Gizzard Lesions in Day-Old Chickens DAVID MILLER AND HARRY W.
TITUS
Poultry Nutrition Laboratory, Bureau of Animal Industry, Beltsville Research Center, Beltsvttle, Maryland (Presented at annual meeting August, 1941; received for publication August 12, 1941)
hatching were obtained. It is one of the purposes of this paper to present some of these data and discuss briefly the mechanism of the formation of gizzard lesions and some of the possible causes of the initial hemorrhages. Another purpose is to give a list of the substances that were found to have no effect on the incidence or severity of gizzard lesions in day-old chickens when added to the diet of the parent stock and a list of substances that likewise had no effect when injected into the eggs on different days of the incubation period. EXAMINATION OF THE GIZZARDS The method of removing the gizzards of the day-old chickens and preparing them for examination was essentially as follows: The chickens were killed by breaking their necks, and their gizzards were removed with the aid of a small pair of scissors. Each gizzard was then opened by cutting with the scissors along the ventral edge from the proventricular opening to a point about half way around. When a gizzard that has been opened in this manner is held with the proventricular junction uppermost and the lining on the side next to the observer, the duodenal opening is in the right-hand portion near the top. In examining the gizzards, a careful search was made for deposits of extravasated blood. This search was greatly expedited by slightly stretching the opened gizzard and holding it between the eyes and a source of light—usually a window but sometimes a 50-watt, inside-frosted, electric lamp. If there were no detectable
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N THEIR studies of gizzard lesions at the Beltsville Research Center the writters have examined during the last two years approximately 300 chicken embryos, 31,000 day-old chickens, 8,000 chickens that ranged in age from two days to eight weeks, and 1,500 chickens that were more than eight weeks old. All the embryos and all but a comparatively small number of the chickens were Rhode Island Reds. The embryos and most of the chickens were from parent stock that had been fed an all-mash diet, which, on the basis of our present knowledge of poultry nutrition, was adequate in every way. The remainder of the chickens were from parent stock that had received modifications of this diet or diets that were formulated for the purpose of studying the effect of various feedstuffs and combinations of feedstuffs on the incidence and development of gizzard lesions in the offspring. Of the 31,000 day-old chickens that were examined about 10 percent were hatched from eggs into which various individual substances had been injected on certain selected days of the incubation period. None of the diets fed to the parent stock and none of the substances injected into the eggs had any apparent influence on the incidence or severity of the gizzard lesions. However, a large number of data were accumulated on the incidence of gizzard lesions in day-old chickens and on the distribution of the different "severity scores." Also, some data regarding the changes in the severity score between the eighteenth day of incubation and the tenth day after
I
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DAVID MILLER AND HARRY W. TITUS
deposits' of extravasated blood a severity score of 0 was given; if one or two pinpoint deposits of extravasated blood (evidence of hemorrhage from the capillaries) were found in the lining or the muscular wall, a score of 0.S was given; if the deTABLE 1.—Distribution1 of the severity scores of lesions in the gizzards of day-old Rhode Island Red chickens Number
Percent
0 0.5 1 2 3
199 1,935 9,591 8,936 7,797
0.7 6.8 33.7 31.4 27.4
Total
28,458
100.0
1
Average severity score = 1.821 +0.005. Standard deviation=0.872. Standard error of an average severity score = vU759945/N.
posits of extravasated blood in the lining were few in number and small in size but large enough that it was unnecessary to hold the gizzard between the eyes and a source of light to see them, a score of 1 was given; if there were a large number of pin-point deposits or one or two ridgelike deposits about 0.5 centimeter long, a score of 2 was given; and if there were two or more large ridge-like deposits or three or more smaller ridge-like deposits, a score of 3 was given. In earlier studies made in this laboratory (Lansing and Miller, 1940) consideration was given to the presence or absence of eroded areas (places where the lining was broken or frayed), as well as to the number and size of the deposits of extravasated blood, but as experience in scoring was gained it became evident that this practice was unnecessary when day-old chickens were being examined. INCIDENCE AND SEVERITY OF THE LESIONS Among 28,458 day-old Rhode Island Red chickens, the gizzards of which were
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Severity score
examined and given a severity score, only 199, or about 0.7 per cent, exhibited no evidence of hemorrhage from the capillaries in the gizzard. The distribution of the severity scores that were given is shown in Table 1. This group of 28,458 day-old chickens consisted of 611 smaller groups that ranged in number from 4 to 160 and contained on an average 46.6. These smaller groups consisted of chickens that were hatched at the same time from the eggs of pens of hens that received various diets. The most common average severity score of the smaller groups was 1.9, but the average severity score of the 28,458 day-old chickens was 1.821 ± 0.005. The average severity scores of the 611 smaller groups ranged from 0.9 to 2.9. In most cases a difference of 0.6 or more between two average severity scores was highly significant from a statistical standpoint, but differences of this order of magnitude were frequently observed between two different hatches from the same parent stock on the same diet. This was considered as very good evidence that factors other than the diet of the parent stock had a greater effect on the severity score than the diet of the parent stock. That gizzard lesions in day-old chickens are very common is shown by the findings of Tepper (1941) and Lansing, Miller, and Titus (1939). Tepper examined 1,737 dayold chickens from 62 hatcheries located in 12 different states and found that nearly 74 percent had gizzard lesions. Lansing, Miller, and Titus reported that they examined a group of 600 one-day- and two-dayold chickens and found that fully 75 percent had gizzards that were not normal. The incidence of gizzard lesions reported in this paper is very much higher than that previously reported. This probably is attributable to an improvement in the skill of the writers in detecting the lesions.
GIZZARD LESIONS IN DAY-OLD CHICKENS
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FIG. 1. Changes in the average severity score of the gizzard lesions between the eighteenth day of incubation and the tenth day after hatching. CHANGES IN T H E SEVERITY SCORE BETWEEN T H E EIGHTEENTH DAY OF INCUBATION AND- THE TENTH DAY AFTER HATCHING
In order to follow the development of the lesions, examinations were made of the gizzards of embryos on the eighteenth, nineteenth, twentieth, and twenty-first days of incubation and of chicks on the first, second, fourth, sixth, eighth, and tenth days after hatching. In examining the gizzards of the embryos it was found that essentially the same method of scoring as that used in the case of day-old chickens was applicable. However, in the case of the chickens that were more than one day old and,
hence, had eaten feed for a day or more it was necessary to give attention to the number and size of the eroded areas as well as to the number and size of the deposits of extravasated blood, because many of the latter had been transformed into eroded areas. Inasmuch as the two systems of scoring are strictly, comparable, it was possible to follow the changes that took place in the severity score. These changes are shown in Figure 1 for representative groups of embryos and chicks. According to Figure 1, there was little or no difference between the severity scores on the eighteenth and nineteenth days of
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206
DAVID MILLER AND HARRY W.
TITUS
TABLE 2.—Substances that had no effect on the incidence or severity of gizzard lesions in day-old chickens when included in the diet of the parent stock Substance Alfalfa leaf meal /Alfalfa leaf meal \and crude soybean oil Alfalfa leaf meal, hexane extract of
Fluorine (as NaF) Gelatin Hempseed meal Iodine (as KI) Kelp Lecithin, from soybeans Lettuce Limestone Linoleic acid Linseed oil Liver meal, whole, freshly made Liver meal, whole, old stock Liver meal, Argentine Magnesium carbonate Manganese (as MnS0 4 .4H 2 0)
15 percent /15 percent \14 percent Equivalent to 30 percent of alfalfa leaf meal and 4 g. per bird 3 times per week for 7 weeks then 6 times per week for 9 weeks (4 g. of extract were equivalent to 100 g. of alfalfa leaf meal) 75 parts per million 40 milligrams per day 240 U.S.P. units per 100 g. of diet /160 U.S.P. units per 100 g. of diet \ 80 U.S.P. units per 100 g. of diet /120 U.S.P. units per 100 g. of diet \120 U.S.P. units per 100 g. of diet / 80 U.S.P. units per 100 g. of diet \160 U.S.P. units per 100 g. of diet 70 percent 1 percent / 0.5 percent \ 10 and 50 parts per million 0.05 percent 5 percent 0.1 pound per bird per day 2.8 g. per bird 6 times per week 2 and 6 percent 0.85 c.c. per bird per day 0.25 g. per bird per day 15 and 30 parts per million 5 percent 60 parts per million /20 parts per million \30 parts per million /20 parts per million \10 parts per million 20 parts per million 10 parts per million 30 parts per million 1.5 percent 3 percent 15 and 30 parts per million 67 percent 40 percent 5 percent 15 percent 5 percent 240 U.S.P. units per 100 g. of diet (See also under animal provitamin D) 10 parts per million 5 percent 5 and 15 percent 10 parts per million 2 percent 1 and 2 percent 0.1 pound per bird per day 2.34 percent (substituted for oystershell) 0.5 and 2 percent 2 percent 5 percent 5 percent 5 percent 1 percent '200 parts per million (See also under cobalt)
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Aluminum (as A1 2 (S0 4 ) 2 .18H 2 0) p-aminobenzoic acid Animal provitamin D, activated /Animal provitamin D, activated 1 and irradiated ergosterol /Animal provitamin D, activated 1 and irradiated ergosterol /Animal provitamin D, activated \and irradiated ergosterol Barley, finely ground Bile, ox, desiccated /Bile, ox, desiccated \and 2-methyl-l, 4-naphthoquinone Borax (Na 2 B 4 O 7 .10H 2 O) B-Y feed Cabbage Calcium gluconate Charcoal, granular Chlorophyll in oil (Grade F) Choline chloride Chromium (as K 2 Cr 2 07) Citrus pulp meal Cobalt (as Co(N0 3 ) 2 - 6H 2 0) fCobalt (as Co(N0 8 ) 2 .6H 2 0) (and manganese (as MnS0 4 .4H 2 0) /Cobalt (as Co(N0 3 ) 2 .6H 2 0) land nickel (as NiS0 4 .6H 2 0) Cobalt (as Co(N0 3 ) 2 .6H 2 0) \ nickel (as NiS0 4 .6H 2 0) [and manganese (as MnS0 4 .4H'20) Cod liver oil, ordinary Cod liver oil, fortified Copper (as CuS0 4 .5H 2 0) Corn, yellow Corn, white Corn oil (Mazola) Cottonseed meal Cottonseed oil, refined , Ergosterol, irradiated
Quantity given or in the diet
GIZZARD LESIONS IN DAY-OLD CHICKENS
207
TABLE 2.—Continued
Substance Meat scrap Mercury chloride (Hg2Cla) 2-methyl-l, 4-naphthoquinone /2-methyl-l, 4-naphthoquinone \and linoleic acid Molybdenum (as Na 2 Mo0 4 .2H 2 0) Nickel (as NiS0 4 .6H 2 0)
Tall oil Thiamin (vitamin Bi Vitamin C Vitamin D Vitamin G Wheat Wheat bran Wheat germ meal Wheat germ oil Wheat middlings Yeast, brewers', dried Zinc(asZnS0 4 .7H 2 0)
incubation. The difference between the scores on the nineteenth and twentieth days of incubation depended on the development of the embryos. When the shells were not pipped on the twentieth day, the difference was not great; it was somewhat greater if the shells were pipped and appreciably greater when the chicks hatched on the twentieth day. There was an increase in the severity score on the twentyfirst day of incubation, and this increase was slightly greater if the shells were pipped on the twentieth day than if they were not. The severity score was about the
12 percent (as sole source of animal protein) 6 and 9 parts per million 10 parts per million (See also under bile) /50 parts per million \ 0.5 and 2 percent 54 parts per million 60 parts per million (See also under cobalt and manganese) 10 parts per million 77 percent 30 percent 10 percent 0.05 percent 0.5 percent 200 micrograms per 100 g. of diet 15 and 20 percent 10 percent 1.4 percent 0.375 percent 2 percent 0.5 and 1 percent added to that already in diet 0.5 and 1 percent per bird / 0.12 g. per bird per day \ 0.13 g. per bird per day 12 percent 14 percent (See also under alfalfa leaf meal, hexane extract of) 0.5 and 2 percent 1.2 parts per million 0.35 g. per bird per day See under animal provitamin D and ergosterol, irradiated See under riboflavin 22.5 and 25 percent 15 percent 7.5 and 15 percent 0.5 and 1 percent 35 percent 15 percent 36 parts per million
same on the first day after hatching as it was on the twenty-first day of incubation. Thereafter the severity score decreased more or less regularly until the sixth day after hatching. The change in the score after the sixth day depended on the diet of the chicks. If a well-balanced diet .was fed, the severity score increased only slightly or not at all between the sixth and tenth days after hatching; but if a poorly-balanced diet was fed, the severity score tended to increase, but did not reach the score shown at hatching time or the first day after hatching.
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Nicotinic acid Oats Oat hulls Peanut oil cake meal Potassium bromide Potassium chloride Riboflavin (vitamin G) (as fullers earth absorbate of whey) Rice bran Rice polishings Sardine oil, ordinary Sardine oil, fortified Sodium acetate Sodium chloride Sodium sulphate /Sorbitol land sorbitan Soybean meal Soybean oil
Quantity given or in the diet
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DAVID M I L L E R AND HARRY W.
TITUS
TABLE 3.—Substances that had no effect on the incidence or severity of gizzard lesions in day-old chickens when injected into the eggs during the incubation period
Substance
Day of incubation period the injection was made
Quantity injected
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Aconitic acid 8th 10 milligrams Aconitic acid 15th 10 milligrams Allan toin 11th 10 milligrams Allantoin 18th 10 milligrams Aluminum (as A12(S04)3. Na 2 S0 4 .24H 2 0) 8th 0.1 milligram 4-amino-2-methyl-naphthol-HCl . 9th 0 . 1 , 0.5, 2.5, and 5 milligrams p-aminobenzoic acid 10th 1 milligram p-aminobenzoic acid 17th 1 milligram p-aminobenzoic acid 19th 5 milligrams fp-aminobenzoic acid / 1 milligram (and pantothenic acid 10th \ 1 milligram 8th Animal provitamin D, activated 16,000 U.S.P. units 10th Antimony (as KSb0 3 ) 0.03 milligram Antimony (as KSb0 3 ) 17th 0.03 milligram Arsenic (as Na 2 HAs0 4 ) 8th 5 micrograms Barium (as BaCl 2 .2H 2 0) 10th 0.03 milligrams Barium (as BaCl 2 .2H 2 0) 17th 0.03 milligrams Beryllium (as Be(NOs)s) 10th 0.03 milligrams Beryllium (as Be(N0 3 ) 2 ) 17th 0.03 milligrams Beta-alanine 11th 10 milligrams Beta-alanine 18th 10 milligrams Bile, ox, desiccated 9th 15 milligrams Bile, ox, desiccated 15th 200 milligrams Biotin (vitamin H) preparation 8th 10 micrograms Biotin (vitamin H) preparation 15th 10 micrograms Bismuth (as NaBi0 4 ) 8th 0.1 milligram Boron (as Na 2 B 4 O 7 il0H 2 O) 9th 0.03 milligrams Caesium (as CeCl) 8th 0.03 milligrams Choline chloride 9th 5 milligrams Choline chloride 16th 5 milligrams Chondroitin 11th 50 milligrams Cobalt (as CoS0 4 .6H 2 0) 8th 0.05 milligram Copper (as CuS0 4 .5H 2 0) before incubating 0.03 milligram Copper (as CuS0 4 .SH 2 0) 15th 0.03 milligram Corn oil 15th 0.25 cubic centimeter Creatinine 10th 10 milligrams Creatinine 18th 10 milligrams Cysteine hydrochloride 8th 1 milligram Cysteine hydrochloride 15th 1 milligram Cystine 8th 1 milligram Cystine 15th 1 milligram Germanium (as Ge0 2 ) 9th 0.03 milligram Glucosamine 9th 1 milligram Glucosamine 15th 1 milligram Glutathione 8th 1 milligram Glutathione 15th 1 milligram Indium (as InCl 3 ) 0.03 milligram 8th Indium (as InCl 3 ) 9th 0.03 milligram Indium (as InCl 3 ) 15th 0.03 milligram Inositol 8th 3 milligrams Inositol 15th 3 milligrams Iridium (as IrCl 4 ) 8th 0.03 milligram Iridium (as IrCl 4 ) 15th 0.03 milligram /Iron (as FeCl3) / 0.20 milligram \and copper (as CuS0 4 .5H 2 0) 8th \ 0.13 milligram Linseed oil, raw 15th 0.25 cubic centimeter Magnesium (as MgC0 3 ) 8th 0.15 milligram Mannose 9th 5 milligrams Mannose 16th 5 milligrams Methionine 8th 1 milligram Methionine 15th 1 milligram /2-methyl-l, 4-naphthoquinone f 0.1 milligram land sodium glycocholate \ 0.5 milligram 9th
GIZZARD LESIONS I N D A Y - O L D C H I C K E N S
209
TABLE 3.—Continued
Substance
Phthiocol Pyridoxine (Vitamin Be) Rhodium (as RhCl 3 ) Rhodium (as RhCl 3 ) Riboflavin (Vitamin G) Rubidium (as RbCl) Silver (as AgN0 3 ) Silver (as AgN0 3 ) Sodium choleate (desiccated bile) Sodium glycocholate Sodium glycocholate Sodium glycocholate Sodium glycocholate • phthiocol and oleic acid Sorbitol Sorbitol Suceiniesacid Succinic acid Tantalum (as Ta 2 0 6 ) Tellurium (as TeCl2) Tellurium (as TeCl2) Thiamin (Vitamin Bi) Thorium (as Th(N0 3 ) 4 . 4H 2 0) Titanium (as Ti0 2 ) Titanium (as Ti0 2 ) Titanium (as Ti0 2 ) Vanadium (as VC12) Vanadium (as VC12) Vitamin C (ascorbic acid) Vitamin D Vitamin E (alpha-tocopherol) /Vitamin E (alpha-tocopherol) \and bile, ox, desiccated Vitamin-K preparation (Klotogen) Vitamin-P preparation Xanthine Xanthine Zinc (asZnS0 4 .7H 2 0) Zinc(asZnS0 4 .7H 2 0) Zirconium (as Zr0(N0 3 ) 2 .2H 2 0)
Quantity injected
/ 0.1 milligram \ 0.5 milligram / 0.1 milligram 9th \ 4 milligrams / 0.1 milligram \ 4 milligrams 16th fl5 milligrams \15 milligrams 9th 9th 0.03 milligram before incubating 0.03 milligram 15th 0.03 milligram 9th 1 milligram 8th 0.03 milligram 15th 0.03 milligram 8th 10 milligrams 15th 10 milligrams 9th 1 and 2 milligrams 10th 1 milligram 17th 1 milligram 5 milligrams 19th (See also under p-amino-benzoic acid) 8th 2.5 milligrams 9th 1 and 2 milligrams 8th 0.03 milligram 15th 0.03 milligram 9th 0.5 milligram 8th 0.03 and 0.15 milligram 10th 0.03 milligram 17th 0.03 milligram before incubating 20 milligrams 8th 2.5 and 100 milligrams 9th 5 milligrams 16th 5 milligrams f 2.5 milligrams 8th i 2.5 milligrams [ 0 . 2 5 cubic centimeter 9th 4 milligrams 16th 4 milligrams 8th 10 milligrams 15th 10 milligrams 9th 0.03 milligram ' 9th 0.03 milligram 16th 0.06 milligram 9th 0.1 milligram 9th 0.03 milligram before incubating 0.03 milligram 9th 0.03 milligram 15th 0.03 milligram 8th 0.3 milligram 15th 0.03 milligram 15th 2.5 milligram See activated animal provitamin D 9th 25 milligrams /15 milligrams \15 milligrams 9th 9th 0.05 and 0.1 cubic centimeter 0.25 cubic centimeter equivalent to 5 g. of 15th citrus meal 9th 10 milligrams 13th 10 milligrams before incubating 0.03 milligram 15th 0.03 milligram 9th 0.03 milligram 16th
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/2-methyl-l, 4-naphthoquinone \and sodium glycocholate /2-methyl-l, 4-naphthoquinone land sorbitol /2-methyl-l, 4-naphthoquinone \and sorbitol /2-methyl-l, 4-naphthoquinone \and bile, ox, desiccated Molybdenum (as Na 2 Mo0 4 .2H 2 0) Nickel (as NiS0 4 .6H 2 0) Nickel (as NiS0 4 .6H 2 0) Nicotinic acid Osmium (as OSO4) Osmium (as Os0 4 ) Oxalic acid Oxalic acid Pantothenic acid Pantothenic acid Pantothenic acid Pantothenic acid
Day of incubation period the injection was made
210
DAVID MILLER AND HARRY W. TITUS
1
Unpublished data.
by Tepper) and average live weight at the age of 12 weeks. He obtained his initial score by taking a sample of 20 chicks from each group that he studied. The writers used Rhode Island Red chickens in their experiments and obtained both an initial severity score and a final severity score. They found no consistent relationship between the average initial severity score and the average live weight at several different ages. Moreover, -they found no correlation between the live weights of the individual chickens at the different ages and the final severity scores of the lesions in the gizzards of the same chickens. SUBSTANCES INEFFECTIVE IN PREVENTING GIZZARD LESIONS The writers have studied the effect of a number of substances on the incidence of gizzard lesions in day-old chickens; some were included in the diet of the parent stock, others were injected into the eggs on different days of the incubation period. All were found to be ineffective. Those that were included in the diet of the parent stock are listed in Table 2 and those that were injected into the eggs are listed in Table 3. . SUMMARY Data are presented on the incidence and severity of gizzard lesions in 28,458 dayold chickens and on the change in the severity score between the eighteenth day of incubation and the tenth day after hatching of representative groups of embryos and chicks. In slightly more than 99 percent of the day-old chickens there was evidence of the hemorrhages that precede gizzard erosions of the type that is commonly encountered. The average severity score of the gizzard lesions decreased more or less steadily during the first 6 days after hatching. The mechanism of the formation of gizzard lesions is discussed briefly. A list is
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THE FORMATION OF GIZZARD LESIONS Lansing, Miller, and Titus (1939) found that hemorrhages from the glandular layer of the gizzard, but originating from the capillaries in the submucosa, are the immediate cause, or forerunners, of gizzard erosions. Tepper (1941) found that if the blood pressure of embryos was increased by injecting adrenaline on the sixteenth day of incubation, hemorrhages took place on about the eighteenth day. He concluded that the taking of the yolk into the body cavity and the establishment of pulmonary circulation and respiration tended to increase the blood pressure and thus contributed to the formation of hemorrhages. The data presented in Figure 1 seem to support this conclusion. However it is not known why there are hemorrhages in some chicks but not in others. Almquist (1938) found that when chicks were fed bile or cholic acid gizzard erosions did not develop. Later, Almquist and Mecchi (1941) demonstrated conclusively that a deficiency of vitamin K was not the cause of gizzard erosions. The writers tentatively offer the suggestion that the hemorrhages that precede the erosions are the result of a delay in the proper functioning of the liver; however, they have no ready explanation of why there is such a delay. Apparently the presence of lesions in the gizzards of young chickens has little or no demonstrable effect on their growth. This observation was reported by Almquist and Stokstad (1937) about four years ago and has been verified by Tepper (1941) and the writers.1 Tepper studied the growth of several different breeds of chickens, including Barred Plymouth Rocks, Single Comb White Leghorns, New Hampshires, and various crossbreds, and found no consistent relationship between the average initial severity score (referred to as "gizzard score"
GIZZARD LESIONS IN DAY-OLD CHICKENS
given of substances that were included in the diet of the parent stock without apparent beneficial effect on the incidence of gizzard lesions in the offspring. Also, a list is given of substances that had no effect when injected into the eggs on different days of the incubation period. REFERENCES
Almquist, H. J., and E. Mecchi, 1941. The influence of bile acids, vitamin K, and cinchophen on erosions of the chick gizzard lining. Proc. Soc. Exp. Biol, and Med. 46:168. Almquist, H. J., and E. L. R. Stokstad, 1937. The gizzard factor of the chick. Jour. Nutr. 13:339. Lansing, A. I., and D. Miller, 1940. Dysfunction of the biliary system and hemorrhages in the gizzard of the chicken. Poultry Sci. 19:258. Lansing, A. I., D. Miller, and H. W. Titus, 1939. The formation of erosions of the gizzard lining in the young chick. Poultry Sci. 18:475. Tepper, A. E., 1941. Studies in gizzard ulceration in chickens. Thesis, University of Maryland.
On the Reading of Scientific Papers* A U D I E N C E E N E M I E S N U M B E R S I TO VI
A
FEW years ago a large international congress was held in one of the most beautiful cities of Europe. The committee on arrangement had planned every detail to perfection. The university buildings were new, the lecture halls ample. Each platform was provided with a two-foot clock that not only pointed out the elapsed time but also turned on a red light at 8 minutes and a big flashing light at 10 minutes. When the meeting started, one could say "Every prospect pleases." Only man was vile. One hour after the opening members realized that the distinguished chairmen of the sections were not holding the speakers to the 10-minute limit so carefully stipulated in the programs. Therefore, every speaker counted on talking IS or 20 minutes. Of course, he saved his most important slides until the end and they were shown in competition with the flashing light plus an obviously nervous chairman. In addition, there were all the other * Reprinted in part from Science, vol. 95, no. 2,463, pp. 273, by permission of author, Dr. Eugene F. DuBois, Department of Physiology, Cornell University Medical College, New York.
minor and major human defects best calculated to torture an audience. Most of the speakers mumbled their words or else turned and lectured to the lantern screen. This was particularly annoying, since the papers were delivered in four different languages, each with its local variants. Most of the lantern slides were photographs of typewritten sheets crowded with data, and few speakers were content to show less than 20. The main points were carefully concealed until the last minutes, by which time the audience had lost all interest. This meeting was perhaps an extreme example, and in our country most of the papers are carefully prepared and carefully delivered. There are, however, enough poorly delivered papers to warrant a discussion of what may be called "audience enemies": 1. "The Mumbler," who drops his voice to emphasize important points or else talks to the lantern screen instead of to the audience. 2. "The Slide Crowder," who packs his slides with typewritten data and shows too many slides. (Continued on page 229)
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Almquist, H. J., 1938. The influence of bile acids on erosions of chick gizzard lining. Science 87: S38.
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