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M. r Liliv.z...a 1": .1 Quart-kl v Y ' ' r--‘\ ,fivvrn‘fa~t:: .0 . 9a 5.3.. f Q's-liar L ABSTRACT THE INFLUENCE OF LIGHT DURATION AND TYPE OF LIGHT ON THE INDUCTION 0F CATARACTS IN BOBWHITE QUAIL By Kenneth Lars Klippen Three hundred day-old Bobwhite quail of mixed sexes were randomly divided into six groups and placed into cages with nine square feet of floor Space. During the next two weeks, all the quail were subjected to continuous light as a 250 watt infrared light (2060 lumens/watt) was used for brooding. Light types and length of duration were changed after two weeks. One pen had three light types, 250 watt infrared (2060 lumens/watt), #0 watt fluorescent (2500 lumens/watt), and 60 watt incandescent (835 lumens/watt) lights operated continuously twenty-four hours a day. The other pen had the same light types Operated cyclically twelve hours a day and absolute darkness the other twelve hours. In the second year of the study, fluorescent lights and 60 watt incandescent lights were replaced with 200 watt incandescent (4010 lumens/watt) lights and 25 watt incan- descent (235 lumens/watt) lights. All the quail received the same ration at appropriate ages. Kenneth Lars Klippen Light duration significantly influenced the induction of cataracts in Bobwhite quail. No significant relationship was observed between type of light and incidence of cataracts. THE INFLUENCE OF LIGHT DURATION AND TYPE OF LIGHT ON THE INDUCTION OF CATARACTS IN BOBWHITE QUAIL By Kenneth Lars Klippen A THESIS Submitted to Michigan State University in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE Department of Poultry Science 1975 ACKNOWLEDGEMENTS The author wishes to express his sincere appreciation to Dr. Theo H. Coleman, Department of Poultry Science and Dr. Janver D. Krehbiel, Department of Veterinary Pathology for their supererogating efforts in making this research a reality. The author is also grateful to Dr. Lloyd R. Champion and Dr. Howard C. Zindel for their guidance and careful review of this manuscript. Sincere thanks are also extended to Dr. John L. Gill, Department of Dairy Science and Mr. Terry L. Wing, Department of Poultry Science for their statistical review of the data. To Dr. H. C. Zindel, Chairman of the Poultry Science Department, the author extends his appreciation for financial support provided. The author is grateful to all individuals in the Poultry Science Department at Michigan State University for their moral support and to Mrs. Barbara Jacobs, Miss Nancy Creed and Miss Patricia Shanks for their technical assistance. ii iii Finally, the author is indebted to his parents and his girl. Patricia, for their never-ending courage and faith that this manuscript will someday be finished. LIST OF T INTRODUCT TABLE OF CONTENTS ABLES O O O O O O O O O O O IOIQ O O O O I O O O O O O 0 LITERATURE REVIEW . . . . . . . . . Dise Drug Exte Inte ase-Related Cataracts . . . -Related Cataracts rnal Stimulation . . . . . rnal Stimulation . . . . . Nutrition Cataract . . . . . . Radi Heat PROCEDURE Expe Expe RESULTS A CONCLUSIO BIBLIOGRA APPENDICI A. B. ation . . . . . . . . . . . and Light Cataracts . . . riment I . . . . . . . . . riment II . . . . . . . . . ND DISCUSSION . . . . . . . N . . . . . . . . . . . . . PHY . . . . . . . . ES Light Influence on Cataract for Experiment I . . . . Light Influence on Cataract for Experiment II Induction Induction Light Influence on Mortality for Experiment I iv Page < \owmmmwmme. A) to P‘ +4 F3 +4 -w 0\ \1 kn \» \p 36 63 72 V Page D. Light Influence on Mortality for Experiment II . . . . . . . . . . . . . . . . 75 E. Quail Diets . . . . . . . . . . . . . . . . . 80 LIST OF TABLES Table Page 1. The relationship of Bobwhite quail mortality to cataract incidence, by light treatment over an eleven month observation period . . . . . I9 2. Proportion of cataracts in Bobwhite quail within treatment combinations . . . . . . . . . . 22 3. Analysis of variance for data summarized in Cpafiole 2 O I O O C O O O O O O O O O O C O O O 23 A. The influence of cataracts on the mortality of Bobwhite quail reared in cages to eleven Inonths Of age 0 O O D O O O O O O O O I O O O O O 25 Appendix A (Experiment I) l. The influence of light treatment on the induction of cataracts in Bobwhite quail from three to eleven months of age . . . . . . . 36 2. The influence of light duration on the induction of cataracts in Bobwhite quail from three to eleven months of age . . . . . . . “5 3. The influence of light type on the induction of cataracts in Bobwhite quail from three to eleven months of age . . . . . . . . . . . . . 5h Appendix B (Experiment IT) 1. The influence of light treatment on the induction of cataracts in Bobwhite quail from four to six months of age . . . . . . , . , 63 2. The influence of light duration on the induction of cataracts in Bobwhite quail from four to six months of age . . . . . . . . . 66 3. The influence of light type on the induction of cataracts in Bobwhite quail from four to Six months Of age 0 O O O O O O O O O O O I O O O 69 vi vii Page Appendix C (Experiment I) 1. The influence of light treatment on mortality of Bobwhite quail to eleven months of age . . . . 72 2. The influence of light duration on Bobwhite quail mortality to eleven months of age . . . . . 73 3. The influence of light type on Bobwhite quail mortality to eleven months of age . . . . . . . . 74 Appendix D (EXperiment II) 1. The influence of light treatment on mortality of Bobwhite quail to thirteen months of age 0 O O O l C O O O O O O O O O O O O O O O O O 75 2. Proportion of dead Bobwhite quail within light treatment 0 O O O O O l O O C O O O O O I O 76 3. Analysis of variance for data summarized in Table 45 O O O I O O O O O O O O I O O O O O O 77 4. Proportion of dead Bobwhite quail within treatment combinations . . . . . . . . . . . . . 78 5. Analysis of variance for data summarized in Table 47 O O O O O O O O O O O O O O O O O O O 79 Appendix E 1. Ingredient analysis . . . . . . . . . . . . . . . 80 2. Ingredients 0 O O O O O O O O O O O O O O O O O O 81 INTRODUCTION The crystalline lens is suspended in the visual axis of the eye by zonular ligaments. Aqueous humor bathes the anterior surface of the lens while the posterior surface abuts the more viscous vitreous humor. Light energy must pass through these refractive indices and focus on the macula densa, a specific point of the retina. Changes in the lens will cause fluctuations in its refractive index deflecting light transmittance (Philipson, 1973). Any alteration in the normal transparency of the lens may be termed cataractous (Bourne, 1937). Attributable factors to cataract induction are innu- merable, but the factors of greatest concern are those that involve ordinary, everyday living. Cataracts in avian species have been noted following subjugation to extended exposures of light energy. To supplement the pinning of this plausible postulate this research has been conducted investigating the influence of light duration and type of light on the induction of cataracts in Bobwhite quail. LITERATURE REVIEW The preventative element of cataracts is still unknown yet the contemporary treatment element of surgical extrac- tion of the lens still utilize the basics as outlined by the French oculist, Jacques David in 1748 (Rucker, 1965). The first reported cataract explanation was by Aurelius Cornelius Celsus, a Roman physician at the begin- ning of the Christian era. Celsus (Bellows, 1944) believed that a large space, Locus vacuus, existed between the cornea and the iris. A cataract, according to his con- ception, was a diseased humor, a suffusion that seeped from the brain into this Space and solidified. Cataract, then meaning, "flowing down", was appropriate. The opaque lens conception was finally recognized by Francous Quarre and confirmed by Weiner Rolfinck in 1656. Disease-Related Cataracts Maternal rubella acting as a teratogenic agent in humans has focused interest on the possible role of viral infections in the production of congenital abnormalities. Lens absence or defective deveIOpment occurred in chick embryos inoculated with Newcastle Disease Virus (Blattner and Williamson, 1951), Influenza A Virus 3 (Williamson §t_§l., 1956) and Enders Strain Mumps Virus (Robertson st 31., 1964). Cataracts were reported in adult hens exposed to Avian Encephalomyelitis (Peckham, 1957; Bridges and Flowers, 1958; Barber and Blow, 1963; Halpin, 1967) and Lymphomatosis (Rigdon. 1959). Drug-Related Cataracts During the summer of 1935, a sporadic outbreak of cataracts, mostly in young women, revealed a cataractogenic drug; dinitrophenol. Its prescribed use was as a metabolic stimulant. Reports of cataracts attributed to this drug flooded medical journals (Allen and Benson, 1935; Kniskern, 1935; Lazar, 1935; Horner §t_§1.. 1935; Shutes, 1935; Whalman, 1936; Spaeth, 1936; Mann, 1936; Hessing, 1937; Horner, 1942). Dinitrophenol experimentation revealed an interference with the metabolism of the rabbit lens (Field et_§1,, 1937). Bourne (1937) postulated that interference with lens metab- olism may lead to cataract formation. The dinitrOphenol cataract was induced in chickens (Buschke, 1947), chicks (Robbins, 1944; Bettman, 1946a; Rigdon EI.El'9 1959), chick embryos (Feldman gt g1., 1958) and in mammals (Bettman, 1946b; Ogino and Yasukura, 1957). 1,4-Dimethanesulfonoxybutane, a radiomimetric chemo- therapeutic drug used in treating chronic myeloid leukemia in humans, produced diffuse opacities in the posterior cortical layers of the rat lens during chronic toxicity Li tests by Solomon.§t 31. (1955). He speculated that the mode of action of this aliphatic compound was due to an alkylation of cytoplasmic or nucleic proteins. Methoxsalen (8-methoxypsoralen), an ingredient used in suntanning lotions, photosensitizes the mammalian lens to ultraviolet light (Cloud et 31., 1960, 1961) and with prolonged use, cataracts developed. Visible light is transmitted by the cornea, the lens and reaches the retina. Ultraviolet light is transmitted by the cornea but is ab- sorbed by the lens. The authors conceded that one omission made in planning these experiments was that no provision was made to determine whether methoxsalen alone was re- sponsible. Polymyxin B Sulfate, an antibiotic, was linked to cataract development in rabbits following intravitreal injections (Cotlier and Apple, 1973). The membranes of the lens fibers contain reactive acidic groups as a part of glycoproteins, phospholipids, polyphosphate nucleic acids and acid mucopolysaccharides. Polymyxin B Sulfate can bind to anionic sites in the lens fiber membranes and eliminate its selective permeability. Electrolyte and water im- balances result, eventually yielding cataractous changes. No lenticular alterations resulted from intravitreal in- jections of streptomycin sulfate, nystatin, bacitracin, penicillin, or chloramphenicol. 2,6-Dichloro-4-nitroaniline, a fungicide used to inhibit the growth of mold on soft fruits, helped to induce 5 cataracts in beagle dogs exposed to both the fungicide and sunlight (Bernstein_gt'31., 1970). The authors indict a conjunction with light because the cataract was located in the visual axis. External Stimulation According to Duke-Elder (1926), Hess (1888) and Kiribuchi (1900) induced cataracts in animals following electrical stimulation via the use of a Leyden jar. Adam and Klein (1945) observed cataracts in a man resulting from an electric current he received in an industrial accident. Duke-Elder (1926) suggested that the electric effect might be complicated by concussion effects. A wedge-shaped Opacification can be produced in the human lens by excessive radial mechanical stress (Fisher, 1973). Internal Stimulation The occurrence of lamellar cataracts in several genera- tions of a family of humans is not very rare. Khan (1926) managed to pedigree this type of cataract but concedes that the pedigree does not fulfill all the requirements of the Mendelian theory. Khan justifies this by citing the diffi- culty involved in accumulating all the data on maternal conceptions. Anderson (1949) attempted a genetic explana- tion of the cortical cataract as a form of dominance with low penetrance; "...an individual possesses a dominant gene for cataract but does not exhibit the condition himself." Anderson conceded that the investigators of the genetic 6 cataracts report such a diversity of findings that the re- sults seem questionable. Nutrition Cataract Laboratory investigations following dietary deficien— cies have revealed several cataractogenic determinates in several Species. Riboflavin deficiency cataracts have been reported in the rat (Day E: 31., 1931, 1937; O'Brien, 1932; Yudkin, 1933; Day and Darby, 1938), mouse (Langston 3:,EER’ 1933), pig (Patek E: 31., 1941; Wintrobe E: 31., 1944) and in the cat (Gershoff St 31., 1959). Gyorgy (1935) was unable to induce riboflavin—deficiency cataracts in the rat, whereas, Day and Langston (1934) reported a 100% incidence. Day 3:.Ei' (1938) also reported that small amounts of riboflavin would arrest further development of this nutri- tion cataract. Baum E: El. (1942) reported that small amounts of riboflavin are needed for cataract development. Ferguson St El. (1954) observed cloudiness in the central portion of the lens of turkey embryos produced by hens fed an all-vegetable protein diet without vitamin E. A second study by Ferguson it 31. (1956) yielded a kera- toconus condition in turkey embryos at 19 days of incuba- tion, with liquefaction of part or essentially all of the lens protein. Young rats develop cataracts when fed a diet deficient in tryptophan (Albanese and Buschke, 1942; Buschke, 1943; von sallmann gt 31., 1959), phenylalanine (Syndestricker §t_§l., 1947; Bowles et 31., 1947; Hall 33 21., 1948), or low protein (Rezende and deMoura campos, 1942; Ferraro and Roizin, 1947). Nutritional-deficiency cataracts have been reported in guinea pigs with tryptophan deficiency (von Sallmann.et 31., 1959), the larvae of the tiger sala— mander with cystine deficiency (Patch, 1941), the pig on a low protein diet (McLaren, 1959) and young rabbits with calcium deficiency (Swann and Salit, 1941). Mitchell and Dodge (1935) reversed the nutritional deficiency investigations by overfeeding lactose and observing cataractous development. Galactose-rich diets also induce cataracts according to some investigators (Krewson gt 31., 1939; Gifford and Bellows, 1939; Kinoshita and Merola, 1964; sippel, 1967; Kuwabara E: 31., 1969). The clinical manifestations of the sugar cataract have been reported in individuals with galactosemia (Lerman, 1959; Kinoshita, 1965) or diabetes (Duke-Elder, 1926). Lens Opacities were noted in studies of thirst (Kudo, 1921) and anoxia (Bellows and Nelson, 1944). Radiation Roentgen Radiation. In 1895 Roentgen discovered the X-ray and two years later chalupecky, as reported by clapp, 1932, demonstrated lenticular opacities in irradiated rabbits, fifty days after exposure. Leinfelder and Kerr (1936) exposed the eyes of several groups of rabbits to various doses of roentgen rays, one eye exposed and the other eye shielded by 2 mm of lead serving as the control. Lenticular changes occurred in all exposed eyes. Cogan and Donaldson (1951) utilized a wider range of roentgen dosage and rabbit age and reported that cataracts occurred with a latent period that was an inverse function of the dose. Rabbits, 4-10 weeks old, were exposed to a single dose of 2000 r (von Sallmann, 1951) and after the first week a spatial disarrangement of nuclei was observed in the bow and preequatorial zone of the lens epithelium. After two weeks, the spatial disarrangement erupted into gaps and disorganization of lens fibers. Reducing the roentgen dosage to 1500 r revealed to von Sallmann (1952) the disappearance of dividing cells thirty minutes after irradiation. This inhibition lasted 3-4 days, then mitosis recurred at an accelerated rate. Pirie (1959) was unable to induce lens opacities in the chick embryo or the chicken, but did note lenticular damage in the rabbit lens following exposure to roentgen rays. Atomic Radiation. Advances in molecular technology have yielded medical repercussions such as cataract devel- opment after atomic radiation exposure. Small vacuoles, thickening of posterior capsule, failure of cells at the equator to differentiate into lens fibers, early migration of cells beneath the posterior capsule toward the posterior pole are some pathological descriptions of the human lens after exposure to the Hiroshima and Nagasaki explosions (Schlaegel, 1947; Cogan gt g1., 1949; Kimura and Ikui, 1951; Cogan gt g1., 1952). 9 Experimentation with radiation induction of cataracts revealed a migration of lens epithelium (Reese, 1939) of the germinative zone toward the posterior pole (Hanna and O'Brien, 1963). Selective irradiation with thymidine- tritium on other areas of the lens required much larger doses to produce lenticular changes than were required to produce changes of the germinative zone (Hanna and O'Brien, 1961). Cyclotron-induced cataracts have been reported by investigators (Abelson and Kruger, 1949; Cogan gt 31.. 1952) to be similar in appearance to radiation cataracts. Heat and Light Cataracts The clinical manifestations of cataracts in occupa- tions that subject people to extremes of heat and light, such as glass-blowers and iron-workers, enticed cataract- ogenic speculation of incident radiant energy on the lens deranging the lens' metabolism (Duke-Elder, 1926). This renders its proteins more prone to coagulation by changes in hydrogen ion concentration, salt content, osmotic changes, or metabolic disturbances. Lenticular Opacification due to heat rays yield posterior polar Opacities in rabbits (Goldmann, 1933) when the rays strike the iris alone and not the whole lens. Goldmann postulated that environmental and metabolic temperatures act on the temperature of the anterior lens surface behind the iris. lO DeVolt (1944) reported lamellar cataracts in chicks brooded in a cellar using electric light bulbs. other procedures did not experience this phenomenon, so he reared a second brood of chicks, but with a shortened time period in the cellar. No cataracts developed in the second brood. The effects of continuous light on the avian eye were first reported to be an enlarged eyeball (Jensen and Matson, 1957). Lauber lm C+ ‘31. (1961) confirmed and extended this research to include: accumulation of vitreous, thickening of retina, reduced thickness of nerve fiber layer and layer of rods and cones. In his studies on the effects of con— tinuous light on the avian eye, he subjected chicks for 10 weeks to an intensity of 3 foot candles (32.28 lux). Lauber gt_al: (1970) prolonged the exposure of chicks to continuous light to 16 weeks and noted an increase in intraoccular pressure. An increase in intraoccular pres- sure disrupts lens metabolism (Brini and Flament, 1973). A disruption in lens metabolism may lead to cataractous development (Bourne, 1937). Zigman and Vaughan (1974) exposed mice to near-ultra- violet (black) light for 12 hours a day over a period of 90 weeks. At 35 weeks they noted inhibition of lens epi- thelial cell differentiation into typical non-nucleated cortical fiber cells in the bow region. Lenticular opaci- ties appeared after 50-60 weeks of exposure to the near- ultraviolet light. Kinsey (1948a) used a Beckman Spectro— photometer to measure the ultraviolet adsorption by the 11 eye. His studies revealed that the lens is chiefly respon- sible for radiant energy absorption of wave lengths shorter than 300 millimicrons. He theorized that radiant energy from the sun would damage the cornea before it damaged the lens. Pirie (1971) and van Heyningin (1973) noted photo-oxidation of lens proteins following exposure to ordinary sunlight. Exposure of chickens to continuous artificial light for several months has led to peripheral anterior synechia, rupture and/or detachment of the retina, metaplasia of the eye wall and cataracts (Lauber and McGinnis, 1966). Light-induced eye abnormalities in turkeys include progres- sive buphthalmus and loss of corneal convexity (Ashton 3331.. 1973). Other investigators have inculpated light for catar- actogenic activity in humans (Milner, 1934), trout (Allison, 1962; Steucke gt 31.. 1968) and rabbits, when light was in conjunction with heat (Langley gt 21., 1960). Bercovitz gt 3;! (1970) measured the thickness of lenses of White Leghorn chickens following light treatments and noted that greater intensities increased the thickness of the lens. A thorough investigation by Krehbiel (1972) of lens opacities in quail revealed that metabolic disturbances, infectious microorganisms, congenital causes, population density, or nutrition did not significantly influence cataract formation but that a continuous light environment 12 for quail as opposed to their natural diurnal experience, had a pronounced effect on cataract formation. ‘tllllll llll'll II [III-I’ll! {III III. II . PROCEDURE Experiment I Three hundred Bobwhite quail (Colinus virginianus) of mixed sexes were hatched from the eggs of Michigan State University stock, wing banded and evenly distributed at random between six identically-constructed compartments. The compartments were three feet by three feet of one-half inch screened cages with four feet by four feet of three-eighths inch plywood intercompartmental dividers. Each compartment possessed one hanging light bulb fixture suspended thirty inches above the floor of the divider so direct light transmittance between compartments was in- hibited. Two light-control pens (capable of complete darkness) had three compartments each. These pens were located in House #2 of the Michigan State University Poultry Science Research and Teaching Center. Brooding infrared lamps were initially installed in the light bulb fixtures for the first two weeks while the quail were provided MSU Quail Starter Ration 72 and water ad libitum. After two weeks, the brooding lamps were re- placed with the experimental lights; 250 watt infrared (2060 lumens/watt) bulbs in compartments 1 and 4, 40 watt Cool White flourescent (2500 lumens/watt) bulbs in 13 14 compartments 2 and 5 and 60 watt incandescent (835 lumens/ watt) bulbs in compartments 3 and 6. Compartments l, 2 and 3 were located in pen G and the light system was set to Operate continuously for one year. Compartments 4, 5 and 6 were located in pen F and operated on a cyclic light system; 12 hours of light, 12 hours of darkness each day. Each pen had one main ceiling outlet into which all three light fixtures were plugged. Via the use of a time clock, this outlet produced either a continuous flow of electrical power (pen G) or the cyclic system (pen F). Monthly eye examinations were performed on each bird. When the eye undergoes cataractous development, light will be reflected from the pupillary region, exhibiting an Opaqueness of some form. Most generally, the afflicted quail exhibited centrally located petechial Opacities which progressed with time into complete cpacification of the lens. By simply shining a high intensity light onto this region, a positive identification of cataracts could be diagnosed. When a cataract was detected, the compartment number, wing band number and particular eye (R,L) was recorded and the bird was returned to its compartment. A one-quarter inch thick plywood, portable intracompartmental divider prevented repeated handling of the same bird. All the birds in one compartment were persuaded to one side, then the divider was inserted. After each examination, the bird was placed on the other side of the divider. When the 15 compartmental examination was finished, the intracomparté mental divider was removed. The birds would then resume their routine activities until the next month's exam. Quail Breeder Ration 72 replaced the starter ration after six months. Experiment 11 Experiment II began with a new hatch of three hundred and thirty-six Bobwhite quail of mixed sexes which were wing banded and randomly distributed among the six original compartments. Newly-incorporated procedures included debeaking (two-thirds of the upper and lower beak), using a Lyons PDQ-2 Debeaker, replacement of the high intensity examina- tion light with a Kowa SL Portable Slit Lamp Microscope and light-type changes. The fluorescent lights in compartments 2 and 5 were replaced with 200 watt incandescent (4010 lumens/watt) bulbs. The 60 watt incandescent bulbs in compartments 3 and 6 were replaced with 25 watt incandescent (235 lumens/watt) bulbs. Infrared lights (2060 lumens/watt) were retained in compartments 1 and 4. Except for these few changes, brooding and operating procedures were identical to those described in Experiment I up to the six month stage, at which time two new light-control pens with three, new, identically-constructed compartments each, were incorporated. At that point, i.e.. after six months, half of the number of remaining birds in each original compartment were transferred to new 16 compartments utilizing the same type of light, but a new light system. For example: half the number of birds in the original compartment 1 (24 hours of infrared light) were transferred to a new compartment that operated on 12 hours of infrared light and 12 hours of darkness. The other half of the birds remained as controls in the original location. - ‘I‘lll‘l'l'l’li‘lllll‘li" ‘r‘lfll,li RESULTS AND DISCUSSION Etiologic investigations of cataracts have yielded two parameters for study concerning light: type and duration. Three commercially-available light types were employed in two different light systems offering two different durations; six treatment combinations in all. With diet, ventilation, temperature, floor space and examination techniques identical for all the quail, the only varying factor was the type and duration of light. All of the diets used met the established protein requirements for optimum growth and maintenance as prescribed by Andrews E: El. (1973). Monthly data collections were analyzed using Chi-Square Analysis (Kempthorne, 1969) to determine if the six treat- ments had any cataract-inducing influence. In the entire two years of study, a significant cataract-inducing in- fluence was attributable to the subjection of Bobwhite quail to the light treatments every month. Eighty-nine percent of the first year's data indicated a high degree of sig- nificance (P<0.005) in treatments influencing cataract induction. 17 The second year and a new brood of quail increased this highly significant percentage to 92% overall. Two more chi-square tests followed each monthly test of sig- nificance attributable to the treatments. Light duration was analyzed for its cataract-inducing influence and in the first year, produced a high level of significance in every month (78% at the 0.005 level and 22% at the 0.01 level of probability). The second year reaffirmed the 100% cataract-inducing influence through light duration with 83% of the data at the 0.005 level of probability. Light type was the third, monthly chi-square test. Only one month in the two year period showed any level of significance (P<0.05). Tables 5 through 31 (see Appendix A) show the chi-square test statistics for the cataract-inducing in- fluences of light in the first year of study. Tables 32 through 40 (see Appendix B) show light influences for the second year. The data records begin at the first month that signs of cataract-afflicted quail are evident in any group. The multi-dimensional contingency (Cochran, 1954), Table 1, reveal a highly significant (P(0.005) relationship of cataract incidence and light treatments to Bobwhite quail mortality. Tables 41 through 43 (see Appendix C) are the chi-square tests used to single out the inculpatory factor. O moo .o v a .HoooflHcmHmi... ....im.m\.,utmm\~1m.o v... w onwo so.o oo.o mm.H o om.oH no.o om.m oo.m m so.o mm.e om.m oo.m e mo.o mm.o o mm.oH m mo.o mo.H om.o o m mm.o am.m oo.m mo.o H ooHo oo>HH omHo oo>HH HooeHoone Haemoz Pompmpmo . omeommxm\mHomeommxmuom>mmmmoo moH oo om oH oom :oH ooH mom ooH so we on mm mHoHop mm 3 w m om mm NH 3 oq 0H s m H o no. em H m m oo o: m o: 13 m H H o m w 1 n I. am 3 m m on mm mm o: om mm H H o e m am. 1. 0 RN mH m m om mm mm mm mm mH mH m oH m 1% m P am 3 m m on mm mm H: mm 3 o o m m m m. H mm “H m m om so oH mm em o oH oH o H m omHo oo>HH ooHo oo>HH HmHoe ooHo oo>HH Hmpoo ommo oo>HH HmHoo omwo oo>HH ecospoono Hmsaoz HomemHmu.1QoHHdH590MIHdee Hmspoz pommmvmo omeommxm om>mmmmo .BOHHmQ coapm>pmmno £9208 Cm>on cm Hm>o pCmEPMmhp pcmfla an .modmoflocw poshmpmo op hpwadphos Hassv mvfisspom 90 mfingOHpmamh ace .H manna 20 Light treatments offer a high degree of significance toward influencing Bobwhite quail mortality, but no significant difference could be isolated in light duration and types analysis. Reinspecting Table l, particularly treatment 5, an unusually high mortality is recorded. An uncontrollable case of cannibalism took its toll on this particular group, thus, influencing the test statistics. To counter such a reoccurrence in the second study, all the quail were de- beaked at one day of age. The second trial (Table 44, Appendix D) shows no significant relationship between light treatments and Bobwhite quail mortality. A radiant energy range of 200 to 400 nanometers (nm) is generally used to produce fluorescent rays. This range involves ultraviolet and the shorter wave lengths of visible light, the blue and violet spectral regions (White and Argauer, 1970). Kinsey in his spectrophotomic work (1948b) has demonstrated that the lens will absorb radiant energy of wave lengths shorter than 300 nm. No wave lengths shorter than 300 nm can be transmitted by glass. Kinsey speculated that solar energy would damage the cornea before damaging the lens. The fluorescent lights used by the author were glassed, tubular encasements which produced the shorter wave lengths of visible light. The first experiment did not pinpoint a relationship between light type and cataract induction. The second experiment eliminated the fluorescent study and incorporated two new incandescent bulbs, 25 watt and 200 21 watt bulbs. These bulbs would offer a wider range of visible light wave length at two different intensities. Can cataractous development be arrested by trans- ferring cataract-free and cataract-afflicted quail from a continuous light system to the cyclic, or can cataractous develOpment be stimulated by a transfer from cyclic to continuous? This question became an objective in the second experiment. Half the number of quail were transferred to a new compartment with the reciprocal light treatment. The remaining quail acted as controls. Table 2 indicates the proportion of cataracts within the treatment combinations. The numbers (12, 24) describe the number of hours of light initially (the first number) and for the last seven months (the second number). The analysis of variance (Table 3) reaffirms the significance of light duration (treatment combination) and exonerates light type. Tukey's Test (Tukey, 1949) revealed that in this study of treatment combinations, the quail that began with 12 hours of light and were switched to 24 hours of light are not significantly different in cataract induction from those that began with 12 hours of light and remained at that light level. 12—-12, 12——24 24-—12, 24--24 There is a significant difference between those groups of quail that began with 24 hours of light and those that began with 12 hours of light. 22 .mmv Hod Pswfla so mHSOQ CH mcchs Cm>om wcflsoaaow exp mow pcmspmmhp one mfl pmnsss ozoomm ms» was Hones: thflm one mp ooPNOchH ma ems we m:p:os Ram 09 a: HCmEPMoHP chflwflmo oce* mm.wsH ms.mm o.m© ON\MH Pemomoccmocfl ppm; mm md.mm m.mm BH\@ PsoommccmOcH ppm; oom on.om o.os om\sH oonmnecH Nfilsm mm.wm ::.wa 0.0H OH\H PcmommocmOcfl ppm; mm oo.NH o.s HN\H HemommocoocH ppm; oom mm.mm m.oH mm\s oosmnccH mHumH mn.©wa . mm.H© m.mn NN\SH Pamomoocmocfi Pew; mm sm.ms H.ms nH\m Femommocmocfl 99m: oom mm.aw w.mm mH\&H wmhmmwcH fiNIdN :m.mm mo.om m.om oH\m HemommocoocH ppm; mm mm.:m w.Hm mm\m HCmomoocmocH ppm; oom om.am A.Hm mm\m omnonccH & .oz #:NINH mQOHPmsHowmsmpp owed Mo mCOHpmcflpsoo pewspmmpe mw Camop< cowppoaohm .mCowpmcflnsoo pCmEPMmHP Canvas Hamsv mpflcsnom Cw mpomhumO mo COHPHomon .N manna mo .ov a .HcooEHcmHm .. .COflPMEhO.HmC.m.HP Cflmohw hp. UQPGHSOHNO .H mm.m: o poppm RH.m mo.msH m wasp HcmHH *md.wa 03.5:w m CQHPMCHDEOO pCmEpmmpe msam>lm meadow cams soommpm mo condom mmmnmmm l .N canny CH omuflnmEESm spec pom cosmem> mo mflmzamc< .m manna 24 The symbols above are a convention for displaying the results of paired comparisons in order of magnitude. The underlined portion shows that these groups of means are not significantly different from one another. The data collected consisted of the proportion of cataract-afflicted quail in the total population within compartments. The possibility that cataracts are lethal to Bobwhite quail would bias the results. Tests conducted on the effects of cataracts on Bobwhite quail mortality over an eleven month period (Table 4) revealed no significant relationship between the two. Light treatments and/or treatment combinations effects on Bobwhite quail mortality were also analyzed (Tables 45-48, Appendix D) resulting in a negative relationship between them. ‘l l 'l‘ .llllnllllal l I.‘ III III).- III 1 i. (Ii . .Hflwsw mmpgnpowpwpwo we pmpesz u z .N .Hflmsv Umpoaflg%muyomuMPMO Mo pmpesz u o .H 5 Sum u HQNAmuom—w «mm m: mmm m: 333 2 mH.o aw.o mofi Hm mwa mm Umflm wN.o 5:.H ow ma :w mm um>flq z o z o z o me\mfimxmlmpov Umpommxm wm>ummno II, .mwm ho mcpcoe Cm>mam op mmmmo Ca vaMmh Handw mpfizanom mo zpflampnos msp so mvomMMPmo mo mQCmSHMcfl mne .3 wands CO NCLUS IO N The exposure of Bobwhite quail to a continuous light environment will lead to cataractous lenses. The type of light utilized will not significantly influence cataract induction. Cataract-affliction in domestically-reared Bobwhite quail will not significantly influence mortality. 26 BIBLIOGRAPHY BIBLIOGRAPHY Abelson, P. H. and P. G. Kruger, 1949. Clyclotron-induced radiation cataracts. Science 110: 655-657. Adam, A. L. and M. {lein, 1945. Electrical cataract: notes on a case and review of literature. Brit. J. Ophthal. 29: 169-175. Albanese, A. A. and w. Buschke, 1942. on cataract and certain other manifestations of trytOphan deficiency in rats. Science 95: 584-586. Allen, T. D. and V. M. Benson, 1935. Late development of cataract following use of dinitrophenol about a year before. J.A.M.A. 105 pt. 1: 795. Allison, L. M., 1962. Cataract among hatchery-reared lake trout. Prog. Fish Cult. 24: 155. Anderson, C. L., 1949. Reduced penetrance in the inheri- tance of cortical cataract. J. Hered. 40: 157-161. Andrews, T. L., R. H. Harms and H. R. Wilson, 1973. Protein requirement of the Bobwhite chick. Poultry Sci. 52: 2199. Ashton, W. L. G., M. Pattison and K. C. Barnett, 1973. Light-induced eye abnormalities in turkeys and the turkey blindness syndrome. Res. Vet. Sci. 14: 42-46. Barber, C. w. and W. L. Blow, 1963. A genetic influence on cataract formation among White Leghorn incrosses following an outbreak of avian encephalomyelitis. Avian Dis. 7: 495-500. Baum, H. M., J. F. Michaelree and E. B. Brown, 1942. The quantitative relationship of riboflavin to cataract formation in rats. Science 95: 24-25. Bellows, J. G., 1944. Cataract and Anomalies of the Lens. C. V. Mosby Company, St. Louis. Bellows, J. and D. Nelson, 1944. cataract produced by anoxia. Arch. Ophthal. 31: 250-252. 27 28 Bettman, J. W., 1946a. Production of cataracts in chicks with dinitrophenol. Arch. Ophthal. 36: 674-676. Bettman, J. W., 1946b. Experimental dinitrophenol cataract, Amer. J. Ophthal. 29: 1389-1395. Bercovitz, A. B., P. C. Harrison and G. A. Leary, 1970. Eye develOpment of White Leghorns subjected to different intensity and spectrum light treatments. Poultry Sci. 49: 1367. Bernstein, H. W., J. Curtis, F. L. Earl and T. Kuwabara, 1970. Phototoxic corneal and lens opacities in dogs receiving a fungicide, 2,6-dichloro-4-nitroani1ine. Arch. Ophthal. 83: 336-348. Blattner, R. J. and A. P. Williamson, 1951. Developmental abnormalities in the chick embryo following infection with Newcastle disease virus. Proc. Soc. Exptl. Biol. Med. 77: 619-621. Bourne. M. G., 1937. Metabolic factors in cataract produc- tion. Physio. Rev. 17: 1-27. Bowles, L. L., V. P. Syndenstricker, W. K. Hall and H. L. Schmidt, 1947. Cataracts resulting from a deficiency of phenylalanine in the rat. Proc. Soc. Exptl. Biol. MGd. 66: 585-586. Bridges, C. H. and A. 1. Flowers, 1958. Iridocyclitis and cataracts associated with an encephalomyelitis in chickens. J.A.M.A. 132: 79-84. Brini, A. and J. Flament, 1973. Cataracta glaucomatosa acuta. Exp. Eye Res. 16: 19-28. Buschke, W., 1943. Classification of experimental cataracts in the rat: recent observations on cataract associated with tryptophan deficiency and with some other experi- mental conditions. A.M.A. Arch. Ophthal. 30: 735-750- Buschke, W., 1947. Acute reversible cataract in chickens due to various nitrocompounds. Amer. J. Ophthal. 30: 1356-1358. Clapp, C. A., 1932. The effects of x-ray and radium radiations upon the crystalline lens. Amer. J. Ophthal. 15: 1039-10440 Cloud, T. M., R. Hankin and A. C. Griffin, 1960. Photo- sensitization of the eye with Methoxsalen 1. Acute effects. A.M.A. Arch. Ophthal. 64: 346-351. 1' l .i. All '1' I r V N \3 Cloud, T. M., R. Hankin and A. C. Griffin, 1961. Photo- sensitization of the eye with Methoxsalen 11. Chronic effects. A.M.A. Arch. Ophthal. 66: 689-694. Cochran, W. 02, 1954. Some methods for strengthening the common X tests. Biometrics 10: 417-451. Cogan, D. G., S. F. Martin and S. J. Kimura, 1949. Atom bomb cataracts. Science 110: 654-655. Cogan, D. G. and D. D. Donaldson, 1951. Experimental radia- tion cataracts 1. Cataracts in the rabbit following single x-ray exposure. Arch. Ophthal. 45: 508-522. Cogan, D. G., D. D. Donaldson and A. B. Reese, 1952. Clini- cal and pathological characteristics of radiation cataract. Arch. Ophthal. 47: 55-70. Cotlier, E. and D. Apple, 1973. Cataracts induced by the polypeptide antibiotic Polymyxin B Sulfate. Exp. Eye ReS. 16: 69-77. Day, P. L., W. C. Langston and C. S. O'Brien, 1931. Cataract and other ocular changes in vitamin C de- ficiency. An experimental study on albino rats. Amer. J. Ophthal. 14: 1005-1009. Day, P. L. and W. C. Langston, 1934. Further experiments with cataract in albino rats resulting from the withdrawal of vitamin G (B2) from the diet. J. Nut. 7: 97. Day, P. L., W. J. Darby and w. C. Langston. 1937. The identity of flavin with the cataract-preventive factor. J. Nut. 13: 389-399. Day, P. L., W. J. Darby and K. w. Cosgrove, 1938. The arrest of nutritional cataract by the use of ribo- flavin. J. Nut. 15: 83-90. Day, P. L. and W. J. Darby, 1938. The influence of different casein preparations in riboflavin-deficient diets upon the appearance of cataract. Biochem. J. 32 pt. 1: 11710 DeVolt, H. M., 1944. Lamellar cataracts in chickens. Poultry Sci. 23: 346-348. Duke-Elder, W. S., 1926. The pathological action of light upon the eye. The Lancet 1: 1250-1254. 3O Feldman, G. L., T. M. Ferguson, R. H. Rigdon, B. L. Reid, M. S. Cross and J. R. Couch, 1958. Effect of dinitro- phenol on the lens of chick embryo. Proc. Soc. Exptl. Bio. Med. 98: 646-648. Ferguson, T. N., R. L. Atkinson and J. R. Couch, 1954. Relationship of vitamin E to embryonic development of the avian eye. Proc. Soc. Exptl. Bio. Med. 86: 868-871. Ferguson, T. N., R. H. Rigdon and J. R. Couch, 1956. Cataracts in vitamin E deficiency. An experimental study in the turkey embryo. A.M.A. Arch. Ophthal. 55: 346-355. Ferraro, A. and L. Roizin, 1947. Ocular involvement in rats on diets deficient in amino acids. Arch. Ophthal. 38: 331. Field II, J., E. G. Tainter, A. W. Martin and H. S. Belding. 1937. Studies on the oxygen consumption of the rabbit lens and the effect of 2-4 dinitrophenol thereon. Amer. J. Ophthal. 20: 779-794. Fisher, R. F., 1973. Human lens fibre tranSparency and mechanical stress. Exp. Eye Res. 16: 41-49. FlowerS, A. 1., L. C. GrumbleS, R. T. Dubose and J. P. Delaplane, 1957. Cataracts: A new flock problem in chickens. Poultry Sci. 36: 1117. Gershoff, S. N., S. B. Andrus and D. M. Hegsted, 1959. The effect of the carbohydrate and fat content of the diet upon the riboflavin requirement of the cat. J. Nut. 68: 75-88. Gifford, S. R. and J. Bellows, 1939. Histologic changes in the lens produced by galactose. Arch. Ophthal. 21: 346-358. Goldmann, H., 1933. Genesis of heat cataract. Arch. Ophthal. 9: 314. Gyorgy, P., 1935. Investigations on the vitamin B2 complex. I. The differentiation of lactoflavin and the “rat antipellagra" factor. Biochem. J. 29 pt. 1: 741-759. Hall, W. K., L. L. Bowles, V. P. Syndenstricker and H. L. Schmidt, Jr., 1948. Cataracts due to deficiencies of phenylalanine and of histidine in the rat. A comparison with other types of cataracts. J. Nut. 36: 277-296. 31 Halpin, F. B., 1967. Opacity of the lens in fowl associated with exposure to the virus of infectious avian ence- phalomyelitis--a case report. Avian Dis. 11: 146-148. Hanna, C. and J. E. O'Brien, 1961. Cell production and migration in the epithelial layer of the lens. A.M.A. Arch. Ophthal. 66: 103-107. Hanna, 0. and J. E. O'Brien, 1963. Lens epithelial cell proliferation and migration in radiation cataracts. Rad. Res. 19: 1-11. Hessing, E. E., 1937. Cataract due to DNP. Report of cases. Arch. Ophthal. 17: 513-515. Horner, w. D., R. B. Jones and w. w. Boardman. 1935. Cataracts following the use of dinitrOphenol. Pre- liminary report of 3 cases. A.M.A.J. 105 pt. 1: 108-110. Horner, w. D., 1942. Dinitrophenol and its relation to formation of cataract. Arch. Ophthal. 27: 1097-1121. Jensen, L. S. and W. E. Matson, 1957. Enlargement of avian eye by subjecting chicks to continuous incandescent illumination. Science 125: 741. Kempthorne, 0., 1969. An Introduction to Genetic Statistics. Iowa State Univ. Press, Ames, Iowa. Khan, W. A., 1926. Pedigree of lamellar cataract. Brit. J. Ophthal. 10: 387-389. ' Kimura, S. J. and H. Ikui, 1951., Atomic-bomb radiation cataract. Case report with histopathologic study. Amer. J. Ophthal. 34: 811-816. Kinoshita, J. H. and L. 0. Merola, 1964. Hydration of the lens during the development of galactose cataract. Invest. Ophthal. 4: 786-799. Kinsey, V. B., 1948. Spectral transmission of the eye to ultraviolet radiations. A.M.A. Arch. Ophthal. 39: 508-513. Kniskern, P. W., 1935. Cataracts following dinitrOphenol. A.M.A.J. 105 pt. 1: 794-795. Krehbiel, J. D., 1972. The pathology of spontaneous cataract in Bobwhite quail. Ph.D. dissertation at NSU. .32 Krewson, C. P., E. J. Schantz and C. A. Elvehjem, 1939. Relation of skim milk feeding to cataract production. Proc. Soc. Exp. Bio. 42: 573-576. Kudo, T., 1921. Studies on the effects of thirst. I. Effects of thirst on the weights of the various organs and systems of adult albino rats. Amer. J. Ana. 28: 399-430. Kuwabara, T., J. H. Kinoshita and D. G. Cogan, 1969. Elec- tron microscope study of galactose-induced cataract. Invest. Ophthal. 8: 133. Langley, R. K., C. B. Mortimer and C. McCullock, 1960. The experimental production of cataracts by eXposure to heat and light. Arch. Ophthal. 63: 473-488. Langston, W. C., P. L. Day and K. W. Cosgrove, 1933. Cataract in the albino mouse resulting from a de- ficiency of vitamin G (B2). Arch. Ophthal. 10: 508-514. Lauber, J. K., J. V. Shutze and J. McGinnis, 1961. Effects of exposure to continuous light on the eye of the growing chick. Proc. Soc. Exptl. Bio. Med. 106: 871-872. Lauber, J. K. and J. McGinnis, 1966. Eye lesions in domestic fowl reared under continuous light. Vis. Res. 6: 619-626. Lauber, J. K., J. E. Boyd and T. A. S. Boyd, 1970. Intra- occular pressure and aqueous outflow facility in light-induced avian buphthalmos. Exp. Eye Res. 9: 181-187. Lazar, N. K., 1935. Cataract following the use of dini- trophenol. A.M.A.J. 105 pt. 1: 794. Leinfelder, P. J. and H. D. Kerr, 1936. Roentgen-ray cataract; an experimental, clinical and microscopic study. Amer. J. Ophthal. 19: 739-756- Lerman, S., 1959. The lens in congenital galactosemia. Arch. Ophthal. 61: 88-92. Mann, Jr., W. A., 1936. Cataract due to di-nitrophenol. Arch. Ophthal. 15: 116-117. McLaren, D. S., 1959. The eye and related glands of the rat and pig in protein deficiency. Brit. J. Ophthal. 43: 78-87. 33 Milner, J. G., 1934. Irradiation cataract. Brit. J. Ophthal. 18: 497-511. Mitchell, H. S. and W. M. Dodge, 1935. Cataract in rats fed on high lactose rations. J. Nut. 9: 37. O'Brien, C. 5., 1932. Experimental cataract in vitamin G deficiency. Arch. Ophthal. 8: 880-887. Ogino, S. and K. Yasukura, 1957. Biochemical studies on cataract. VI. Production of cataracts in guinea pigs with dinitrOphenol. Amer. J. Ophthal. 43: 936-946. Patek, Jr., A. J., J. Post and J. Victor, 1941. Ribo- flavin deficiency in the pig. Amer. J. Physio. 133: 47-55. Patch, E. M., 1941. Dietary production of cataracts in larval Amblystoma tigrinum. J. Nut. 22: 365-381. Peckham, M. C., 1957. Case report--1ens opacities in fowls possibly associated with epidemic tremors. Avian Dis. 1: 247-255. Philipson, B., 1973. Changes in the lens related to the reduction of transparency. Exp. Eye Res. 16: 29-39. Pirie, A., 1959. The effect of X-radiation on the lens of the embryo and the adult hen. Rad. Res. 11: 260-270. Pirie, A., 1961. Difference in reaction to X-irradiation between chicken and rabbit lens. Rad. Res. 15: 211-219. Pirie, A., 1971. Formation of N'-Formy1kynurenine in pro- teins from lens and other sources by exposure to sun- light. Biochem. J. 125: 203-208. Reese, A. B., 1939. Operative treatment of radiation cataract. Arch. Ophthal. 21: 476-485. Rezende, C. and F. A. deMoura Campos, 1942. Cataract in rats fed a low protein diet. Arch. Ophthal. 28: 1038-1041. Rigdon, R. H., 1959. Cataracts in chickens with lympho- matosis. Amer. J. Vet. Res. 20: 647-654. Rigdon, R. H., G. L. Feldman, T. M. Ferguson. B. L. Reid and J. R. Couch. Cataracts produced by dinitrophenol. Arch. Ophthal. 61: 249-257. Robbins, B. H., 1944. DinitrOphenol cataract: production in an experimental animal. J. Pharmacol. Exp. Ther. 80: 264-271. Robertson, G. G., A. P. Williamson and R. J. Blattner, 1964. Origin and development of lens cataracts in mumps-in- fected chick embryos. Amer. J. Ana. 115: 473-486. Rucker, C. W., 1965. Cataract: a historical perspective. Invest. Ophthal. 4: 377-383. Salit, P. W., 1938. Water content and solids of cataractous and sclerosed human lenses. Amer. J. Ophthal. 21: 755. Schlaegel, T. F., 1947. Occular histOpathology of Nagasaki atomic bomb casualties. Amer. J. Ophthal. 30: Shutes, M. H., 1935. Notes, cases, instruments--dinitro- phenol. Amer. J. Ophthal. 18: 752. Sippel, T. 0., 1967. Enzymes of carbohydrate metabolism in developing galactose cataracts of rats. Invest. Ophthal. o: 59-63. Solomon, G., A. E. Light and E. J. DeBeer, 1955. Cataracts produced in rats by l,4-dimethanesulfonoxy-butane (Myioranfih. Arch. Ophthal. 54: 850-852. Spaeth, E. B., 1936. DinitrOphenol cataracts with signs of tetany. Amer. J. Ophthal. 19: 320-323. Steucke, Jr., E. W., L. H. Allison, R. G. Piper, R. Robertson and J. T. Bowen, 1968. Effects of light and diet on the incidence of cataract in hatchery-reared lake trout. Pros. Fish Cult. 30: 220-226. swann, K. c. and P. W. Salit, 1941. Lens opacities associ- ated with experimental calcium deficiency. Preliminary report. Amer. J. Ophthal. 24 pt. 1: 611-614. Syndenstricker, V. P., H. L. Schmidt, Jr. and W. K. Hall, 1947. The corneal and lenticular changes resulting from amino acid deficiencies in the rat. Proc. Soc. Exptl. B10. Med. 64: 59-61. Tukey, J. W., 1949. Comparing individual means in the analysis of variance. Biometrics 5: 99-114. van Heyningen, R., 1973. Photo-oxidation of lens proteins by sunlight in the presence of fluorescent derivatives of kynurenine, isolated from the human lens. Exp. Eye Res. 17: 137-147. 35 von Sallmann, L., 1951. Experimental studies on early lens changes after roentgen irradiation. I. Morphological and cytochemical changes. Arch. Ophthal. 45: 149-164. von Sallmann, L., 1952. Experimental studies on early lens changes after roentgen irradiation. III. Effects of X-radiation on mitotic activity and nuclear fragmenta- tion of lens epithelium in normal and cysteine-treated rabbits. Arch. Ophthal. 47: 305-320. von Sallmann, L., 1957. The lens epithelium in the patho- genesis of cataract. Amer. J. Ophthal. 44: 159-170. von Sallmann, L., M. E. Reid, P. A. Grimes and E. M. Collins, 1959. Tryptophan-deficiency cataract in guinea pigs. Arch. Ophthal. 62: 662-672. Whalman, H. F., 1936. Dinitrophenol cataract. Amer. J. Ophthal. 19: 885-888. White, C. E. and R. J. Argauer, I970. Fluorescence Analysis. Karcel Dekker, Inc., New York. Williamson, A. P., L. Simonsen and R. J. Blattner, 1956. Specific organ defects in early chick embryos following inoculation with influenza A virus. Proc. Soc. Exptl. Bio. Med. 92: 334-337. Wintrobe, M. N., W. Buschke, R. H. Follis, Jr. and S. Humphreys, 1944. Riboflavin deficiency in swine. With special reference to the occurrence of cataracts. J. Hepkins Hosp. Bul. 75: 102-114. Yudkin, A. M., 1933. Occular disturbances produced in experimental animals by dietary changes. J.A.M.A. 101 pt. 1: 921-926. Zigman, S. and T. Vaughan, 1974. Hear-ultraviolet light effects on the lenses and retinas of mice. Invest. Ophthal. 13: 462-465. APPENDIX A 36 me .o v e #5832? .Hflmsv vopofiamwmleomePmo mo popssz m* .Hflmsv mohMlpoMQMPmO ho hopssz n z .m n o .mee mace pm HHde msfl>w>m5m mo hopes: one op Sampson mpHSmop one u + #3.? u QOAmqu—w SN 3 SN 3 338. 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H. mm 0 ON A w: m 0: HH UmHMHHCH H z o z o z o mesa psoEHMoee mxm\NAmeumnov oopooaxm oo>pomno .omw Ho m:p£os o>Hp op HHmso mpanpom CH mpommmpwo Ho COHpososH exp :0 psoapmmmp pstH Ho moCoSHch one .mm mHnme 44 .HHoso oomplpoopopoo Ho Honssz n z .HHoso oopoHprotpoopopoo Ho nonssz u o .N .osHp oan pm HHoso mnH>H>HSo Ho Hones: onp 0p nHopHoQ mpHSmoH one u + moo.o Va JPCMOHHHCmHm 1.1:“. .m .H 8.8.8 n mflmnmuomw mm H. mm H 3.8.8. m 86 oo.m H m AH o 888888 e H O n1 3.5 8H s H m o 888882 m m 0...... s u. mm.H oo.m mH m MN 0 oomoman H mm n a e z 4. mm.H oo.m wH m mH 0H pnoomoonoonH m MN m ooo moo oH e oH m 2888on N m S Nm.H mm.m MH m m w oopopan H z o z o z o .MQHH pnospoope me\NAmxmumnov oopoomxm oo>noono +.omo Ho mnpcOs so>oHo op HHoso opannom 2H mpoopopoo Ho COHposocH onp no pnospoopp panH Ho oosoSHan one .mH oHnoe 59 .HHoso oompupoopopoo Ho Honssz n z .m .HHoso oopoHpronpoonopoo Ho Honszz n o .N .osHp man pm HHosw mnH>H>HSm Ho Hones: onp op nHopHom mpHSmoH one u + .H moH n Hfimnmomw mmH em mmH so 238. No.0 HH.o m: m m: 0H pnoomoocoonH NH.o no.0 om w on : pnoomopoSHm mo.o HH.o mm o Hm oH oonoeecH z o z o z ml 88 QNM\NAmxmnmnov oopooaxm oo>poono + .omo Ho onpnos pnmwo op HHoso opanpom :H mpoopopoo Ho COHposonH onp no omhp panH Ho ooCoSHan one .mN oHpoB APPEND IX C 72 .HHo50 oooc Ho popssz n 0 .HHosw mnH>H>HSo mo Honssz u H .H mOO.OVQ .PCmOHpHCWHm 1.1;. .N 22.8.8 n Tstmuomw moH ooH 8H ooH mHopop Tr 70 no.0 00.0 Nm 0H mm NH pnoooownoonH 0 u“ n1 0 0N.0 0m.0 Nm 0H 0: m pnoomoposHm m. m %M n.+ 05.0 0m.H Nm 0H KN MN nonopan : 0 m B m m. 0m.0 0m.0 Nm 0H 5N mN pnoomoonoocH m "n w 0 om.o 86 mm oH mm No. 888838 N m S HH.o mm.o mm 0H em 0H oonmnncH H 0 A O H D H omhe pnoEpoopB mxm\NAmxmlonov oopoogxm 0o>pompo Co>oHo op HHosw opanpom po poHopnos .omo Ho mnpsos no pnospoomp panH Ho ooQoSHHCH one .H: oHpoe 73 .HHoso oooo Ho mopssz u 0 .N .HHosv mcH>H>msm Ho Hopssz u H .H ia n T5183? 8H ooH 8H ooH 333 00.0 HN.H 50 m0 00H 0: NH 00.0 Hm.H 8 mm om H0 so 0 H o H o H 1:888:21 panH me\NAaxmlonov oopoomxm 0o>pompo .owo Ho mnpsos no>oHo op szHoppoE HHoso opHnspom no COHpopsu panH po oososHan one .N: oHnoe 74 .HHosw oooo Ho popssz u 0 .N .HHosv mcH>H>psm po sonszz u H .H H05 u HQNAmuovh—w 00H 00H 30H 00H oHopop mm.0 Hm.0 00 mm 00 0: psoomounoonH 00.0 mm.H 00 mm mm 5N pnoomonosHm 0N.0 00.0 00 mm H0 0m nonopan 0 H 0 H 0 H oHHe mxm\NAmxmlmnov copoogxm 0o>momno .omo Ho mnpnos no>oHo op HpHHoppos HHosw opanpom no omhp panH Ho oososHan one ..m: oHHoB APPENDIX D 75 .ooHo Heep HHooo 8o Hooeoz u o .oo>H>H5o ponp HHosw Ho Honssz n H .H .N 00.: u HENHHIOVHQ 0 00m 00m mHopop 00.H No.0 H 00 0: pnooooocoonH p8; mm 0 m 00.H No.0 H H0 00 pnoomoosoocH w ppm; oom m m s W. 00.H N0.0 H Hm N0 oopopan H Hm. w. m o o H on om pnoomoocoocH m P903 mm m 3 1. t. M. 0 0 H :0 :0 pnoomonsoonH "H u ppm; oom m m we oo.H mo.o H mm Hm ooHoHHnH H H H 0 H H omhe psospoope me\NAmxmlonov oopoomxm 0o>pompo .omo Ho manOE noopHan Op HHosv opHnsnom Ho HpHHoppos no pnospoomp panH Ho oonosHan one .3: oHnoe 76 m0.NN 0m.HH 0.m H0\N pnoomoonoonH 1HNHH o.m mm\m 888.858 0 0 0 UoHoHHCH & .oz mHSOm NH 00.mN MH.m 0.N H0\H pnoomoonoonH Hm.m 0.H 00\H pnoomoHOSHm eNHH o.m mm}. 8888 & .oz mp:om HN COHpospopmcopp oooo Ho W «Hmong 8.93.89on psospoone .pnospoomp panH anpHs HHozv opHnspom poop p0 COHpHomopm .0: oHnme 77 .COHPproamcmhp Camonm >9 UmpmHSOHmo .H Hm.mm N hoppm oom.o 5.0H m waxy pnmflq Noo.o m.m H soapwpzw pswflq mzam>|m mpmsvm Gama Eocmmhm mo mopSOm mmmpmmo .m: mapwp CH omNAMMSESm mpmc pow mocmflpm> %o mflmzamc¢ .0: magma 78 .hmc\mpsos CH mzpcoe cm>mm mcflsoaaom may now PCmEPMmpp map ma ampszc ucoomm mgp Ucm HmDESC thfih mSP hp UmPNOHUCH mH wmm Ho mSPCoE XHm 0P Q3 PCGEmehP HNCHwfiho w£6* :o.mm mu.~m o.mH om\m pcmommocmocfl ppm; mm no.0m o.:m mm\m pcoommvcmOcfi ppm; oom NH.:N 5.0H :m\: cmpmpMcH mfludm mo.om mm.m: m.mm :m\:fi psoommucmocfi ppm; mm oa.mfi m.w mm\m pCmommccwocH ppm; oom Hfl.mm d.ma wm\d copaywcH Nflumfi ou.mn mm.ad m.: mN\H pcmommucmocfi yam; mm no.0m 0.:m om\m p:mommg:«ocfi ppm; oom om.mm m.am mm\m umpmpch #Nuém mo.mw ma.um m.om :m\m pCmommccwoca Ppwz mm :m.ofi m.m :m\m pcmommccmocfi pp“: com Nw.ma m.aa 0N\m UmpmpmcH R .02 #:NINH W mCOflpgpommcmnp v.86 (Ho m: owvwcflnEoo Pamspwmue Camoh< Coappoaopm .mCOHpmcflpEoo pamevmmpp Canvas HHMSU mvflczpom cmmv we soappomomm .nd manme 79 .COflpmsuowmcmup Camohw hp UmPMHSOHmo .H m:.HuH w goppm moa.o mm.mH N mgzp pgmflq mam.o mH.m: m COprcHQEOQ pamspmmpe mzam>um muwswm cams Eovmmmm mo mopsom mmoummo .Nfi mfiflmu. CH UmNHHNEESm .mPMU .HOrH mocwflhdkr .HO mflthmCafl .wd mfiflwm. APPENDIX E MSU 72-15 Starter Protein-~g/g diet 0.29 Metabolizable energy--kcal/g 3.02 (Prot/M.E.) x 100 9.60 Methionine--% of prot. 1.94 Ca--% 1.02 P, avail.--% 0.65 Fat--% 8.2 Fiber--% 3.2 80 Quail Diets RSU 72-16 Breeder 0.235 2.88 8.15 1.95 2.75 0.53 8.4 3.1 81 Quail Diets GS 72 Ingredient Starter Pounds per ton Corn, #2 Yellow 767 Soybean Meal, 49% 846 Fish Meal 62 Meat Scrap, 50% 70 Alfalfa Meal, Dehy. 90 Animal Fat, Stabl. 112 Limestone --- Dicalcium Phosphate 26 Choline Chloride, 50% 6 Methionine Hydroxy Analogue 2 Salt, Iodized 7 Mineral Mix A 6 Vitamin Mix A 6 Antioxidant (Ethoxyquin/ or BHT) 113 .O .6 g QB 72 33222: 900.4 654 100 90 114 100 113.6 g M'TITI'l‘fiflfilflzllMIHEII'IIIIIJ'I'IJTI'IMMJFLITU’I‘IWES