Understanding the development of the human adenohypophysis is dependent on visualizing the growth of Rathke's pouch. This embryonic structure gives rise to bilateral anterior and posterior, superior and inferior segments. These segments differ in their potential to produce various types of hypophyseal chromophils. The potential differences are described in the text.Further, by application of specific staining procedures it has been possible to determine the approximate time that specific chromophils appear in the adenohypophysis. The chromophils of the adenohypophysis develop in the order: cell type 111, I, IV, 11, V, VI and IX. There may be a relationship between the development of certain chromophils and the onset of function in target endocrine glands.Present descriptions of the cytogenesis of hypophyseal chromophils are incomplete (Romeis, '40; Pearse, '52; Falin, '61). Two apparent reasons are the lack of a range of suitable material for study and the use of staining procedures that were not specific for individual cell types.In previous studies I have attempted to evaluate the specificity of the available staining methods and to provide a description of the chromophils of the adult adenohypophysis (Conklin, '66, '68). In all, seven specific chromophils as well as variant forms were identified.The specific chromophils and the hormone tentatively secreted by each are as follows: cell type I: somatotropic hormone (STH); type 11: lactotropic hormone (LTH) ; type 111: adrenocorticotropic hormone (ACTH) ; type IV: thyrotropic hormone (TSH); type V: luteinizing hormone (LH); type VI: follicle stimulating hormone (FSH) (see Ezrin, '63; van Ordt, '65; Conklin, '66 for terminology). The significance of three other cell types, i.e., VII, VIII and IX is not clear. Cell types VII and VIII appear to be variant forms of the definitive chromophils while type IX is a definitive cell of unknown function.In the present study, the methods employed to demonstrate each of the above chromophils have been applied to the fetal hypophysis in order to determine the time of appearance and origin of each cell type.ANAT. REC., 160: 79-92. MATERIALS A N D METHODSThe material employed in this study consisted either of whole embryos, heads of fetuses or fetal pituitary glands obtained from the Embryology Research Collection of the Department of Anatomy, The University of Michigan. Thirty-eight specimens ranging in crown-rump (CR) length from 11.5 mm to 365 mm (term) were used. The specimens were fixed in either 10% neutral formalin or Bouin's solution. Tissue sections were stained by several different staining procedures and identification of specific chromophils was achieved by the use of methods described in previous publications (Conklin, '66, '68).Particular attention was given to (1) the histogenesis of various regions of the hypophysis and (2) the time, based on crownrump measurements, of appearance of tinctorially distinct chromophils. The staining reaction of intracellular cytoplasmic inclusions was the basis for identifyin...
The protein fractions of 7-18 day chick serum, allantoic and amniotic fluid and egg white were demonstrated by acrylamide gel electrophoresis.The similarity in protein fractions suggests that most of the amniotic fluid proteins are derived from egg white while serum contributes most of the allantoic fluid proteins.Several protein fractions which are unique to the respective fluids may be produced by components of the extraembryonic membranes.The nature of the proteins found in both serum and allantoic fluid suggests a selective transfer of protein between the two fluids.An interest in the function of the chorioallantoic membrane of the chick embryo has prompted investigations (Conklin, '66) of the membrane and the allantoic Jluid. One of the unanswered questions about the allantoic fluid is the initial source of its primary componcnts. It has been suggested (Romanoff, '60) that avian allantoic fluid is produced either by the allantoic membrane or excreted into the cloaca and thence into the allantoic lumen ( o p . c i t . ) , while the amniotic fluid may originate as a transudate of serum or as a secretory product of the amnion.An obvious way to determine whether serum might contribute to the formation of either fluid would be by comparison of the protein content of the serum and the amniotic and allantoic fluids. Strangely, however, no successful comparison of the protein components of these fluids and of embryonic serum has been made. Indeed, earlier attempts to detect similarities between the fluids and embryonic and adult serum, using paper electrophoresis, failed to demonstrate any proteins in amniotic fluid until after the thirteenth day when, following the rupture of the seroamniotic plate, the proteins of amniotic fluid were identical to ovalbumin (Marshall and Deutsch, '5.0). These authors were able to demonstrate nine protein fractions in 13 day chick serum.Shepard and Hottle ('49) also employed paper electrophoresis and demonstrated three protein fractions in 13 day allantoic fluid. These fractions reportedly were unlike any found in embryonic plasma, J. EXP. ZOOL., 162: 257-262.
Thirty‐two sacrococcygeal neoplasms of germ cell origin were assessed with respect to pathology and natural history. There were 20 mature teratomas, four immature teratomas, one embryonal carcinoma and seven mixed teratomatous neoplasms (teratocarcinomas). All but four neoplasms occurred in infants aged 2 years or younger and 23 of these had visible tumor masses at birth. Only one neoplasm which was present at birth as a visible mass recurred metastasized and caused death. Neoplasms that made their appearance sometime after birth were more frequently malignant. Seventy‐eight per cent of the neoplasms occurred in females. The histologic patterns of growth in these germ cell neoplasms were the same as those encountered in the gonads with the exception that no germinomatous or choriocarcinomatous elements were found. Thirty‐eight per cent of the tumors were histologically malignant although not all behaved so clinically. All mature and immature teratomas were clinically benign. Six of seven teratocarcinomas recurred, metastasized and caused the patients' deaths. The one embryonal carcinoma behaved in a very aggressive manner and caused death of the patient 2 months after diagnosis.
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