Biomedical subjects
G E Shambaugh
Publications and source records attributed to G E Shambaugh.
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)
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.
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.
Antibiotic treatment of children with secretory otitis media.
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Fluoride therapy for otosclerosis.
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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.
Microbiology of the tonsils and adenoids.
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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.
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.
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.
Objective changes in trypsin, alpha 1-antitrypsin, and alpha 2-macroglobulin values as a result of sodium fluoride treatment in patients with otosclerosis.
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Experimental studies on pathology and therapy of otospongiosis.
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Endolymphatic sac valve implant surgery. I: The technique.
A resurgence of interest in surgery on the endolymphatic sac (ELS), not only for relief of vertigo but also for stabilization or improvement of hearing, has emerged. With the concept of operating early in the course of the disease after the diagnosis is well established, various modifications of existing procedures on the ELS have been utilized in an attempt to improve the overall results. One such major modification is the unidirectional inner ear valve implant modified from the eye valve for glaucoma. This valve implant has produced impressive one-year results for both hearing improvements and relief of vertigo in patients who were scheduled for labyrinthectomy. Subsequent preliminary reports by several investigators show good to excellent results for the hearing (AAOO--Class B or A) as well as the vertigo without consideration for the stage of the disease. This study presents primarily the step by step technique with drawings and a color atlas to facilitate the correct performance of this surgery.
Hypocalcemia accompanying agranulocytosis during propylthiouracil therapy.
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The fenestration operation in 1979.
While it is rarely indicated today, fenestration of the horizontal semicircular canal has left its mark in otologic history. A significant number of patients with fenestrated ears are alive today requiring continued care. A review of both the technique of fenestration as well as the particular postoperative problems is presented to familiarize younger otologists involved in their management.
Subcellular alterations in cyclic AMP-binding and protein kinase activities during ontogeny in the rat cerebellum.
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