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Windle WF. Physiology of the Fetus. (1940) Saunders, Philadelphia.

1940 Physiology of the Fetus: 1 Introduction | 2 Heart | 3 Circulation | 4 Blood | 5 Respiration | 6 Respiratory Movements | 7 Digestive | 8 Renal - Skin | 9 Muscles | 10 Neural Genesis | 11 Neural Activity | 12 Motor Reactions and Reflexes | 13 Senses | 14 Endocrine | 15 Nutrition and Metabolism | Figures

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Chapter XIV The Fetal Endocrine Glands

Our knowledge of endocrine functions during prenatal life is fragmentary as may be expected from the fact that adult glands of internal secretion are still incompletely understood and their relationship to one another only partly determined. There seems to be little doubt that a few of the maternal hormones do influence embryonic deve1opment, but not all can pass the placental barriers The present deftciency of information concerning placental transmission of hormones is a factor limiting any discussion of their activities in the fetus. Perhaps the secretions of the fetus itself are equally or more important than those of the mother for the well being and normal metabolism of the new individual. It is with their functions that we shall be especially concerned.

The Suprarenal Cortex

Among all the endocrine glands of the human fetus the suprarenals manifest the most remarlcable peculiaritiesks 3 Examination of them in the still—born infant reveals that they are proportionately very much larger than at any time after birthx in fact they form o.2 per cent of the entire body weight. Those of the adult constitute only o.o1 per cent.4 The reason for their great size is found in an hypertrophy of the innermost cortical cells forming a layer to which the names, X-zone, fetal cortex and androgenic zone have been applied. Only the outer rim of the embryonic gland differentiates into the characteristic suprarenal cortex of the adult, and it does not come into prominence until after prenatal life.

The androgenic zone of the fetal suprarenal undergoes involution rapidly after birthF and as it disappears the size of the gland becomes actually -as well as relatively smaller. The growth curve of the human suprarenal gland is reproduced in Fig. 66.C The gland loses one—third of its birth weight during the first postnatal week, one-half in the first three months and fouplifths by the end of the first year. Thereafter, a slow growth takes place and at puberty the suprarenal again attains the weight it had at the end of the fetal life ; but the androgenic Zone is no longer recognizable. This characteristically fetal part of the suprarenal gland has been identiiied in the cat,7 Inouse,8 rabbit9 and in one strain of rats.10 It seems to be absent, or at least not present as a comparable distinct layer of cells, in the albino rat and some other animals.

The physiologic signiHcance of the hypertrophiecl fetal cortex of the suprarenal gland is not understood. That it is closely related to other endocrine organs is quite certain. A possible influence of Inaternal sex hormones upon the growing feta1 suprarenal is suggestecl by the closely parallel growth curve of the uterus in prenatal and early postnatal life (Fig. 67) . Involution of the X-2one of young male Ihice is accomplished under the influence of testicular hormone.

Fig. 66. — Growth of the human suprarenal glands (weight) during fetal like (c—B) and after birth. (scammon: «The Measurement of Maus« Und: dünn. Press.)

It has been suggested that the fetal suprarenaLgland elaborates an anclromirnetic substance.I2- I« Its ability to maintain the prostates of the castrated immature mouse and rat, which degenerate when gonads and suprarenals are removed, demonstrates an andromimetic property quite clearly-P«- 15 «« Recentlzy however, evidence has been advanced which indicates that carefully prepared extracts of fetal and of other X—2one—bearing glands do not have androgenic propertiesss but it is possible that the amount of suprarenal tissue extracted was too small to produce eifects. should it prove that androgens are laclcingx one would have to discard the attractive hypothesis that the androgenic cortex serves directly to protect the fetus against an excessive iniluence of maternal estrogens reaching it through the placental barrier.

Fig. 67. - Growth of the hutnan Uterus (length) during ketal like (c-—B) and after birth. (scammon: «The Measurement of Man," Univ. Minn. Press.)

The possibility that cortin or a cortin-like hormone is forrned by the feta1 suprarenal gland has received attention. Some investigators have reported that the survival times of adrenalectomized cats and dogs are prolonged during advanced pregnancy.17szI9 Others failed to substantiate this at the end of gestation,20 but even if it is true there is no proof that a fetal secretion protected the mother. Progesterone maintains life and growth in ferrets and rats in the absence of suprarenal glands,2I-««’3 and the functional corpus luteum of pregnant adrenalectomized anirnals does the Same« Adrenalectomy of pregnant rats during gestation results in an increase in weight of the fetal glandsW as will be seen in Table 22.

Tanm 22

Tun Bringe-IS or Aussicht-Demut Denn-ro Pagen-mer III-on kur- Wntenks or rat; Fast-Hi« sur-Hauptn- Gunvs

Time of adrenaleetomy No. of Average Ist. Ave. set. of suprarenal of mothek litters of fetuses (gm.) glands of fetuses (mg.) « d« 9 o« 9 Unoperated eontrols . . . . . . 18 5 .84 5.t»)8 0.90 0.82 14th day of FeSUItIOIL . . . . 15 4 .96 4.78 LLZ I .l8 7th day of Feste-tion . . . . . . 10 4 .70 4.51 1.17 Lls

Attempts have been made to destroy the suprarenal g1ands by means of intrauterine surgery to observe effects on other fetal endocrine organskk but it proved impossible to obtain clear—cut results because of the magnitude of technical difficulties.

The Suprarenal Medulla

The medulla of the suprarenal gland has an embryonic origin very different from that of the cortex. It is formed by cells which arise from the primordia of sympathetic ganglia and which begin to migrate into the already prominent cortical bodies at about seven weeks gestation in man. cells of the suprarena1 medulla as well as of certain other small glandular bodies of similar embryonic origin (e.g., the aortic paraganglia) possess a retnarld able afkinity for chrome compounds with which they take on a brown color. This chromaffin reaction has been demonstrated to be elicitable iirst at about the time extracts of embryonic suprarenal tissue begin to produce pharmacologic responses characteristic of epinephrin749

Many have investigated the activities of the embryonic and fetal suprarenal medulla by this histochemical method as well as by other chemical and sensitive physiologic techniques Epinephrindilce reactions are obtainable from suprarenal extracts prepared from chiclc embryos as early as the eighth day of incubation although similar extracts of other embryonic tissues give negative resultsFHI Epinephrin is formed, or at least stored, in the medulla of the glands in many fetal mammals before the middle of gestation.32-39 The medullary cells show the chromaliin reaction at the 17th to 18th day in the pig and both physiologic and histochemical tests reveal the presence of an epinephrins lilce substance at the time migration of medullary cells into the cortical bodies is first observablekssfs The epinephrin content of fetal glands has been reported to be greater than in the adult; more was found in female than in rnale fetuses. A correlation between appearance of epinephrin in the suprarena1 of the rat and the origin of fetal movements has been suggested but this seems to be coincidental.

In sharp contrast with results obtained in most rnamma1s, human fetal suprarenal extracts give negative or only very slightly positive tests for epinephrine 4144 However, in full term infants as well as prematures which lived for a short time somewhat more definite reactions were obtained. The near fai1 ure to obtain epinephrin-lilce responses from human fetal suprarenal extracts may be contrasted with the observation that the paraganglia yielded definite amounts of epinephrin in one instance:43

Human suprarenal at birth - 0.0I arg. epinephrin per OR? Hm. Fluid.

Human paraganglion at birth - 0.24 rag- epinephrin per 0.1I Hm. sind.

Any relationship between low content of epinephrin and the presence of a very prominent androgenic cortical zone in man is undetermined.

The Sex Hormones

An excellent consideration of embryologic development of sex with a review of all but the latest literature has appeared recently.45 We are limited here to only a small part of this interesting subject.

The male gonads produce substances with androgenic properties in prenatal life. 1t was demonstrated that extracts prepared from the testes of fetal calves are similar to those from the adult and the hormonal yield per unit weight of tissue is greater. 46 It is probable that the male sex glands begin to elaborate secretions about as soon as their sex can be differentiated, which is the sixth day in the incubating chiclc and the seventh weelc in man. The ovary is recognizable as such about a weelc later than the testes.

The best indication we have that fetal androgens are active in early prenatal life is that forthcoming from a study of freemartins in cattle.47 48 The freemartin is an intersexed or masculinized female calf which deve1ops under conditions of chorionic fusion in which vascu1ar anastomoses are estab1ished between the placentas of adjacent male and female fetuses. The male is always a normal individual: It is believed that the hormone elaborated by the fetal male gonadscirculates in the conjoined blood streams, acting upon the female twin’s Miillerian or female duct derivatives to inhibit their normal development and upon its Wolllian or masculine duct derivatives to stimulate their abnormal dilferentiatiom When vascular connections are not established between adjacent fetuses of opposite sex no freemartin results, but the calves are normal male and female.

A similar freemartin condition has been described in swine.49 It should be noted that the placentas of both cattle and swine are relatively ineflicient from the standpoint of permeabi1ity. A high degree of placental fusion, apparently with vascular union, was observed in one instance of synchorial twinning in the cat.50 The fetuses were of opposite sexes, were sexually normal in every way, and were sulliciently advanced in development to make it appear certain that the female twin would not have become a freemartin. similarly synchorial twins of opposite sexes are encountered in other animals and man,51- 32 but freemartins have not been reported. It will probably be prolitable to- learn how the transmission of fetal male sex hormones across the placental barrier is related to the phenomenon in question. It is difficult to see how the freemartin condition can be so limited unless the diffusibility of embryonic testicular hormones is greater in the deciduate types of placentas which therefore never allow hormones to accumulate in suilicient amounts to stimulate the Wolflian derivatives of the genetically female twin.

It would carry us too far alield to inquire deeply into the extensive experimental studies on production of pseudohermaphrodism in the lower animals« success has been attained in mams mals at several laboratories recentlyks Injections of pregnant rats with large doses of testosterone and related preparations bring about abnormal development of the potentially male ducts of genetically female young. It is necessary to administer the hormone before the 16th day of gestation to obtain the most marked effects.54 This is about one day before the WolHian ducts begin to regress The intersexed individuals produced experimentally resemble the naturally occurring freemartins in certain particulars.

Male offspring of rats receiving large doses of estrogens before the Izth day of gestation have been markedly feminizedPs Thus a converse of nature’s freemartin has been induced with excessive female sex hormones. The extent to which the mother’s own hormones may inliuence normal development of sex in the fetus is not understood. It is known that the fetal uterus exhibits a marked hypertrophy and diminishes in size after intimate contact with the mother is abolished by birth. The mammary glands of newborn infants of both sexes show enlargement and may secrete transientlys It is possible that this production of «witch milk" is stimulated by the same maternal hormonal mechanism that leads to the preparation of the mother’s breasts for lactation.

The Thyroid Gland

The ability of the fetal thyroid to secrete at an early period seems to have been established. Iodine has been identilied in the gland at the 2nd or zrd month of gestation in cattle, sheep and swiness and in man at least as early as the 6th month» The amount is said to increase toward the end of prenatal life but to be low as compared with the adult gland, perhaps because storage of colloid is not so marked in the fetus« There is no close correlation between the maternal and fetal blood content of hormone iodine, a fact which suggests that the fetus is secreting its own hormone. The presence of thyreoglobulin in the human fetus at the zrd and 4th months has been established by means of an immunologic precipitin reaction.59

Amphibian metamorphosis and growth can be inlluenced by extracts and transplants of avian and mammalian fetal thyroid glands. In several, it may be said that the thyroid« becomes active at about the time its structure begins to resemble that of the adult. This is on the iith day of incubation in the chickW In calves colloid is present as early as the end« and differentiation is comp1eted between the 4th and 6th prenatal monthsz at this time extracts serve to bring about metamorphosis in the axolotl, a salamander which normally retains the larval state throughout life.30 Extracts prepared from the glands of pig fetuses 7 cm. long proved to be inactive, but those from 9 cm. pig fetuses produced reactions comparable with adult thyroids; correlatively, the adult structure was nearly attained at 9 cm.» When bits of the thyroid gland from a 3-months-old human fetus (1o cm. C. R. length) were transplanted into larvae of a toad, accelerated development took place, and trarisplants from 5-months-old human fetuses had more marked efkectsYs Control experiments with bits of fetal muscle gave negative results. It was found that the thyroid gland of the youngenfetus had already deve1oped col1oid Iilled vesicles.

Little is known about placenta! transmission of the thyroid secretions. In swine, horses, cattle and sheep, animals with adeciduate placentas, it appears that there is no transmission. In geographical regions where iodine deliciency is prevalent the offspring of these animals are born in a state of athyreosis while the mothers show little or no evidence of the iodine lack.C4- S« It seems sthat the fetal requirements of iodine are greater than those of the mother and that the fetus cannot draw upon the mother’s hormone but must manufacture its own. Iodine feeding during pregnancy corrects this deliciency, and the newborn pigs are then normal. In man, on the other hand, it seems probable that the mother’s hormone is available to the fetus because it can traverse the placental barrier. Human infants born without or with atrophic thyroid glands exhibit none of the symptoms of myxedema, but a latent athyreosis soon manifests itself.S3-71

The Parathyroid Glands

Practically nothing is known of function of fetal parathyroid glands. Injections of parathyroid hormone into dog fetuses bring on an elevation of the calcium level of the fetal, but not the maternal blood. This suggests that the parathyroid secretion does not pass the placenta in the species studied.72 Attempts have been made to determine the effects of fetal glands of dogs after thyroparathyroidectomy of the mothers. It was found that tetany developed just as soon as it did in nonpregnant animalsJss ««

The Thymus

Although the thymus is usually considered with the glands of internal secretion, it is doubtful if it logically belongs there. By 3 months in man, the thymus has the appearance of a lymphoid organ with cortex and medulla already in evidence. There is no anatomical basis for the belief that the sgland elaborates a hormone and few attempts have been made to study the fetal thymus from the standpoint of its endocrine function.30

Extracts of thymus seem to exert no elfects when fed to tadPoles, although opinion has been divided on this questions«- «« An extract of calf thymus, to which the name "thymocrescin" was given, has been reported to produce marked acceleration of growth in young rats when injected in daily doses as small as 1 mg.79

Another extract prepared in an entirely different way resulted in even more marked effects in the hands of Rowntree and his colleaguesko This material was injected intraperitoneally in i cc. doses into rats over long periods including gestation and lactation; the young of succeeding generations were similarly treated. Elfects on the olkspring of the first animals were not signijicant but the second and subsequent generations showed remarkable changes. They were larger at birth, more of them survived and their postnatal development was delinitely speeded. The young rats became sexually mature precociously. Maximum effects were found in the eighth and tenth generations. It was necessary to keep giving the treatments and not miss a generation or the effects were promptly dissipated. From the more recent reports it seems that it was necessary to inject the extracts into females only.

Other investigators have attempted to reproduce these very interesting results. but so far no adequate confirmation has been reported» The biologic effects of certain iodine-reducing substances (glutathione, ascorbic acid, cysteine) have been found to simulate those of the thymus extracts in certain particulars.

The Hypophysis

A few studies have been made on placental transmission of hypophyseal extracts but we know Iittle about hormone elaboration by the fetus itself. When pituitrin was injected into rabbit fetuses no muscular contractions were observed in the mother.83 This suggests, but does not prove, that the substance failed to pass the placenta. Anterior lobe extract did not produce any evidence of its usual gonadotropic activity in the mother when it was introduced into the fetuses« Furthermore, this hormone failed to appear in the fetal fluids after it had been injected into the mother; at least, the administration of these fluids to other adult rabbits fai1ed to bring about ovulatory changesss These experiments seem to show that there is very little if any transmission of the large molecules of the anterior lobe gonadotropic factor even in the hemosendothelial type of placenta.

The fetal hypophysis seems to be capable of elaborating several active principlesPss VHV A pressor substance has been found at 6 months in man. similar studies have been made in fetuses of cattle, sheep and swine in which the response was found relatively earlier. The guinea pig uterine strip method served to demonstrate the oxytocic princip1e about as early as the pituitary glarid can be recognized macroscopicallzn It was found in appreciable amounts in pigs and sheep at term.

The melanophore expanding hormone has been identified in the fetal hypophysis It was found in the glands from calf fetuses of 3 months gestation but was not there at 2 months. It was present in pigs of only 2o mm. c. R. length.30- 88

Gonadotropic and growth promoting factors of the anterior lobe seem to make their appearance rather late in fetal life, and the former is later than the latter.90 In fetal pigs the gonadotropic response was obtained from glands at the 2o to 21 ern. stage, a short time before the end of gestation but was not found earlier. The general body growth response could be obtained at the 9 to 13 cm. stage which was just about the same time the thyroid hormone made its appearancesEs 90


Extracts of the proximal portion of the fetal small intestine have been found to cause secretion of pancreatic juice when injected into adult animals with pancreatic Hstu1as.9I·9f The earliest period at which secretin has been obtained from the human fetus is 414 months. The exact source of the hormone is unknown and attempts to ascribe it to the chromalkn cells of the duodenum93 seem to be entirely unjustified

The Endocrine Pancreas

The endocrine function of the pancreas is vested in the cells of the islands of Langerhans These make their appearance in the third month of human gestation but it is not known how early they become capable of secreting. The acinar portion of the gland does not begin to produce its proteolytic ferment before about the 5th month,93 and Banting and Best took advantage of the fact that island tissue is functional earlier when they chose the pancreas of the fetal calf as a source of antidiabetic principle in their early search for insulin.97 Many have discussed the possibility that fetal insulin plays an important röle in carbohydrate metabolism of the fetus and have pointed to a correlation between the appearance of glycogen in the liver and the development of island tissue in the pancreassss 99 but the relationship is still somewhat unsatisfactorily established because the influence of maternal secretion acting through the placenta is diflicult to evaluate. It is said not to pass the placenta from fetal to maternal sides.83 Administration of insulin to pregnant cats failed to reduce the blood sugar level of the fetuses near term. This suggests that the placenta is impervious at the time, but at earlier stages similar results were not obtainedEoo Further discussion of this question will be found in Chapter XVI.

In birds, where all metabolic processes must be managed by the fetus itself, an insulin-like substance has been found in the unincubated eggJOI However, it is not present in the tissues of the early chick embryo until after the pancreatic islets are formed.

The offspring of diabetic animals are not diabetic and as a ruIe seem to possess healthy glandsW This is not always true in man where hypertrophy and hyperplasia of islands and postpartum hypoglycemic deaths are encountered in infants born of diabetic women. Although hyperplastic pancreatic islands are not found in all instances, careful searching might show the condition to be more prevalent.

The possibility that during prenatal life fetal insulin can protect the diabetic mother has been discussed by several investigators. It was discovered by Carlson and his colleaguesIM W that the urine of completely pancreatectomized dogs remained free from sugar when the .operation was performed in late stages of pregnancy. This suggested that fetal island tissue had, supported both the mother and fetuses, for after parturition the mother exhibited glycosuria. These experiments have been adequately confirmedW and similar conditions app«arently occur in the human.I07 Completely depancreatized dogs maintained in good hea1th by diet and insu1in therapy can conceive and give birth to normal pups. They show an increased carbohydrate tolerance kor only about two weeks prior to labor. However, an even greater tolerance appears after birth during lactationz it would seem that the results previously ascribed entirely to ketal insulin are more probab1y due largely to increased utilization of carbohydrates by the fetuses and, after birth, by the nursing puppies. We cannot be sure that the ketal insulin plays any part in protecting the diabetic mother. It is quite reasonable to suppose that it is more important kor the utilization of sugar received by the fetus krom the mother.

Glycogen appears in the liver of the deve1oping chick at 7 days of incubation. This is about three days before delinitive islands of Langerhans make their appearance. Between the tenth and thirteenth days the glycogen content of liver cells diminishes and the metabolic rate and respiratory quotient increase, although there is no rise in the blood sugar concentration. Thus it appears that an increased utilization of carbohydrate by the embryo is correlated with the advent of kunction in suprarenal medulla pancreatic islands and thyroid glands.

References Cited

1. Needham, J. i93i. chemical Embryology, Macmillan, N. Y.

2. Gro11man, A. i93s. The Adrena1s, Williartis sc Wi1kins, Baltimore

3. Rogokk, J. M. 1932 chap. as, vol. 2 in cowdry: Special cytology, I-Ioeber, N. Y.

4. scammon, R. E. i923. Chap. z, vol. i in Abt: Pediatrics, saunders, Philadelphia. «

5. Elliott, T. R. sc R. G. Arnioun igi i. J. Path. sc Bach, is: 4si.

6. scammon, R. E. i93o.» Pt. IV in The Measurement of Man. Univ. of Minn. Press, Minneapolis

7. Davies, s. ig37. Quart. J. Mic. sci., so: si.

8. I-Ioward-Mil1er, E. i927. Am. J. Anat» 4o: 25i.

9. Roak, R. i935. J. Anat., 7o: ists.

10. Bacsich, P. sc s. J. Folley. i939. J. Anat» 73: 432.

11. Martin, s. J. ig3o. Proc. soc. Exp. Bio1. sc Med., Es: 4i..

12. Reichstein, T. i93s. I-Ielv. chi. Acta, i9: Les.

13. I-Ioward, E. i937. Am. J. Physiol» ii9: 339.

14. BurrilL M. W. sc R. R. Greene. i93g. Proc. soc. Exp. Bio1. sc Meds., 403 IS?

15. Howard, E. i939. Am. J. Anat., s5: io5.

16. Gersh, I. sc,A. Gro1lman. i939. Am. Physiol» us: 3ss.

17. stewarch I-I. A. i9i3. Proc. i7th latet-nat. Gang. Magd» secr. z, Pt. g,

18. stewart, G. N. sc J. M. Rogolk t9es. Pt·oc. soc. Exp. Biol. sc Med» ee: sg4 and es: tgo.

19. Rogokh M. sc G. N. stewarr. t9e7. Am. Physiol» 79: so8.

20. cotsey, E. L. tge7. Proc. soc. Exp. Biol. sc Med» es: t67.

21. Gaunt, R» W. 0. Nelson sc E. Loomis. t9s8. Ibid» s9: st9.

22. Gaum, R. sc H. W. I-Iays. t9s8. Science, 88: s76.

23. Greene. R. R., J. A. Wells sc A. c. Ivy. t9s9. Pt·oc. soc. Exp. Biol. scCMed» 4o: 8s.

24. Rogokh J. M. sc G. N. stewarr. tgeg. Am. J. Physiol» 88: t6e.

25. Ing1e, D. J. sc G. T. Fishetn t9s8. Proc. soc. Exp. Biol. sc Med» s9: t49.

26. Tobin, C. E. t9s9. Am. J. Anat» 6s: tst.

27. Weymanth M. F. t9ee. Anat. Rec» e4: e99.

28. Howard-Miller, E. t9e6. Am. J. Physiol» 7s: e67.

29. 0lcuda, M. t9e8. Endocrin» te: s4e.

30. I-Iogben, L. T. sc F. A. E. Stets. t9es. Brit. Exp. Biol., t: t.

31. Lutz, B. R. and M. A. case. tges. Am. J. Physiol» 7s: 67o.

se. Langlois. J. P. and J. Rehns. t899. comp. Rend. soc. Biol., st: t46. ss. Fengetx F. t9te. J. Biol. chem., it: 489 and te: ss.

34. cevolotto, G. t9t6. chem. Abstt·» to: tete.

35. Mccord, c. P. t9ts. J. Biol. chem., es: 4ss.

36. svehla, K. t9oo. A1ch. exp. Path. u. Phaxm» 4s: set.

37. Moore, B. sc c. 0. Purinton. t9oo. Am. J. Physiol» 4: s7.

38. Lewis, J. I-I. tgt6. J. Biol. chem., e4: e49.

39. saito, s. t9e9. Toholcu J. Exp. Med» te: es4.

40. Panlusatz D. s. t9st. Anat. Rec» 49: st.

41. Ingietx A. sc G. schmorL 191 t. Miinch. med. Wochenschr» t9tt, e4os (Abstt·.) .

42. samelson, P. t9te. Ztschtn i. Kinderhlk s: 6s.

43. Elliott, T. R. Personal to G. Batget, t9t4. The simpler Natural Bases, Longmans Green, London (p. 9s).

44. Krametx D. t9t8. Monatschtx f. Kinderhllg t4: sst.

45. Williety B. H. t9s9. chap. s in E. Allen’s «·sex and Internal secres tions," Williams sc Wilkins, Baltimore.

46. Womaclh E. B. sc F. c. Koch. t9st. Proc. end 1nternat. cong. set: Res» t9so, P. se9.

47. Linie, F. R. t9t7. Etcp. Zool» es: s7t.

48. Linie, F. R. t9e3. Biol. Ball» 44: 47.

49. Hughes, W. t9e9«. Anat. Rec» 4t: et s.

50. Wisloclus G. B. sc G. W. D. Hamletr. t9s4. Ibid» 6t: 97.

51. Hamlett. G. W. D. sc G. B. Wisloclti. t9s4. Ibiii» St: st..

52. Wisloclci, G. B. t9s9. Am. Anat» 64: 44s.

53. Gt·eene, R. R» M. W. Burrill sc A. c. Iyy. t9s8. Am. Obst. sc Gyn s6: tos8.

54. Butrill, M. W. sc R. R. Greene. tgs9. Am. J. Physiol» te6: 4se.

55. Greene, R. R. sc M. W. Burrill. t9s9. Ibid» te6: sto.

56. Nosalca, T. t9e7. chem. Abs» et: s9ts.

57. Mauretx E. t9e7. Ztschtu i. Kinderhllc» 4s: t6s.

58. Mcclendon, J. F. sc c. E. McLennam t9s9. Proc. soc. Exp. Biol. sc

Med., 4o: sss. sg. I-Ielctoett, L. sc K. schulhoL t9es. Proc. »Natl. Acad. sei» tt: 48t. eo4

. Wegelin, C. sc J. Abelin. . Thomas, E. sc E. Delhougne

. snyder, F. F. s: F. M. Hoskins.

. Leu-is, D. . snydeiy F. F. i9es. Am. J. Anat» 4i: s99.

. Bell, G. H. sc M. Robson. i9s7. Quart. J. EZcp. Physiol» e7: eo5. . sinith, P. sc c. Dortzbaclx . Hallion, L. 8c P. Lequeux. . camus, L. i9o6. Ibid., 6i: 59. . Pringle, H.

. Banting, F. G. s: c. H. Best. . Aron, M. . Port-in, R. sc M. Aron. i9e7. coinp. rend. soc. Biol., 96: e67. . Britton, s. W. i9so. Am. J. Physiol» 95: i78.

. shilcinamh Y. i9es. Tohoku J. Exp..Med.,sp io: i.

. Willieiy B. H. Personal to J. Needham. i9si. cheiii. Emb., Mac millan, N. Y.

. Abbott, A. C. 8c J. Prendergasr. . i9s7. can. Med. Assoc. J., s6: ees. . Rumph, P. 8c P. E. smith. i9e6. Anat. Ren, ss- es9.

. Schuhe, W» W. schmitt sc K. Hölldobler. . smith, G. E. s: I-I. Welch. i9i7. J. Biol. chem., e9: ei z. . smith, G. E. . siegen.

i9es. Endolcrin., e: e.

i9i9. Endocrin., s: e6e.

i9ei. Verh.«deuts. Gesel. Kinderhllsp ee: s64.

Kot-her, T. is9e. Deuts. Ztschr. chirurg.,-s4: 556.

i9ei. Arch. exp. Path. u. Pharm., sg: ei9. i9e4. Virchow’s Arch. path. Anat. u. Physiol» e4s: eoi .

. Kraus, E. J. i9e9. Beitr. path. Anat. allg. Path., se: e9i. . sgalitzey K. i9ss. Ibid., ioo: es5. . Hoslcins, F. M. sc F. F. snyder.

i9e7. Proc. soc. Eis-P. Biol. sc Med., es: e64. ·

. Vassale, G. i9o5. Art-h. ital. biol., 4s: i77. . Werelius, A. i9is. Sarg. Gyti. sc Obst» i6: i4i. . Trinlca, L.

i9i4. Publ. biol. Ecole Hautes Etudes Vet. de Brno (in czechz cited by J. Needham, i9si) . —

. Macchiariilo, 0. i9so. Riv. ital. di Gin., ii: s57. . Gudernatsch, F. . Allen, B. M. i9eo. J. Exp. Zool., so: is9.

. Asher, L. i9ss. Abderhalden’s Handb. biol. Arbeits-method. Abt. s,

i9i4. Am. J. Anat., is: 4si. Teil sB (e): 9e9.

. Rowntree, L. G., J. H. clarlc sc A. M. Hans-on. i9s4. science, so: e74. . Rowntree, L. G., A. steinberg, N. H. Einhorn 8c N. K. schaffen

i9ss. Endocrin., es: 584.

. Nelson, W. 0. i9s9. chap. ei, in E. Allen’s «sex and Internal Secre tions," Williams 8c IVillcinsk Baltimore i9e7. Anat. Rec., s5: es.

Wisloclci, G. B. sc F. F. snydeix i9se. Proc. soc. Exp. Biol. sc Med., so: i96. . Goodman, L. s: G. B. Wisloclci. i9ss. Am. J. Physiol» io6: ses. schlimperh H. i9is. Monatschix Geh. u. Gyn., ss: s.

i9i6. J. Exp. Med., es: 677.

i9e9. Anat. Rec., 4s: e77. i9o6. comp. rend. soc. Biol., 6i: ss.

i9ii. Physiol» 4e: 40 P.

. Koschtojanz c. i9si. Pllügeks Arch., ee7: s59. . parat, M. i9e4. comp. rend. soc. Biol., 9o: wes. . Ibrahim, J. i9o9. Biochem. Ztschr., ee: e4.

i9ee. J. Lab. s: Glitt. Med., 7: 464. i9es. comp. rend. soc. Biol., s9: is7, is

me. Jos1in, E. P. 1915. Boston Mai. sc: Sarg. J., 173: 841.

103. smyth, F. s. 8e M. B. 01ney. 1938. J. Pediat., is: 772.

104. Car1son, A. J. 8e F. M. Drennam 1g11. Am. J. Physiol» es: 3g1.

105. car1son, A. J» J. s. Ort· 8e W. s. Jones. 1914. J. BioL Odem» 17: 19.

106. cuthberiz F. P., A. C. Ivy, B. L. Isaacs se: Gray. 1936. Am. J. Physiol us: 480.

107. Lawrence, R. D. 1929. Quart. J. Mai es: 191. Los. Daltorh A. J. 1937. Anat. Ren, 68: 393.

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