Louis L. Tureen

Ultrastructural changes in chick cerebellum induced by vitamin E deficiency

SummaryFocal lesions were induced in the cerebellum by feeding chickens a diet high in unsaturated fats and deficient in vitamin E. Ultrastructurally, the lesions consisted of central and peripheral zones. The central zone was characterized in the cortex and white matter by enlargement of the intercellular space, swelling of astrocytes, vacuolization of oligodendrocytes, ballooning of nerve fibers, degenerative changes in small blood vessels, and extravasation of plasma and blood cells. The peripheral zone was characterized by enlargement of the intercellular space in the white matter, swelling of astrocytes in the cortex, and the accumulation of dark bodies in the endothelium of small blood vessels. The results suggest that this nutritional encephalopathy is caused by alterations in the permeability of the vascular bed due to the dietary stress of unsaturated fatty acids in the absence of vitamin E.

Histological observations on the evolution of nutritional encephalomalacia in chick cerebellum

SummaryA study was made of the histological alterations which occur in the development of nutritional encephalomalacia in the chick cerebellum. 3 categories of chicks were discernible according to severity of symptoms.The earliest changes consisted of focal edema in the folial and medullary white matter. These became progressively more severe and resulted in widespread spongy degeneration. Edema of the Purkinje layer consistently appeared and led to a separation of this layer from the underlying granular layer. Apparent capillary proliferation was noted in all layers and distention of blood vessels finally resulted in hemorrhage and in necrosis of the folia.Clinical signs occasionally occurred without apparent morphological alterations. The edematous process, when noted, was considered to be intracellular, involving glial elements in the white matter and the Golgi epithelial cells (Bergmann astroglia) in the Purkinje layer. The condition results from altered permeability of the cerebellar blood-brain barrier which is selectively affected by the metabolic changes brought about by vitamin E deficiency.ZusammenfassungDie histologischen Veränderungen in der Entwicklung von nutritiver Encephalomalacie im Kleinhirn des Huhnes wurden untersucht. Nach der Schwere der klinischen Symptome wurden 3 Gruppen von Tieren unterschieden.Die frühesten Veränderungen bestanden in Ödemherden im Läppchenmark und Marklager, die progredient an Schwere zunehmen und ausgedehnte spongiöse Degeneration bewirken. Ödem der Purkinje-Zellschicht trat regelmäßig auf und führte zu ihrer Ablösung von der darunterliegenden Körnerschicht. Deutliche Capillarproliferation war in allen Schichten erkennbar. Die Gefäßerweiterung führte schließlich zu Blutungen und Nekrosen in den Läppchen.Klinische Symptome traten gelegentlich ohne manifeste morphologische Läsionen auf. Der ödematöse Prozeß wurde, wenn nachweisbar, als intracellulär aufgefaßt. Er betraf Gliaelemente des Markes und die Golgi Epithelzellen in der Purkinje-Zellschicht (Bergmann Astroglia). Diese Veränderung ist bedingt durch Permeabilitätsveränderungen der cerebellaren Bluthirnschranke, die selektiv betroffen erscheint, wenn der Stoffwechsel durch Vitamin E-Mangel gestört wird.

Comparison of Plasma Protein Changes in Antioxidant Deficiency Muscular Dystrophy and Genetic Muscular Dystrophy in the Chicken.

Summary and conclusions 1. Chickens on an antioxidant and sulfuramino acid deficient diet, develop nutritional myopathy. Plasma protein changes, progressively developing during the course of the disease, are characterized by a significant reduction in the albumin fraction, a significant rise in the B globulin fraction and a significant fall in the A/G ratio. 2. Paralyzed chickens of a genetic dystrophic strain fail to show such changes. The plasma protein profile is comparable to that of healthy chickens on a control diet. 3. Genetic dystrophic chickens on an antioxidant and sulfuramino-acid deficient diet grow poorly, develop the most severe degree of paralysis, and have a shorter survival period. The plasma protein profile is characterized by a significant decrease in total protein concentration, although a rather normal plasma protein electrophoretic pattern is maintained. 4. It is concluded that the metabolic defect in genetic dystrophic chickens is one localized to the muscular system, while that in antioxidant and sulfuramino acid deficiency is a generalized one. 5. The significance of the protein changes is briefly discussed.

Immunophoretic Evaluation of Blood Serum Proteins in Chickens. I. Changing Protein Patterns in Chickens According to Age.

Summary and Conclusions 1. Immuno-phoresis was performed in a series of 42 normal chickens from ages 1 to 210 days. Rabbit serum immunized against normal mature chicken serum was used for antibodies. Bar-bital buffer at pH 8.6, ionic strength 0.1 was used. 2. Identification of fractions was attempted by designating precipitation curves in the chick serum preparation with the names used for curves of known fractions in identical position and of identical shape in human serum preparations made under identical conditions. 3. Significant findings in chicken serum indicate that all fractions are more abundant in neonatal life than at later periods. 4. Prealbumin becomes less abundant after the 12th day of life, and is not detected in the preparations after the 20th day. 5. Precipitation curve in the position of the beta lipoprotein fraction is not observed in preparations after the 8th day of life. 6. Additional fractions of gamma globulin appear in some preparations after the 12th day of life. 7. The findings are significant for comparison with serological protein profiles of chickens on vit E-deficient diets.

Phenotypic Expression in Chickens Heterozygous for Hereditary Muscular Dystrophy

Summary Chickens heterozygous for muscular dystrophy have been compared with homozygous normals and homozygous dystrophies with respect to plasma enzyme activity, pectoral muscle function, and muscle histology. Results for the heterozygote include increased mean plasma CPK and GOT, diminished pectoral muscle function, and alterations in muscle histology suggestive of dystrophy. These findings are discussed in relation to other hereditary animal dystrophies and human muscular dystrophy.

Enzyme Changes within Muscle Fibers in Genetic and Nutritional Muscular Dystrophy

Summary and Conclusions Biopsy preparations of pectoral and gastrocnemius muscles from normal and genetic dystrophic chicks, and from chickens developing myopathy following diets deficient in vitamin E and sulfuramino acids, were examined histologically; serial sections were prepared to demonstrate activity of several glycolytic and oxidative enzymes. Histological and histochemical characteristics of genetic and nutritional myopathies are similar in pectoral and gastrocnemius muscles, but more intense in the former. Coagulation necrosis attacks individual fibers or portions of fibers in the earlier stages of the disease. Before other histological alterations appear, white fibers enlarge and manifest the oxidative enzyme characteristics of red muscle fibers. Apparently, muscle fibers early in the myopathic process contain more enzymes, both oxidative and glycolytic, than do the normal muscle fiber. With the development within a muscle fiber of coagulation necrosis, reactions for both oxidative and glycolytic enzymes are diminished or completely absent. The early and extensive vulnerability of the pectoral muscle of chickens for dystrophic change is an index of its high white fiber content. With reference to enzyme activity in the muscle fibers undergoing myopathic changes, apparently two processes occur during the process: at first some enzymes are increased in amount; then when necrosis occurs, various enzymes examined in this study are lost from the damaged fibers.

Form of the Reflex Response in Relation to the Pattern of Afferent Stimulation

The contraction curve and the after discharge of the flexor reflex response to selective ipsilateral afferent stimulation were studied on 52 cats. Action potentials of the afferent impulses in the popliteal or saphenous nerve, tibialis anticus muscle reflex in spinal cats were recorded. In this group of experiments, discharges from a small condenser (.001 mf) furnished the stimulus. Larger condensers (.02 mf) were used in a second group of experiments which included also decerebrate animals. It was established that with the larger condensers repetitive firing of groups of fibers of the afferent nerve followed a single shock; only the lower threshold fibers fired twice with small voltages. As the strength of stimulus was increased, more of the fibers were repeatedly stimulated, while the higher threshold fibers were fired once. Large voltages repeated the entire action potential with each shock. With the small condenser discharges, a single stimulus fired only once all fibers within the threshold of that stimulus. The rate of stimulation varied from 1 to 15 per second, and in most instances periods of stimulation did not exceed 10 seconds. Results. Voltages within the threshold range of the large fibers of the A group, including the alpha, beta and gamma fibers, produced excitatory responses in the contraction curve which persisted during the period of stimulation at a constant level. Cessation of stimulation resulted in prompt relaxation of the muscle, without indication of an after discharge. Action potentials indicated that alpha fiber threshold coincided with 1.5 v at .001 mf. The rest of the alpha, beta, gamma fibers of the A group were fired with shocks of 3–4.5 v. Stronger voltages (6 v) produced a slightly stronger contraction, which decreased after an initial maximum. An after discharge was manifest in the delay in relaxation of the muscle at the conclusion of stimulation. Progressively stronger voltages produced initially stronger contractions which, however, fell off more rapidly during stimulation, and were followed, after stimulation stopped, by after discharges, occurring as separate slow contractions, a latent period intervening. With 6 volts the lower threshold fibers

Effect of High Linoleic Acid and Antioxidant Deficient Diet on Blood Serum Proteins in Chicks.

Summary and conclusions 1. Chicks fed on an experimental diet, high in linoleic acid and deficient in antioxidants, developed a progressive disease manifested by integumentary changes and signs of central nervous system impairment. 2. Blood serum protein patterns were altered and were characterized by an increase in total protein, a decrease in the A/G ratio, and an increase in beta and alpha 2 globulin fractions. 3. Despite a decreasing A/G ratio, chicks on the experimental diet did not develop exudative diathesis. 4. It appears that the blood serum protein changes are a manifestation of Vit. E deficiency.

Myocardial Catecholamine Contents in Vitamin E and Sulfur-Deficient Chickens.

Summary Dystrophy in chickens due to Vit. E and sulfur deficiency is associated with an elevation in myocardial catecholamines. The catecholamine content of the heart of the normal rooster is significantly greater than that of the normal hen.

Post-mortem Changes in Mineral Salt Distribution in Nerve Cells.

An analysis, by microincineration, of the distribution of inorganic salts in anterior horn cells following temporary vascular occlusion of the spinal cord (Tureen 1 brought forward the necessity of examining the post-mortem changes in these elements in similar tissues. It seemed to be especially advisable also because of recent reports on the ash distribution in human nerve cells in various pathological conditions. Tissues were removed from etherized and bled cats at intervals ranging from 5 minutes to 27 hours. One series of animals was permitted to remain at room temperature; a second series of animals was kept in the ice box at 60° F. for similar periods. Sectioning and incineration were carried out as suggested by Scott. 2 Alternate sections of the series were stained with hematoxylin and eosin as controls. The incinerated sections were studied by dark field illumination. The findings will be related briefly in two parts, the first of which is the appearance of incinerated anterior horn cells after immediate fixation. The results are in general in accord with those for similar types of material described by Scott 3 and by Patton. 4 , 5 The first consideration is to establish a “normal” picture—a task admittedly difficult since there is considerable variation in the appearance of the anterior horn cells even under optimum conditions. In general the ash residue of the well-fixed anterior horn cell is uniformly distributed throughout the cytoplasm. This mineral is in small deposits approximately 1 to 2 microns in diameter. It is in this cytoplasmic ash that the greatest variation occurs. In some cases, for example, the remains of the Nissl substance are clearly discernible, in others not. It is as yet impossible to assign this variation to a definite physiological state of the cell.