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Biomedical subjects

G E Shambaugh

Publications and source records attributed to G E Shambaugh.

At least 37 records · Page 2Linked to original sources
PubMed1993

Insulin-like growth factors and binding proteins in the fetal rat: alterations during maternal starvation and effects in fetal brain cell culture.

Maternal malnutrition adversely affects fetal body and brain growth during late gestation. We utilized a fetal brain cell culture model to examine whether alternations in circulating factors may contribute to reduce brain growth during maternal starvation; we then used specific immunoassay and western blotting techniques, and purified peptides to investigate the potential role that altered levels of insulin-like growth factors (IGFs) and IGF binding proteins (IGFBPs) may play in impaired growth during maternal nutritional restriction. Fetal, body, liver, and brain weight were reduced after 72 hr maternal starvation, and plasma from starved fetuses were less potent than fed fetal plasma in stimulating brain cell growth. Circulating levels of IGF-I were reduced in starved compared to fed fetuses, while levels of IGF-II were similar in both groups. In contrast, [125I]-IGF-I binding assay demonstrated an increase in the availability of plasma IGFBPs following starvation. Western ligand blotting and densitometry indicated that levels of 32 Kd IGFBPs were 2-fold higher in starved compared to fed fetal plasma. Immunoblotting and immunoprecipitation with antiserum against rat IGFBP-1 confirmed that heightened levels of immunoreactive IGFBP-1 accounted for the increase in 32 Kd IGFBPs in starved plasma. Levels of 34 Kd BPs, representing IGFBP-2, were unaffected by starvation. Reconstitution experiments in cell culture showed that IGF-I promoted fetal brain cell growth, and that when they were supplemented with IGF-I, the growth promoting activity of starved fetal plasma was restored to fed levels. These changes were measured using MTT to assess mitochondrial reductase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

A new method for the detection of viable cells in tissue sections using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT): an application in the assessment of tissue damage by surgical instruments.

This report describes a new method using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) to visualize live viable tissue at the microscopic level. The visualization of the MTT stained tissue provides a metabolic assessment of tissue damage, and can be utilized as an extension of conventional hematoxylin-eosin (H & E) staining. In this report, several tissues were studied with MTT and H & E staining after incisions had been made by a variety of surgical dissecting instruments. A marked improvement in the detection of tissue damage was seen using MTT, regardless of how the damage was caused, i.e., physical, heat, or photon energy. In addition, a distinct zone of damage not noted on conventionally prepared and stained tissues is readily apparent. Thus MTT staining will have utility in both clinical and research studies, concerned with assessing the viability of tissues.

Animals↗
PubMed1993

Sodium fluoride therapy.

As a medical treatment for otospongiosis-otosclerosis, sodium fluoride influences the underlying bony changes in the labyrinth so as to arrest or prevent the onset of hearing loss. Sodium fluoride is an enzyme inhibitor and reduces osteoclastic bone resorption and, if the dosage is more than 60 mg a day, may rebuild pseudohaversian bone.

Administration, Oral↗
PubMed1992

Otitis media.

Explore the source record for details and available documents.

Child↗
PubMed1992

Retardation of fetal brain cell growth during maternal starvation: circulating factors versus altered cellular response.

Maternal starvation inhibits fetal brain development during late gestation in the rat. To determine whether intrinsic or extrinsic factors might be the principal contributor to altered growth, brain cells from 20 day fetuses were cultured in a 96 well plate with MEM and 10% adult rat serum. Tissue growth was monitored by spectrophotometric measurement of the mitochondrial reduction of a chromagen 3-(4,5 dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide (MTT). After 1, 4 or 6 days incubation, MTT activity in non confluent cultures was shown to be directly related to tissue mass. When fetal brain cell cultures were incubated with 1% and 10% concentrations of adult rat serum, an 11-fold increase in MTT activity paralleled a 15-fold increase in tritiated thymidine incorporation. The impact of maternal starvation on fetal brain cell growth was examined by measuring MTT activity in fetal brain cells from fed and starved mothers. When cultures were incubated for 6 days with graded concentrations of fed adult serum (1.25-10%), the MTT response was slightly but consistently lower in cells from starved when compared with cells from fed mothers. By contrast, a marked difference in MTT activity which was paralleled by a lower DNA content became apparent when fetal rat brain cells were incubated with starved adult serum. Fetal serum and adult male serum were found to support growth equally well, while incubation of fetal brain cells with maternal sera resulted in lower MTT values than with the corresponding fetal sera. When cells were incubated with fetal sera pooled from starved mothers, MTT activity was decreased by 42 to 45%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Vincent's violent vertigo. An analysis of the original diagnosis of epilepsy vs. the current diagnosis of Meniére's disease.

The authors propose to correct the historical misimpression that Vincent van Gogh's medical problems resulted from epilepsy. Rather, the authors propose his main medical problem was Meniére's disease. The authors have reviewed the 796 personal letters written by van Gogh. The symptoms of his Vertigo attacks, their presentation and duration as described in these letters, taken as a whole, are consistent with the clinical picture of Meniére's disease, not epilepsy. They point out that Prosper Meniére's description of his syndrome was not well known at the time of van Gogh's death, and was often misdiagnosed as epilepsy. During the last years of his life, van Gogh was labeled epileptic, although no rigid criteria for this diagnosis are evident. This diagnosis is still prevalent in the art history literature today. His symptoms included episodic vertigo and dizziness, physical imbalance, hearing symptoms, ear noises (tinnitus) as well as a presumed secondary psychological reaction to his physical symptomatology. van Gogh's diagnosis of epilepsy is based on written diagnosis in his medical records in 1889 when he was interred (voluntarily) in St. Remy at an asylum for epileptics and lunatics.

Art↗
PubMed1990

Van Gogh had Menière's disease and not epilepsy.

We intend to correct the historical error that Vincent Van Gogh's medical problems resulted from epilepsy plus madness, a diagnosis made during his life but for which no rigid criteria are apparent. Review of 796 personal letters to family and friends written between 1884 and his suicide in 1890 reveals a man constantly in control of his reason and suffering from severe repeated attacks of disabling vertigo, not a seizure disorder. His own diagnosis of epilepsy was made from the written diagnosis by Dr Peyron, the physician at the asylum of St Remy (France), wherein on May 9, 1889, Van Gogh voluntarily committed himself to the asylum for epileptics and lunatics. However, the clinical descriptions in his letters are those of a person suffering from Meniere's disease, not epilepsy. The authors point out that Prosper Meniere's description of his syndrome (an inner-ear disorder) was not well known when Van Gogh died and that it often was misdiagnosed as epilepsy well into the 20th century.

Art↗
PubMed1990

The impact of maternal serum on development of enolase activity in fetal rat brain cell culture.

The effect of gestational age on serum-mediated changes in enolase activity was tested in a fetal rat brain cell culture. After 6 days exposure to graded concentrations (10 and 20%) of nonpregnant female rat sera, enolase activity in brain cell cultures increased from 2.83 +/- 0.03 to 3.74 +/- 0.19 mumol/min/mg protein, P less than 0.01. By contrast, similar concentrations of 20-day maternal serum progressively decreased enzyme activity from 1.52 +/- 0.14 to 1.19 +/- 0.08 mumol/min/mg protein. The inhibitory effect was apparent at 14 days gestation and became progressively greater during late gestation to reach a maximum at 20 days. Combining equal concentrations of 20-day pregnant with either nonpregnant or adult male serum neutralized the inhibitory activity. When serum from 20-day pregnant rats was partitioned by a dialysis membrane with a 50,000 MW pore size, inhibitory activity could be similarly neutralized by male or nonpregnant female serum. When 20-day maternal serum was passed successively through filters with a greater than 300,000, 100,000, and 50,000 MW exclusion, the inhibitory activity was apparent in all fractions excluded by a molecular weight of 50,000. No inhibition was apparent in fractions that were not excluded by 50,000 MW pore size. Inhibition of enolase activity was greatest in the fraction with MW greater than 300,000. Binding of IGF II could also be demonstrated in this fraction. Binding of IGF II was evident in the fraction greater than 100,000 MW but could not be demonstrated in fractions with a lower molecular weight. The presence of mRNA for IGF II in 20-day fetal rat brain cell cultures was evident when total cellular RNA was analyzed by an RNAase protection assay. It is proposed that a high-molecular-weight component of maternal serum in late gestation can bind endogenously generated IGF II. Such binding, by depleting the necessary growth factors, could inhibit in vitro growth and development of enolase activity.

Animals↗
PubMed1989

Etiology of otospongiotic sensorineural losses.

The etiology of otospongiotic-otosclerotic disease is enzymatic; the proteolytic enzymes released by the otospongiotic-otosclerotic foci damage the inner ear and are also the basis of the bony rebuilding of the OW niche leading to stapedial fixation. The trigger may be an autoimmune process due to the reaction of the enchondral otic capsule against the embryonic cartilaginous remnants, genetically determined to be located in the otic capsule and mainly in the fissula antefenestram.

Antibody Formation↗
PubMed1989

How and when to prescribe sodium fluoride.

Sodium fluoride has now been used for 24 years in an effort to slow down or arrest sensorineural hearing nerve deterioration in patients with stapedial otosclerosis or after stapedectomy, as well as in patients with pure cochlear otosclerosis. Extensive clinical experience in thousands of patients with this therapy has demonstrated its value in arresting previously progressive sensorineural hearing loss. For a long time there were those who objected to this therapy on the basis that it had not been adequately proven by double-blind, placebo-controlled studies. They have been answered by Bretlau's study in Denmark and Fisch's from Switzerland; both investigators confirmed on small groups the value of sodium fluoride by double-blind, placebo-controlled studies. Extensive research by Professor Petrovic of Strasbourg while at our tissue culture laboratory at Northwestern University demonstrated the action of sodium fluoride on bone. A nicely designed study with radioactive strontium by Linthicum, House, and Althaus demonstrated its value in promoting maturation of a spongiotic focus. Today there is no reason to hesitate in prescribing this useful, effective, and safe medication to promote maturation of otospongiotic lesions, and thus to slow down or to arrest progression in sensorineural hearing loss.

Hearing Loss, Sensorineural↗
PubMed1989

Zinc: the neglected nutrient.

Zinc was first recognized as essential for animals at the University of Illinois School of Agriculture in 1916, when it was found that zinc-deficient baby pigs were runty, developed dermatitis on their legs, and were sterile. Zinc deficiency was first recognized in man by Dr. Ananda Prasad of Detroit 26 years ago when he measured serum and hair zinc levels in young male Egyptian dwarfs who had failed to mature and were small in stature. By simply adding zinc to their regular diet, they grew in height and became sexually mature. It is now recognized that dwarfism in males is frequent around the Mediterranean, where wheat is the staple of life and has been grown for 4,000 years on the same soil, thereby resulting in the depletion of zinc. Professor Robert Henkin first suggested that zinc deficiency might cause hearing-nerve impairment. Assay of the soft tissues of the cochlea and vestibule revealed a zinc level higher than that of any other part of the body. Previously, the eye was considered to have the highest level of zinc of any organ. To diagnose zinc deficiency clinically, we use serum zinc assays made at the Mayo Clinic Trace Element Laboratory. With zinc supplementation in patients who are marginally zinc deficient, there has been improvement in tinnitus and sensorineural hearing loss in about one-third of elderly adults. We believe zinc deficiency is one causation of presbycusis; by recognizing and correcting it, a progressive hearing loss can be arrested.

Cochlea↗
PubMed1988

Developmental pattern of poly (ADP-ribose) synthetase and NAD glycohydrolase in the brain of the fetal and neonatal rat.

Poly (ADP-ribose) synthetase and NAD glycohydrolase were examined in nuclear fractions from rat brain at sequential times during late fetal and the first two weeks of neonatal life. In whole brain, both enzymes were demonstrable at all stages of development, but followed separate patterns. Activity of the synthetase which was greatest in fetal life, fell steadily with fetal maturation from 3.90 +/- 0.06 nmol/mg DNA at 16 days, to reach a nadir of 1.36 +/- 0.09 nmol/mg DNA on the 4th postnatal day. Subsequently it underwent a non sustained neonatal rise reaching a peak of 2.46 +/- 0.07 nmol/mg DNA on the 8th day. By contrast, NAD glycohydrolase activity increased steadily throughout late fetal and during the first two weeks of neonatal life, from 12.77 +/- 0.40 nmol/mg DNA on day 16 of gestation to 25.80 +/- .95 nmol/mg DNA on neonatal day 12. In neonatal cerebellum the activity of poly (ADP-ribose) synthetase was greater at 8 than at 4 days, could be stimulated with graded concentrations of sonicated DNA up to 100 micrograms, but was inhibited by higher concentrations of DNA and by all concentrations of exogenous histone. In an in vitro culture system of fetal rat brain cells, the activity of poly (ADP-ribose) synthetase increased steadily over six days. Cycloheximide 10(-3) M completely inhibited the activity of this enzyme. NAD glycohydrolase activity increased progressively in vitro, and after 6 days in cycloheximide (10(-3) M), the cultures contained significantly greater levels of enzyme activity. It is suggested that changing activities of poly (ADP-ribose) synthetase and NAD glycohydrolase could both provide potential markers for brain cell differentiation in this system.

Animals↗
PubMed1988

Nutrition and fetal brain maturation. II. Impact of maternal starvation on changing levels of acetylcholinesterase and enolase in vitro.

The impact of maternal starvation during Days 17-20 of gestation was examined in 20-day fetal rat brain tissue cultured for 6 days in MEM and 10% adult rat serum. Acetylcholinesterase (AChE) activities were consistently greater in fetal brain cell cultures from starved mothers. When fetal tissues from starved mothers were continuously exposed to 72-h fasted serum, AChE activities increased from 1.03 +/- 0.14 to 1.59 +/- 0.21 mumol/h/mg protein (P less than 0.001). In fetal tissues from fed mothers, lower AChE activities were increased from 0.78 +/- 0.09 to 1.04 +/- 0.07 mumol/h/mg protein (P less than 0.05) when 72-h fasted serum was used to replace the fed serum during incubation. When fetal brain cell cultures from fed mothers were exposed for 6 days to graded concentrations of fed serum (2.5-15%), the activities of AChE fell reciprocally from 1.34 +/- 0.10 to 0.82 +/- 0.12 mumol/h/mg protein (P less than 0.05). The levels of AChE activity in tissues exposed to fasted serum were consistently greater, but fell similarly from 1.62 +/- 0.10 to 0.97 +/- 14 mumol/h/mg protein (P less than 0.01), when serum concentrations were increased from 2.5 to 15%. AChE activities were 30% higher in tissues incubated with cycloheximide 10(-3) M (P less than 0.02). Unlike AChE, fetal brain enolase activities were unaffected by maternal starvation. In fetal brain cell cultures from fed mothers, enolase fell from 1.85 +/- 0.10 to 1.37 +/- 0.12 mumol/min/mg protein following exposure to fasted instead of fed serum (P less than 0.02). In fetal cultures from starved mothers, enolase activities were depressed similarly from 1.76 +/- 0.08 to 1.41 +/- 0.09 mumol/min/mg protein when fasted replaced fed serum (P less than 0.02). Thus, the fetal brain cell cultures appear to maintain enzymatic realignments imposed by maternal starvation for at least 6 days. In addition, serum from fasted animals has significant growth inhibiting properties manifested by heightened activities of AChE and lower activities of enolase.

Acetylcholinesterase↗
PubMed1988

Tuning fork tests: forgotten art.

Four examples are cited in which tuning fork tests helped in proper selection of patients for surgery, after audiometric air and bone tests were equivocal or gave the wrong diagnostic and prognostic indication.

Adult↗
PubMed1987

Nutrition and fetal brain maturation. I. Responses in vitro and in vivo.

The glycolytic enzyme enolase increases during the perinatal period of brain development and was utilized as a marker for examining the effect of culture environment on differentiation of cells from 20-day fetal rat brain. Enolase activity in cell cultures increased from 0.91 +/- 0.03 (Day 0) to 2.11 +/- 0.10 mumol/min/mg protein (Day 6). Comparable levels were not reached in vivo until neonatal pups were 15 days old. The in vitro increase was inhibited by both cycloheximide and actinomycin D. Enolase activity in the cells responded to alterations in both incubation media and homologous serum. After 6 days in culture, cells incubated in rat serum (10%) added to MEM or RPMI produced twice as much enolase activity as cells incubated similarly in Ham's medium, i.e., 1.96 +/- 0.09 and 1.85 +/- 0.21 vs 1.02 +/- 0.09, P less than 0.001. Results of a comparable magnitude were obtained when fetal calf serum replaced adult rat serum, but enolase production was somewhat lower when newborn calf serum replaced adult rat or fetal calf serum. When cells were incubated for 6 days with graded concentrations of adult rat serum (2.5-15%), enolase activity increased progressively. The pattern of enolase response suggests that the fetal rat brain cell model described herein will provide a sensitive probe with which to gain insight into nutrition and fetal brain development.

Animals↗