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Immunoglobulin heavy and light chains and C3 were detected on amyloid deposits in cutaneous nodular amyloidosis (NA) by a direct immunofluorescence method. These immunoglobulin chains and C3 could be removed except lambda (lambda) light chain after treating sections with 0.05% Tween 20 solution, 0.1 M glycine buffer pH 7.4 or 0.5% Triton X solution. Lambda light chain was detected consistently after these treatments. Amyloid filaments were not altered with these treatments. Immunoelectron microscopy demonstrated persistent antigenicity of lambda light chain on amyloid filaments. It was suggested that lambda light chain is an inherent component of amyloid filaments in NA, whereas other chains and complement represent nonessential absorption on amyloid material.

Cross-banded filamentous aggregations (CBFA) with a periodic banding pattern (850–1250 A) have been found frequently in the stroma of squamous cell carcinomas and malignant melanomas of the skin. In these tumors, the aggregations were commonly associated with the basal lamina and abnormal fibrils. No CBFA was found where collagen fibrils did not show degradative changes. Less frequently, CBFAs were found in the skin lesions of primary and secondary amyloidoses, in inflammatory foci of a halo nevus, and in other skin lesions. CBFAs were similar to the Luse's bodies which have previously been found in normal and abnormal tissues of the central nervous system. Although some investigators have equated the aggregates with the fibrous-long-spacing (FLS) type of collagen, FLS collagen prepared in our laboratory showed a longer periodicity (2,200 A) than that of CBFA. Staining with ruthenium red significantly increased the electron density of CBFA, suggesting that CBFA contains acid mucopolysaccharides.

Histochemically identifiable amyloid associated with actinic keratosis was studied with the electron microscope. Typical amyloid filaments forming islands identical to collagen strands were found in the upper dermis. Beyond the lesion of actinic keratosis, no amyloid was found. In the healing wound of a previously biopsied lesion, amyloid was regenerated only when the epidermis covered the wound. In such epidermis-covered granulation tissue, electron-dense amorphous substance was initially formed in the upper dermis and amyloid filaments subsequently emerged within it. In both original and regenerated lesions, perivascular spaces were free from amyloid, and actinic elastosis was absent. It was concluded that secondary amyloidosis associated with actinic keratosis is produced by local fibroblastic cells under an abnormal influence of the epidermis.

We studied the recovery phase of immune response-associated (Ia)-positive or ATPase-positive epidermal Langerhans cells (ELCs) after ultraviolet B (UVB)-induced depletion by using mouse ear epidermal sheets. An area 3 mm in diameter was irradiated with 300 nm UVB light (40 mJ/cm2). A time sequence study was carried out to 56 days. During this period the Ia-positive ELC population increased stepwise, i.e., first a rapid increase between day 7 and day 14, which we called the early recovery phase, and next a gradual increase between day 42 and day 56, which we called the late recovery phase. During the early recovery phase, we found polymorphous ELCs in the irradiated area which were giant or normal in size, dendritic or round in shape, and single or paired in distribution. Electron microscopy revealed some of round and some of paired ATPase-positive ELCs to be in metaphase or telophase of mitotic division. Within the entire observation period of our study, there was no evidence suggesting migration of ELCs from hair follicles or from the nonirradiated epidermis. These findings indicated that mitosis of ELCs contribute to their repopulation during the early recovery phase.

The thermodynamic parameters of the CO-equilibria of isolated chains of hemoglobin A and of two α-chains in hemoglobins M Milwaukee-I and Saskatoon at 25°, pH 7.0 were determined. The parameters for the binding of the first CO molecule to the hemoglobins M were ΔH′=−17 and −18 kcal/mole heme and ΔS′=−30 and −29 e.u. for hemoglobins M Milwaukee-I and Saskatoon, respectively. In contrast to this the characteristics of the second step of the binding were ΔH′=+5.9 · and +4.3 kcal/mole and ΔS′=+51 and +49 e.u. These values for the second step were also significantly different from those of the isolated α-chain (ΔH′=−15 kcal/mole and ΔS′=−11 e.u.).

Two cases of transient bullous dermolysis of the newborn are reported. The first patient, a white boy, had normal skin at birth, but multiple blisters soon developed. The oral mucous membranes were not affected. All lesions healed within 4 months without scars but with many milia. At the age of 17 months the boy was reexamined and was found to have no blisters or milia. The second patient, a Japanese baby girl, had extensive denudation of her hands at birth. Generalized blisters and involvement of the oral mucous membrane developed. Blistering stopped within 1 1/4 months, and all lesions healed without scars. Histologically the blisters were subepidermal in both cases. Some lesional basal cells contained periodic acid-Schiff-positive inclusions. Electron microscopy revealed collagenolysis, diminution or loss of anchoring fibrils, and stellate inclusions in dilated rough endoplasmic reticulum in the keratinocytes of the lower epidermis. These stellate inclusions consisted of filamentous bundles with 25 to 33 nm cross-striations.

The mouse monoclonal antibody AFH1 was produced using formalin-fixed, sham paraffin-embedded human melanoma cell culture line A375 as immunogen. Reactivity of this antibody was assessed by immunohistochemical techniques against formalin- or acid alcohol-fixed paraffin-embedded tissue as well as formalin- or acid alcohol-fixed unembedded lesions. Ninety-seven nevomelanocytic lesions, neurofibromas, epithelial lesions, and a plasmacellular infiltrate were evaluated. AFH 1 was immunoreactive on 54 of 55 nevocytic lesions (98.2%), 15 of 16 primary melanomas (93.7%), a lentigo maligna, and nests in 21 of 21 dysplastic nevi (100%). Of 100 consecutive basal melanocytes of intraepidermal melanoma cells counted in each lesion, mean AFH1 immunoreactivity for nonnested basal melanocytes in nevocellular nevi was 3.8%; for dysplastic nevi, 13.8%; and for intraepidermal melanoma cells, 78.0%. When nonnested basal melanocytes were subdivided into cytologically normal and abnormal cell groups, AFH1 immunoreactivity was 9.4% and 72.6%, respectively. AFH1 recognition of the lentiginous portion of dysplastic nevi corresponds statistically to the appearance of abnormal melanocyte cytology, nest formation, or both. Using 50% immunoreactive nonnested melanocytes as the criterion, AFH1 seems to distinguish primary melanoma from dysplastic nevi with a sensitivity of 93.8% and a specificity of 95.8%.

A new monoclonal antibody NKH-1 was developed using human subepidermal basement membrane zone substances as immunogen. NKH-1, IgG1 kappa light chain, labeled proteins in the subbasement membrane zone in a linear fashion. It also labeled oxytalan fibers and elaunin fibers in the papillary dermis. Mature elastic fibers were labeled only in their peripheral microfibrils (elastofibrils) and the center core of elastin was nonreactive. Basal lamina itself was not decorated with NKH-1 even at the immunoelectron microscopic level. Skin appendages such as eccrine and apocrine glands, arrector pili muscle, hair follicle, and sebaceous gland were surrounded with NKH-1 -positive substances. This substance was in linear fashion closely associated with the basal lamina but deposited linearly outside of it. Species specificity tests were performed only in nonprimates: mouse and guinea pig skins were nonreactive with NKH-1. NKH-1 seems to recognize a new substance in the sub- basal lamina region (subbasal lamina proteins) which cross-react with elastic fiber microfibrils.

A lupuslike disease with cutaneous manifestations secondary to the use of chlorpromazine (Thorazine) is presented. Skin biopsy specimens demonstrated classic findings consistent with lupus erythematosus and abundant mucin deposition in the cutaneous lesions—a finding not previously reported to occur in drug-induced lupuslike disease. Laboratory and serologic examinations included a positive antinuclear antibody titer, presence of single-stranded deoxyribonucleic acid (DNA), absence of double-stranded DNA, presence of antihistone antibodies, normal complement level, increased IgM level, and prolongation of partial thromboplastin time. These data confirmed our clinical and histologic diagnosis. Cessation of the medication (chlorpromazine) led to resolution of the skin abnormalities. Electron microscopy revealed electrondense drug metabolites in vascular endothelial cells, as well as tubuloreticular inclusion bodies. This is only the second reported case of chlorpromazineinduced lupuslike disease with cutaneous manifestations.

Intercellular spaces of the secretory coil of the human eccrine sweat gland were studied with the lanthanum permeation technique. It was demonstrated that the interstitial connective tissue, basal lamina, lamina lucida, and the basal intercellular spaces were continuously permeated with lanthanum. This route was thought to represent the physiological pathway of the interstitial fluid, i.e., the source of the eccrine sweat. It was postulated that the fluid is absorbed from the basal intercellular spaces into the clear cells and then excreted into the main lumen through a sodium pump. Whereas desmosomes were only occasionally seen in the basal intercellular spaces, the periluminal intercellular spaces had a series of desmosomes and tight junctions. Although some of the more proximally located tight junctions were circumvented, one of the luminal tight junctions stopped the permeation of lanthanum. With the lanthanum method, the luminal tight junctions were shown to be composed of complicated arrays of negatively stained septations and lanthanum-filled spaces. Only a small number of pinocytotic vesicles were seen in the clear cells. It was thought that they do not contribute to the absorption of the intercellular fluid.

The apocrine duct extends from the apocrine secretory segment to the pilosebaceous follicle. Because apocrine glands are limited to a few areas, and even in these areas are few in number, the structure of their ducts has been largely ignored in descriptions of the ultra-structure of the epidermis and its appendages. Charles (1) and Zelickson (2) have briefly described the apocrine duct in their studies which were concerned primarily with the apocrine secretory segment.

One case of solitary Osler's disease with typical clinical and histopathologic pictures was examined with the electrom microscope. Most of the affected (dilated) vessels were identified as small venules in the upper submucosa or dermis. In these venules, flattened endothelial cells were junctioned by a defective overlapping of terminal villi of the extended cytoplasm. Affected venules thus showed many endothelial gaps which were stopped up with thrombi. At the edges of these gaps, intact villi of endothelial cells were present, suggesting that clear-cut separation by slipping of overlapped villous junctions formed the gaps. The lanthanum permeation method showed that the tight junctions exist between these villi. However, lanthanum often leaked into the lumen. Perivascular connective tissue showed many abnormal changes. This was thought to be an important etiologic factor because these small venules lacked other perivascular support, such as pericytes, smooth muscles, and elastic fibers.

This study was undertaken in order to describe the fundamental differences between normal skin and the oral mucosa mainly from the standpoint of keratinization.A brief survey of the literature dealing with the human oral mucosa reveals that Sognnaes and Albright (1,2), Fasske and Themann (3), and Zelickson and Hartmann (4) have done electron microscopic work on the human oral epithelium, Listgarten (5) and Kurahashi and Takuma (6) on the human gingival epithelium, Melcher on the oral connective tissue (7), and Frithiof and Wersall on some organelles (8). Until now, however, no electron microscopic work has been done on the posterior buccal mucosa of the human oral cavity, although the anterior buccal mucosa has been studied by Zelickson and Hartmann (4); and there has been no comparative study of the human mucous membrane with either adult or embryonic human skin.In this study it was found that the normal human posterior buccal mucosa is very similar to the immature embryonic epidermis in all aspects; and that despite a complete lack of keratinization, the plasma membranes of the posterior buccal epithelial cells in upper layers become considerably thicker than those of the lower layers, thus suggesting that this thickening process is a phenomenon independent of keratinization.MATERIALS AND METHODSBiopsy specimens were taken from the normal human buccal mucosa, posterior or lateral to thesecond molar tooth, of ten healthy white men and women between the ages of 17 and 50. Five specimens were obtained from the oral lesions of pemphigus vulgaris, and one from the lesion of stomatitis of the posterior buccal mucosa. All specimens were immediately sliced into small pieces, fixed in 1% osmic acid in veronal buffer (pH 7.2) containing 4.5% sucrose. After fixation for one hour, the tissues were dehydrated through a series of graded alcohols and propylene oxide, and were embedded in Araldite. Thin sections were then cut with an LKB Ultrotome at 400-600 A. The sections were stained first with 1% uranyl acetate in 50% etha-nol, and then, before completely dried, re-stained with lead citrate (9). Some specimens were stained for acid phosphatase before osmic acid fixation using the method of Barka and Anderson (10).RESULTSBasement membrane and basal layer. The basement membrane measured approximately 600 A in thickness. Occasionally, phagocytes, lymphocytes, and leukocytes were seen crossing the basement membrane (Fig. 1). In such areas the subepithelial reticular fibrils were thick, and re-duplication of the basement membrane, as reported by Caulfield and Wilgram in erythema multiforme (11), was observed (Fig. 1). The basal cells here contained fewer tonofilaments than the epidermal basal cells (Fig. 1). Intercellular spaces were rather wide, with numerous slender villi of the basal cells projecting into them (Fig. 1). Some basal melanocytes contained well-developed, rough-surfaced endoplasmic reticulum and were actively producing all gradients of maturation of melanin granules in their melanosomes (Fig. 2). The dendritic processes of these melanocytes, found between the basal cells and squamous cells, contained a greater number of more mature (larger and denser) melanin granules than did the body of the melanocytes. This phenomenon can be explained by assuming that the melanocytes inject their melanin granules into the surrounding cells as soon as the granules reach maturity. The basal cells and the squamous cells contained varying numbers of injected melanin granules (Fig. 2).As the basal cells moved up into the squamous512ULTRASTRUCTURES OF THE BUCCAL MUCOSA513*-i

With the advent of the electron microscope, investigators of elastic fiber have used two major approaches: first, the method of teasing out tissue fragments with or without additional shadow casting technics (replication method) (1-7), and second, that of using tissue sections (8-14). Several workers in each group have shown interest in the elastic tissue of the skin, either normal (2-4, 6, 10), or abnormal (9, 11-13).

Calcifying epithelioma is a rare, solitary tumor which often occurs in young individuals (1), most frequently on the face and the arms (1, 2). Since Malherbe and Chenantais (3) described “calcified epithelioma of sebaceous glands” in 1880, the histogenesis of this tumor has been attributed to various skin appendages such as sebaceous glands (3, 4) and hair (2, 5, 6, 7). Lever and Griesemer (7) regarded the basophilic cells in calcifying epithelioma as primary epithelial germ cells with a tendency to differentiate into keratotic hair cells. Forbis and Helwig (1), in their recent study on 240 specimens, agreed with the opinion of Lever (2) and Lever and Griesemer (7) that calcifying epithelioma arises from primitive cells of the hair matrix. They pointed out that the broad dense transitional zone from basophilic to shadow cells of this tumor, where sulfhydryl groups are abundant, is analogous to the kera-togenous zone of the hair. They also demonstrated that hyalinized shadow cells in some instances show a brilliant birefringence, as does the keratogenous zone of the hair.

As an extension of our histochemical studies of the skin (1, 2), the distribution and activity of cholinesterases were studied in the skin of the rat. The development of cholmesterase activity was followed during the histogenesis of the skin, with special reference to the nerve elements.

Although there have been several electron microscopic studies of human axillary apocrine glands (1, 2, 3, 4) the exact mechanism of apocrine secretion remains an enigma. Hibbs (1) denied true apocrine secretion in normal human axillary apocrine glands because he was unable to find the secretory cells in the process of extruding its contents. In addition, he could not visualize any secretion product within the lumen. He assumed, therefore, that the principal mode of secretion is by droplet formation at the apex of the cell and that secretion by disruption of the cell probably occurs only under extreme conditions, if at all. Montagna (2) suggested that the secretory granules are dissolved in the apical cytoplasm and excreted either by a fragmentation of the luminal microvilli or by oozing out through the plasma membrane. Charles (3) also failed to see cellular debris in the lumen, but did report disruption of the apical membrane through which he thought the contents of the secretory cell had been extruded. Observations similar to Mon-tagna's, e.g., that the secretory granules are dissolved in the apical cytoplasm, were made by Kurosumi et al. (4) ; they further described the formation of expanded apical secretory projections and were inclined to defend the classical decapitation secretion theory. They denied that secretion occurred through fragmentation of the luminal microvilli. The following report will be concerned primarily with the maturation of the apocrine secretory granules and their mechanism of excretion from the cell. A multiplicity of secretory mechanisms of the apocrine glands was found in this investigation, including decapitation secretion.

A glomus tumor of the multiple type was examined by electron microscopy. Except for a single layer of endothelial cells lining the vascular lumen, the remainder of the tumor cells are smooth muscle cells. What have been called “glomus” or “epithelioid” cells in the past are transversely sectioned smooth muscle cells. There is no ultrastructural similarity to the hemangiopericytoma.

Electron microscopic studies were performed on the hair cone and intraepidermal hair canal formation in the scalp and eyebrow skin using 11 Negro embryos of the menstrual ages of 9 to 18 weeks. While most of the previous observations of light microscopists were confirmed, information on several fine structural features was added. (1) The hair cone formation represented the very initial keratinization of the cells of future Henle and Huxley layers. These cells were connected by desmosomes, tight junctions, and intercellular cement. (2) The intraepidermal portion of the hair canal was formed by keratinization and vacuolization of the organized hair canal matrix cells. Lysosome-like dense bodies were present and thought to play a role in self-destruction of the matrix cells. (3) The cellular envelopes of the hair cone cells and of the wall cells of the hair canal became twice as thick as the plasma membranes of their matrix cells. An 80–100 A thick cytoplasmic band, i.e., the newly synthesized marginal band, was found to be responsible for this thickening.

A Negro female infant with recurrent respiratory infections, nodular generalized skinrash, lymphadenopathy, and hepatosplenomegaly was studied from 3 to 34 months of age. Initially she had inadequate delayed immune response, which became normal at 34 months. She had a persistently elevated IgM antibody level. Skin and lymph node biopsies on electron microscopy showed paramyxovirus-like intracytoplasmic inclusions similar to those seen in systemic and discoid lupus erythematosus and in dermatomyositis. The infant and mother did not have clinical or laboratory evidence of systemic lupus erythematosus. The rubella hemagglutination inhibition titers were persistently elevated during the period of follow-up.

Human tonenail cells keratinized by accretion of cytoplasmic filaments and without the formation of keratohyaline granules. Clumping of cytoplasmic filaments first formed prekeratin fibrils which eventually filled the entire cytoplasm and became keratin fibrils. Within some of the prekeratin, and in the majority of the keratin fibrils, filaments measuring 65–75 A showing a central core were observed. Numerous free ribosomes and a number of round, rough-surfaced cisterns of endoplasmic reticulum were present in the keratinizing nail cells. A marginal band formed and was responsible for the doubling of the thickness of the cellular envelope. This was not derived from the material of the membrane-coating granules. The marginal band was protease resistant. The original plasma membrane did not increase in thickness and was observed outside the marginal band.

The various junctions by which cell-to-cell contact is maintained in normal oral mucosa and skin are described. Disruptions of cellular junctions are seen in such disorders as pemphigus and pemphigoid.

Merkel cells identical to those described in the skin were found in the gingival mucosa and in the vermilion border of the lip. They were often clustered in rete ridges but also found individually in the basal layer. Unmyelinated axons (neurites) of presumably a sensory afferent nerve surrounded the basal half of these cells within the epithelium. Occasional desmosomes connected the Merkel cell to the neighboring keratinocytes, but neither desmosomes nor other junctional devices were found between the Merkel cell and the neurite. The Merkel cell is characterized by membrane-surrounded dense granules, measuring between 800 and 2000 A, which seemed to derive from Golgi saccules. Some Merkel cells contained lysosome-like dense bodies and transferred melanosomes.

Animal Material. Twenty-five rats of the Wistar strain were used. Twelve of these were embryos (3 each on the 12th, 14th, 16th and 18th days of gestation), 2 were new-born (the period of gestation varied from 19 to 21 days), 3 were ten-day-old, 3 were fifteen-day-old and 5 were adults. The adult rats weighed approximately 100 g. New-born and older rats were killed by a blow on the neck without anesthesia. Hair was shaved off the back, and skin specimens were taken from there and cut into small square pieces. These pieces were immediately immersed for about five minutes into ice-cold 0.1 M Sorensen's phosphate buffer and then used for frozen sections. (The buffer had a pH of 7.6 for the study of the succinic dehydrogenase system and a pH of 7.4 for the study of the malic and lactic dehydrogenase systems). In embryos, skin was removed from the back while they were still alive. Frozen sections, approximately 20 in thickness, were made from the fresh skin specimens. Histochem feat Demonstration of the Succinic Dehydrogenase System (SDS). Ogawa and Zimmerman's method (7) was employed to demonstrate the succinic dehydrogenase system. As a rule, nitroneotetrazolium chloride (nitro-NT) was used as an electron acceptor. Occasionally, however, nitro-blue tetrazolium (nitro-BT) was used, instead.

Perifollicular nerve endings of the human lanugo hairs have been studied with the electron microscope. The endorgans are arranged in palisade along the periphery of the follicle and are composed of an axon and an enveloping Schwann sheath. Spaces between the endorgan are largely free from collagen and cellular elements. This arrangement of endorgans perpendicular to the follicle may be most efficient to detect the movement of the follicle, and the empty spaces between the organs permit a maximum deformation of the terminal axon. The axon produces a subcytomembrane dense layer at the follicular end but is, with rare exceptions, separated from the external root sheath cells by the basal lamina. The endorgan can attach to any portion of the follicle including the cellular junctions, indicating that there is no specialization on the follicular side at the site of attachment. In fact, half-desmosomes and subbasal dense plaques are regularly seen on the basal surface of the follicular basal cells.

The formation of the intradermal eccrine sweat duct lumen began in the 15-week-old embryo with a dissolution of the desmosomal attachment plaques, followed by the separation of apposing inner cells and subsequent formation of microvilli at the luminal surfaces. The luminal cells possessed numerous microvilli and crypts and a periluminal band of tonofilaments. In the secretory portion of older embryos (22 weeks old), columnar secretory cells extended from the basement membrane to the luminal border. The presence in these secretory cells of microvilli, Golgi elements, mitochondria, small secretory vesicles, dense secretory granules and abundant endoplasmic reticulum, implies that preparation for secretory functioning begins in embryonic life. The pyramidal myoepithelial cells differentiated from the basal cells seen in younger embryo, and rested upon a basement membrane. In the oldest embryo examined (22 weeks) there was as yet neither intercellular canaliculi nor sufficient difference in the amount of glycogen to enable one to distinguish between dark and light secretory cells. Isolated cilia of 9 + 0 type were occasionally found in the luminal cells of the duct and the secretory segment.

1. 1. Electron microscopic studies of two cases of typical benign leukoplakia (oral hyperkeratosis) revealed that basal cells contain an abundance of thick, stranded tonofilaments and RNP particles. 2. 2. The squamous layer was thick, often comprising more than twenty cell layers. Squamous cells, unlike those in normal mucosa,1 were filled with abundant, thick tonofilaments which formed a heavily interwoven network in the cytoplasm. Other cellular organelles were compressed and masked by these tonofilaments. 3. 3. In the upper squamous layer and in the granular layer, RNP particles became aggregated in many foci in the cytoplasm and appeared to produce a dense material. As these aggregations enlarged, the dense material masked individual particles of RNP, and keratohyaline granules were formed. Even in large keratohyaline granules, RNP particles were still distinctly visible at their periphery. 4. 4. In spite of the presence of many layers of horny cells, the keratinization of these cells was still parakeratotic. Parakeratotic cells were characterized by the retention of nuclei, visible bundles of filaments, and the presence of lipid bodies. 5. 5. In the basal layor, melanocytes were actively producing melanin and transferring melanosomes to neighboring cells. Either Langerhans' cells or dense cells (which are similar to dermal histiocytes and Langerhans' cells except for Langerhans' granules) were very often found in the vicinity of the melanocytes.

In 1952 Lutz (1) described a peculiar serpiginous keratotic eruption that was present on the sides of the neck of a 21-year-old man for 8 years. He named the lesion keratosis follicularis serpiginosa. Histologic studies of the keratotic wall showed that it was composed of a cystic structure containing horny lamellae situated just beneath the epidermis and that it appeared to have arisen from the hair follicles. Under the same title, Beening and Ruiter (2) in 1954 described the eruption in a 13-year-old girl who had developed ring-formed and semi-circular lesions on the side and nape of her neck. When first seen 3 years before, these lesions consisted of a number of closely-set hailstone-sized, hard, reddish papules. The summit of each papule revealed a keratotic plug which when removed revealed a deep depression. The center of the rings appeared depigmented but not atrophic. Three years later most of the lesions had undergone involution. Histologic study of specimens removed by biopsy showed a markedly acanthotic epidermis which contained horny lamellae. Serial sections demonstrated that the horny masses penetrated into the cutis in some places. Where they remained in contact with connective tissue, inflammatory infiltrate containing small round cells, histiocytes and occasional giant cells were found. The hyperkeratosis appeared to have a direct relationship to the hair follicle and the cyst formations were apparently connected with the sweat glands. Neither of the aforementioned authors elucidated the true nature of the horny lamellae found in the cysts.

The intercellular spaces of the human eccrine sweat duct were investigated using lanthanum as a tracer. In the coiled and straight portions of the intradermal duct, lanthanum permeated the interstices, basal lamina, lamina lucida, and the basal and luminal intercellular spaces, but was stopped at the luminal ends by the luminal complex of tight junctions. Since there were no tight junctions in the basal intercellular spaces, it was postulated that the reabsorbed precursor fluid of eccrine sweat may be dissipated into the interstices without being reabsorbed into the basal cells. In the keratinized portion of the intraepidermal duct, there was no connection between the luminal intercellular spaces and those of the epidermal cells since the distal tight junctions of the granular cells prevented the permeation of lanthanum.

Recently, morphologic evidence that epidermal Langerhans cells (ELC) undergo a mitotic cycle in normal mouse ear skin has been presented. In the present study, using immunohistochemical staining, we examined the mitotic activity of Thy-1-positive dendritic epidermal cells (Thy-1+DEC) in the normal murine epidermis. A small number of Thy-1+DEC showed round, cleaved, paired, and paired dendritic morphologies, which are identical to those occurring during ELC mitosis. We conclude that normal Thy-1+DEC undergo mitosis within the epidermis to maintain their population in the murine epidermis.

Electron microscopic examination of a verruca vulgaris has revealed the intranuclear inclusion of tonofibrils. Although many intracellular inclusions may be related directly to the virus, nonviral inclusions may also be present.

Milia developed in two patients with different chronic dermatoses after 2 weeks of treatment with clobetasol propionate ointment. Routine histologic and immunohistochem-ical analysis showed the cysts to be of eccrine gland origin.