This review deals with the comparative observations of brown fat tissue in the bat, a hibernator, and in man, a nonhibernator. In both mammals, the brown fat is distributed in restricted portions of the body and brought into a thermogenetic activity by an acute drop in ambient temperature.
Light microscopic examination was performed on the interscapular brown fat of bats captured monthly throughout one year; electron microscopic observations were made using a bat captured in April and another in September. Human perirenal brown fat was investigated light-microscopically on tissues derived from 215 fresh necropsy cases (Japanese) of both sexes aged from one month to 93 years. Brown adipose tissue was recognized only in 162 (75%) of the 215 samples, because brown fat cells were reduced by transformation into white fat cells.
Human brown fat cells were classified into six types according to the morphological features of their lipid droplets. These reflect different functional states of intracellular heat production. The Type 1 (D) cell is a fat-depleted brown fat cell with a darkly stained cytoplasm; it is specific to humans. Human perirenal brown fat cells begin to show a transformation into white fat cells already at the infantile stage. This change occurs from the peripheral toward the central portion of the lobule, so that various functioning cell types remain only in the central area of the lobules. In contrast to humans, bat interscapular brown fat cells exhibit regular seasonal changes in size and lipid droplet content, so that the cells could not be classified as in humans into definite types according to the features of their lipid droplets.
The most conspicuous difference between brown fat tissue in the nonhibernator and hibernator is that in the latter, white fat cells never occur within the brown fat tissue. In the hibernator, thermogenesis in the brown fat is necessary for both the arousal from hibernation and the maintenance of hibernation as well as rutting. In human perirenal brown fat tissue, darkly stained fat-depleted cells (D) occupy, with other cell types (CR, CR'), an important part in the reversible heat production cycle of the brown fat tissue. The “hypothermic” or “cold syndrome (cold injury)” is a disorder affecting inadequately protected infants in severely cold seasons, accompanied by lethargy, hypothermia and lactation refusal and revealing hemorrhagic pneumonia in necropsy. The brown fat tissue in such infants is composed exclusively of fat-depleted brown fat cells. Similar fat depletion can be recognized in the remaining brown fat of adult subjects succumbing to overexposure to cold and other causes including burning and hemorrhaging both of which cause excitation of the sympathetic nerve. Thus, in forensic medicine, changes in the brown fat tissue may indicate the cause of death.
This review further details electron microscopic observations of bat brown adipose tissue and its sympathetic innervation.

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The ultrastructure of the cardiac ganglia of streptozotocin-induced diabetic rats was studied at survival times of 3 and 7 days, 1, 3, 6, 9 and 12 months. At 3-7 days post-induction, some intracardiac neurons showed an overall increase in electron density, with the dendrites darkening first. Some of the affected dendrites appeared jet black and their intracytoplasmic organelles were hardly distinguishable except for some swollen mitochondria. Both electron dense and lucent types of degenerating axon terminals were observed in the interstitial spaces. Several myelinated and unmyelinated axons also showed early signs of degeneration.
At 1-6 months post-induction, numerous myelinated and unmyelinated axons were shown to be degenerated. The majority of the intracardiac neurons appeared to be normal. Numerous macrophages containing phagosomes were found in the interstitial spaces. At 9-12 months post-induction, macrophages containing engulfed debris were still commonly observed amongst the neuronal profiles, which appeared to be morphologically normal.
It is concluded that degenerative changes occur in the cardiac ganglia of streptozotocin-induced diabetic rats and that these changes appear to be both progressive and prolonged.

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The presence of Langerhans cells in the developing mucosal epithelium of mice was investigated by ATPase histochemistry and by electron microscopy. In the stratified squamous epithelium of the tongue and forestomach, a few ATPase-positive Langerhans cells could be recognized at 1 or 2 weeks after birth. They increased in number by 3 weeks of age, but the density was lower than that in the epidermis. The ATPase-positive cells in the mucosal epithelium had longer (18-22μm) dendritic processes; each cell thus occupied a large space. The mucosal Langerhans cell with elongated dendritic processes may well be responsible for the surveillance of a wide area in the defense system of the mucous membrane. The cells had a clear cytoplasm among keratinocytes in the basal cell layer and, under the electron microscope, showed characteristics similar to those of the epidermal Langerhans cells; Birbeck granules were also recognizable in the cytoplasm.

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In combination with transmission electron microscopy (TEM), histochemistry for acetylcholinesterase (AChE) and immunohistochemistry for vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY) were carried out on the intraepithelial nerve fibers of the guinea-pig nasal gland.
AChE-positive nerve profiles and VIP-immunoreactive nerve profiles were detected in abundance within the epithelium of the glandular acini and within the epithelium of intralobular excretory ducts including the intercalated and striated ducts. Intraepithelial NPY-immunoreactive nerve profiles were also considerably large in number in the nasal gland, but less frequent than the other two types of nerve profiles; furthermore, the NPY-immunoreactive nerve profiles appeared absent within the epithelium of the striated duct.
All the intraepithelial nerve varicosities were in close spatial contact with the epithelial cells of the acinus and the duct and also with the myoepithelial cells, which were commonly seen in the acinus and the intercalated duct. Throughout the present study, however, no membranous specializations could be found between the nerve varicosities and the epithelial cells or the myoepithelial cells.
The present results suggest an intense and delicate regulation through the collaboration among ACh, VIP and NPY of the secretory activity of the guinea-pig nasal gland, including the emission of acinar secretions into the duct through contraction of the myoepithelium and modification of the secretion contents by the duct epithelium.

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The secretory function of the natural killer (NK) cells has been considered to be essential for cytolytic activity against their target cells. In this study, the distribution and spatial relationship of various cell organelles which participate in the secretory process, i. e., Golgi apparatus, vesicles, granules and microtubules, were examined ultrastructurally in nontreated and OK-432-activated rat NK cells bound to the tumor cells, with special reference to the rod-cored vesicles which are the most characteristic structure of the NK cells. Rod-cored vesicles and their closely related structures, “empty” vesicles, were derived from the end portion of the Golgi trans cisternae and became accumulated in the central area which was surrounded by the Golgi apparatus, nucleus and contact surface. Some of the vesicles appeared to be further transported to the contact area along the microtubules extending from the centrioles toward the bound targets. The access of the vesicles to the contact surface occurred at that portion where subplasmalemmal actin lattice was thin. The distribution of the dense granules and multivesicular bodies was similar to that of the vesicles, but the area of their occurrence was a little wider. At the outer aspect of the Golgi apparatus was situated the endoplasmic reticulum from which transitional vesicles came to the inner or cis cisternae of the apparatus. The present observations indicate that the cell organelles of the conjugated NK cells are purposefully arranged in the cytoplasm in such order that the generated rod-cored veislces and “empty” ones are efficiently directed toward the bound tumor cells.

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Combined light and electron microscopic observations of the carotid labyrinth of the newt, Cynops pyrrhogaster, revealed the occurrence of glomus cells with melanosomes (MG cells), a finding so far unreported in the amphibian carotid labyrinth. These melanosomes, which derived from melanophores, were electron-dense and usually oval (250-700nm in diameter). They occurred in groups enclosed by a limiting membrane, and the diameter of clusters was approximately 1.5μm. These clusters were surrounded by a large number of dense-cored vesicles (60-100nm in diameter), which were predominantly located in the glomus cell cytoplasm. The density of dense-cored vesicles in MG cells was higher than that in regular glomus cells (G cells).

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Fibronectin has been believed to be involved in vasculogenesis. This study demonstrates by immunohistochemistry the distribution of fibronectin around the systemic arteries of chick embryos during the periods of aortic arch formation, and examines the possible relationship between the distribution of fibronectin and the obliteration of the arch artery.
In embryos at stage 23, no obliteration of arch arteries was recognized on sections. At this stage, intense staining with an anti-fibronectin antibody was seen in the developing tunica media of the carotid artery and dorsal aorta. Staining around, the arch arteries was much weaker. At stage 26, the intensity of anti-fibronectin antibody staining was weaker around the left arch artery, although the diameter of the 4th arch artery was not different between the left and right. At stage 27, which is the early period for the obliteration of the left 4th arch artery, the intensity of the anti-fibronectin antibody staining for the left arch artery was much less than that for the right arch artery.
These results show that fibronectin does not accumulate around the left 4th arch artery during aortic arch formation and suggest the possibility that a smaller amount of fibronectin is responsible for the obliteration of the left 4th arch artery.

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Direct conversion of typical fibroblasts to chondrocytes in the mouse fibrous connective tissue induced by bone morphogenetic protein (BMP) was observed by light as well as electron microscopy. A pellet containing BMP obtained from a murine osteosarcoma was transplanted into the dorsal subfascia of 5 week-old mice. Until 3 days after implantation of BMP, all the connective tissue cells in the pellet region of the dorsal subfascia showed the fine structural features of typical fibroblasts. The cells in the pellet region changed their shape from spindle-like to polygonal by 5 days after implantation. At this time, small vacuoles 150-450nm and vesicles 40-60nm in diameter, containing a homogeneous substance of low electron density, appeared in the cytoplasm of the cells. A small amount of extracellular substance, showing metachromasia by toluidine blue staining, was seen around the cells. Moreover, autoradiography of ³⁵S revealed the uptake of sulfur by the cells and its accumulation in the extracellular substance around the cells in the pellet region at 5 days. The rough endoplasmic reticulum and Golgi apparatus increasingly developed with time and after 7 days both elements were distributed throughout the cytoplasm. The cytoplasmic small vacuoles and vesicles also increased in number with time, and the metachromatic extracellular substance containing fine filamentous meshwork and many tiny particles, which was regarded as the matrix of cartilage, also increased rapidly in amount. By 9 days, the cells in the pellet region became oval or round in shape, showing many short cytoplasmic processes. This finding indicates that the fibroblasts in the BMP pellet region transform to chondroblasts at least by 5 days after implantation, and become typical chondrocytes by 9 days.

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Adenohypophysial cells having a glucocorticoid receptor were immunohistochemically determined in rats. For detecting the presence of the glucocorticoid receptor, we used the monoclonal antibody for a glucocorticoid receptor (BuGR-2), and immunohistochemically examined the phenotypes of the cells that exhibited BuGR-2-immunoreactivity. The immunoreaction for the glucocorticoid receptor was confined to the nuclei of the majority of corticotrophs (70%) and of some somatotrophs in intact animals. Following adrenalectomy, all corticotrophs became significantly hypertrophic, losing their immunoreactivity for the glucocorticoid receptor. In contrast, somatotrophs that had also lost the immunoreactivity for the glucocorticoid receptor in the nuclei greatly diminished in size. Intraperitoneal administration of corticosterone was performed in adrenalectomized animals to supplement glucocorticoids. This treatment restored BuGR-2-immunoreactivity in the nuclei of some corticotrophs. In intact rats, immunolabeled corticotrophs were classified into two types, stellate and polyhedral. However, the immunoreaction for the glucocorticoid receptor was equally evident in the cell nuclei of these different types of cells. It is concluded that, in rats, both corticotrophs and somatotrophs are target cells of glucocorticoids, although these cell types display opposite growth responses to the removal of glucocorticoids.

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The localization of spot 35 protein, a cerebellar Purkinje cell-specific protein, was studied in guinea pig taste buds by means of electron-microscopic immunocytochemistry. The immunoreactivity was localized in the cytoplasmic matrix of discrete bud cells. The ultrastructural features of the reactive cells indicated that they corresponded to the Type III or gustatory cells making a synaptic contact with the intragemmal nerves. All other cells specified as basal, Type I, and Type II were immunonegative for spot 35 protein. This finding indicates a method for specifically demonstrating the gustatory cells in the guinea pig taste bud and, further, gives new evidence that paraneurons may share neuron-specific substances with neurons.

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