea were attributed to the known irritancy of MA and BA. In the BA subgroups kept for a 6-month post-exposure observation, reconstructive effects, such as replacement of altered olfactory epithelium with respiratory epithelium, and partial regression of corneal neovascularization were observed.

Acrylates↗
PubMed1990

Repeated transplacental transmission of Neospora caninum in dogs.

Four litters of German Shorthaired Pointers from one owner developed a toxoplasmosis-like illness. According to the records, 29 of 39 dogs had hind limb paralysis. Six dogs from 2 litters were necropsied and had generalized encephalomyelitis. Tachyzoites and tissue cysts of Neospora caninum were found in the brain and spinal cord of each dog. Lesions were found in the eyes, extraocular muscles, or both in all of the dogs, and N caninum was detected microscopically in the eyes (retina and choroid in 1 dog), extraocular muscles, or both in 5 of the 6 dogs. Ocular lesions consisted of focal retinitis, choroiditis, mild nonspecific iridocyclitis, and myositis of extraocular muscles. Organisms stained with anti-N caninum serum, but not with anti-Toxoplasma gondii serum in an immunohistochemical test, except in 1 dog. In one dog, aged thick-walled N caninum tissue cysts reacted mildly with anti-T gondii serum.

Animals↗
PubMed1990

Immunohistochemical characterization of rat central and peripheral nerve tumors induced by ethylnitrosourea.

Ethylnitrosourea-induced central and peripheral nerve tumors in Sprague-Dawley rats were tested for GFAP (Glial Fibrillary Acidic Protein), S-100 protein, NSE (Neuron Specific Enolase) and Anti-Leu 7 (HNK-1) immunoreactivity utilizing the ABC method (avidin-biotin-complex) for GFAP, S-100 protein and NSE, and the PAP method (peroxidase-antiperoxidase) for Anti-Leu 7. Peripheral nerve neurinomas were consistently positive for S-100 protein and consistently negative for GFAP and Anti-Leu 7. Neurinomas would occasionally exhibit positive staining for NSE (2 of 55 tumors). The staining intensity for S-100 protein varied from strongly positive in differentiated neurinomas to weakly positive in anaplastic tumors. Neoplastic and reactive astrocytes exhibited positive staining for both S-100 protein and GFAP. Variation in the GFAP staining intensity of glial tumors correlated with the degree of differentiation as anaplastic tumors did not stain with the same intensity as their more differentiated counterparts. Oligodendrogliomas exhibited occasional immunoreactivity to S-100 protein (3 of 36 tumors). NSE reactivity in oligodendrogliomas was rarely observed (1 tumor in 36) and immunoreactivity against GFAP or Anti-Leu 7 was consistently absent. Anti-Leu 7 and NSE proved to be of little value in the classification of ENU-induced neural tumors.

Animals↗
PubMed1990

Characterization of N-nitrosourea-induced tumors of the nervous system; their prospective value for studies of neurocarcinogenesis and brain tumor therapy.

Two decades of research with resorptive neurocarcinogens firmly established the high potency of methyl and ethylnitrosourea (MNU and ENU) as neurocarcinogens, particularly in rats. There are significant differences in susceptibility to these agents among species. There are also differences among age groups. Fetuses are between 50 to 100 times more susceptible than adult rats. One single iv inoculation of 20-50 mg/kg ENU into pregnant rats may produce neurogenic tumors in 100% of the offspring. The tumors produced by these compounds have been well characterized morphologically, biologically, biochemically and histochemically. Tumors produced by both compounds are mostly gliomas and neurinomas (Schwannomas), however, clear differences exist between ENU and MNU produced neoplasms. Transplacental exposure to ENU generally results in a high number of anaplastic neurinomas and mostly differentiated gliomas (astrocytomas, oligodendrogliomas or mixed gliomas). In contrast, multiple exposures of adult rats to MNU result in a moderate number of mostly differentiated neurinomas and a high number of anaplastic gliomas. Tumors usually start out as well differentiated oligodendrogliomas or astrocytomas. As they grow larger, they become more mixed and anaplastic. In contrast to spontaneous gliomas in old rats, MNU and ENU-induced astrocytomas can be readily identified with well established biomarkers such as the S100 protein and particularly GFAP (glial fibrillary acidic protein). Neurinomas are also strongly positive for S100 protein. No reliable markers exist for oligodendrogliomas. Neurogenic tumors induced by MNU or ENU, as well as derived cell lines and clones from such tumors, have been successfully used as models for neurocarcinogenesis and therapeutic screening.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of nerve growth factor on the transplacental induction of neurinomas by ethylnitrosourea in Sprague-Dawley rats.

Administration of nerve growth factor (NGF) to the offspring of Sprague-Dawley rats transplacentally exposed to 50 mg/kg ethylnitrosourea on the 20th day of gestation resulted in a significant reduction of trigeminal and peripheral nerve neurinomas. Forty, 60, and 80 micrograms of NGF was administered in five s.c. doses, one dose on each of days 12-16, 90-94, and 210-214 postnatally. Of the 34 rats in the NGF-treated group, 11 animals were affected with trigeminal nerve neurinomas as compared to 18/34 in the NGF-untreated group (P less than 0.05). In the peripheral nerves (spinal cord nerve roots) there were five and 11 neurinomas, respectively, in each group of 34 rats. When the total numbers of neurinomas (trigeminal and peripheral nerves) between these groups were compared (16/34 versus 29/34), the significance of neurinoma reduction was P less than 0.01. Five trigeminal and two peripheral neurinomas in the NGF-untreated group were shown by immunohistochemical staining to contain nerve growth factor receptor protein, whereas none of the neurinomas in the NGF-treated group were positive for the receptor protein. The results obtained from this experiment lend support to the hypothesis that NGF has the capability to reduce the oncogenic consequences of ethylnitrosourea exposure perhaps by the process of maturation and/or differentiation of the transformed cells, and that this effect may depend upon the presence of receptor binding sites.

Animals↗
PubMed1988

A quantitative morphological assessment of the effect of lidoflazine and deferoxamine therapy on global brain ischaemia.

The effect of the combination of two drugs, i.e. lidoflazine (a calcium antagonist), and deferoxamine (an iron chelator) was evaluated following 15 min global brain ischaemia (GBI) and reperfusion in dogs in a randomized blind study. GBI was produced by complete cardiac arrest of 15 min duration. Histopathological analysis performed on in situ fixed brains 40 h post-resuscitation revealed diffuse microhaemorrhages in the control group. These were noted rarely in the treatment group, the mean value of foci of microhaemorrhages/20 low power fields (LPF) being 5.2 in the treatment group versus 28 in the control group (p less than 0.001). Diffuse coagulative necrosis of neurons (ischaemic cell change) in the cerebral cortex, especially lamina 3, hippocampus, striatum, brain stem and cerebellum was present in all cases. Quantitation of the degree of cellular damage obtained by counting the number of anoxic neurons (in consistent regions of the brain) with the use of an image analysis system, revealed no significant difference between the 2 groups. The mean percentages of the ischaemic neurons in the control group in the various areas studied were: parietal cortex, 22.25; hippocampus, 50.37 and cerebellum (Purkinje cells), 66.75; and in the treatment group 25.3, 55.04 and 70.6 respectively. Thus, the lidoflazine-deferoxamine regimen significantly reduced the incidence of microhaemorrhages in the brain, but it did not have any protective effect against anoxic neuronal injury 40 h post-ischaemia in this experimental model of GBI of 15 min duration.

Animals↗
PubMed1987

Cerebral endothelial microvilli following global brain ischemia in dogs.

Cerebral blood vessels (BVs) of dogs subjected to global brain ischemia by complete cardiac arrest of 15 min followed by 8 h of reperfusion, were studied in neocortex and hippocampus by means of transmission electron microscopy. Widespread endothelial microvilli were present in the postischemic animals. The number of endothelial microvilli in the postischemic animals (mean/BV in the neocortex = 3.26 and in the hippocampus = 2.54) was significantly larger than that in the non-ischemic controls (mean/BV in the neocortex = 1.39 and in the hippocampus = 0.84), P for both regions being less than 0.05. Arterioles, venules and capillaries, all were equally affected. Endothelial pinocytotic vesicles were also observed frequently in the postischemic dogs. Marked pericapillary swelling of astrocytic foot processes was present in the surrounding neuropil. It is concluded that the prominent cerebral endothelial microvilli recognized after 8 h of reperfusion following cardiac arrest in this experimental model of global brain ischemia, may play a significant role in the development of delayed postischemic hypoperfusion.

Animals↗
PubMed1987

Modulation of growth and of morphological characteristics in glioma cells by nerve growth factor and glia maturation factor.

Anaplastic glioma T9 cells were treated with either nerve growth factor (NGF) or glia maturation factor (GMF) or both. It was found that, when T9 cells were treated with these factors in a chemically defined medium, both NGF and GMF induced characteristic changes of cell morphology and growth pattern. Several differences in the effects of NGF and GMF were noted. NGF retarded growth rate, whereas GMF did not. The cells treated with NGF were characterized by a flattened extended cytoplasm with numerous protruding processes. The cell masses were somatically connected by cell bridges. GMF, on the other hand, produced slender cells with long, branching processes forming an interconnecting cell net. Concomitant administration of NGF and GMF retarded cell growth as was demonstrated with NGF alone and induced morphological changes predominantly attributable to GMF. The maximal effect of either NGF or GMF or both was attained after 4 days of treatment. A withdrawal of the factors from the medium following various periods of treatment revealed that the effects of GMF were readily reversible while morphological changes induced by NGF persisted in its absence.

Animals↗
PubMed1987

Ultrastructural and ionic studies in global ischemic dog brain.

A time course of tissue ionic changes, and their relation to ultrastructural findings during reperfusion following a 15-min global ischemic brain insult was studied in a dog model. Parietal cortex was analyzed for Ca, Na, K, Mg and Fe in controls and after 10 min, 2, 4, and 8 h of reperfusion. After 8 h of reperfusion, the mean values (mumol/g tissue wet wt.) for Ca (control = 1.43, 8 h = 2.76) and Na (control 60.4, 8 h = 107.4) doubled and K (control = 90.4, 8 h = 48.5) decreased to half that of the control. Ultrastructural studies and subcellular localization of calcium in parietal cortex of in situ-fixed brains after 8 h showed cortical neurons with clumping of nuclear chromatin, dilatation of endoplasmic reticulum and disruption of plasma membranes. Large amounts of electron-dense precipitates of calcium were present within dilated astrocytic processes, synaptic vesicles, cytoplasm of edematous dendrites and mitochondria. Cortical neurons from postischemic dogs without reperfusion showed only slight chromatin clumping and edema of astrocytic processes, but no calcium accumulation. The large ionic shifts noted between 4 and 8 h of reperfusion, indicate a progressive inability of the cells to maintain normal transmembrane gradients of these ions and may reflect a membrane destructive process, as demonstrated ultrastructurally at 8 h. Enhanced calcium entry into the neuron during reperfusion appears to be a part of the cytotoxic mechanism leading to neuronal necrosis.

Animals↗
PubMed1987

Effect of flunarizine on global brain ischemia in the dog: a quantitative morphologic assessment.

The effects of flunarizine, a calcium antagonist, were evaluated in an experimental model of global brain ischemia produced by 15 min of cardiac arrest followed by resuscitation and reperfusion. One group of dogs received flunarizine (0.1 mg/kg intravenously during a 10-min period) at the onset of resuscitation. Another group of dogs underwent cardiac arrest, resuscitation, and reperfusion but did not receive flunarizine. A third group served as nonischemic control. In situ-fixed brains of all animals (nonischemic controls and the postischemic dogs after 8 h of reperfusion) were examined for anoxic ischemic injury. Quantitation of the ischemic neurons was carried out in parietal cortex, hippocampus, and cerebellum by using an image analysis system. Significant difference in the number of necrotic neurons between the flunarizine-treated group and the ischemic controls was noted in the hippocampus only; the mean percentage of necrotic neurons in the two groups being 14.8 +/- 9.6 and 29.3 +/- 12.1, respectively (P less than 0.05). These results indicate that flunarizine has an ameliorating effect on neuronal injury in the hippocampus that follows cardiac arrest in this experimental model of global brain ischemia. However, flunarizine was not found to be effective in reducing the ischemic neuronal damage in the cortex or the cerebellum.

Animals↗