Lectin-binding affinities of human breast tumors.

Paraffin-embedded sections from a variety of breast lesions were stained with a number of lectins labeled with fluorescein isothiocyanate and examined by fluorescence microscopy: 95 non-neoplastic tissues and 69 malignant tumors were examined. Lectin binding was demonstrated in all malignant tumors, the fluorescence being confined to the plasma membrane of the tumor cells. Normal and hyperplastic tissues either failed to stain or showed a grossly diminished level of fluorescence. The significance of the staining reaction is discussed.

Histochemical studies of experimental fetal intestinal obstruction.

Experimental intestinal atresia can be produced by mesenteric disruption in fetal lambs. In previous reports, a detailed histochemical study of the bowel in this atresia model demonstrated: (1) hyperplasia of ganglion cells in the dilated proximal segment, (2) involutional changes in the area of maximal distension, (3) decreased to absent adenosine triphosphatase (ATP-ase) production in the area of the atresia, (4) gradual increase of ATP-ase production to normal proximally, and (5) greater reduction of ATP-ase production along the antimesenteric border compared to the mesenteric border. In the present study, a model of fetal intestinal obstruction by simple ligation of the bowel has been created to observe the effects of pure obstruction of the lumen of the fetal bowel without the possible ischemic effects of any vascular interruption. Studies with this model reveal: (1) hyperplasia of ganglion cells in the dilated proximal segment, and (2) decreased ATP-ase production proximal to the obstruction, but (3) no involutional changes in the area of maximal distension. These findings show a pattern of disturbance of bowel morphology and function caused by obstruction of the fetal bowel that is similar to but less severe than that seen with intestinal atresia.

Fluorescein-concanavalin A conjugates distinguish between normal and malignant human cells: a preliminary report.

A method is described for using a fluorescein isothiocyanate concanavalin A conjugate to stain human cell membranes in formalin fixed paraffin embedded tissue. 57 neoplastic and normal tissue sites were examined. In 54 malignant tumours, bright green fluorescence was confined to the cell membranes while in 23 benign tumours and normal tissue sites, the membranes were unstained or showed a diminished level of fluorescence. The distinction between malignant and hyperplastic or normal cells was clear cut and definite.

Lectin-binding affinities of human epidermal tumors and related conditions.

Paraffin-embedded sections from a variety of epidermal lesions were stained with fluorescein isothiocyanate-labeled concanavalin A and examined by a fluorescence microscope. Seventy-six normal, hyperplastic, and neoplastic tissues were examined. Lectin binding was demonstrated in all malignant tumors, the fluorescence being confined to the plasma membrane of the tumor cells. Normal and hyperplastic tissues either failed to stain or showed a grossly diminished level of fluorescence. The distinction between malignant and normal of hyperplastic cells was clear-cut and definite.

Pathogenesis of vascular injury in rejecting rat renal allografts.

Unmodified rejection of rat renal allografts was characterized by the early onset and rapid progression of endothelial damage in venules and capillaries which culminated in ischemic cortical necrosis. This pattern of endothelial injury correlated with lymphocyte accumulation in vascular lumens and could not be duplicated by renal perfusion with alloantibodies or prevented by C'3 depletion. In contrast, endothelial integrity and normal graft function were maintained over study intervals extending to 200 days when Brown Norway (BN) rat kidneys were transplanted into Lewis (Le) rat kidney recipients subjected to neonatal thymectomy or lymph drainage. Vascular lesions occurred when syngeneic thoracic duct lymphocytes were transfused into these recipients, but irreversible endothelial injury could be prevented by simultaneous injections of immune plasma. These findings indicate that the destruction of donor endothelium is mediated by thymus-dependent immune mechanisms which can be altered by thoracic duct drainage to promote indefinite survival of renal allografts across major histocompatibility loci.

Specialized structure and metabolic activities of high endothelial venules in rat lymphatic tissues.

Microscopic, histochemical and ultrastructural techniques were used to define characteristics of high endothelial venules (HEV) in rat lymphatic tissues. This endothelium contained acetyl esterase and acid hydrolase activities which were not altered by lymphocyte depletion. No immunoglobulins were detected on luminal surfaces of HEV by fluorescent antibody staining. Only minor structural differences were seen between HEV within lymph nodes and Peyer's patches. At both sites, high endothelial cells were linked together by macular junctional complexes and interlocking basal foot processes. Endothelial cell cytoplasm moulded about surfaces of lymphocytes migrating through the venular wall, and flocculant deposits of basement membrane formed over lymphocytes penetrating the basal lamina. The endothelium was ensheathed by three to five layers of overlapping reticular cell plates and connective tissue. Each plate was linked to the reticular meshwork of the node by collagen bundles and anchoring filaments which inserted into the plate's external limiting membrane. This permitted individual paltes to separate or approximate each other as tissue and intravascular pressure varied, and lymphocytes moved across the sheath by insinuating themselves into gaps between overlapping plates. This composite structure of the HEV wall appeared to facilitate lymphocyte entry into the node and minimized vascular leakge.

Microvascular changes in lymph nodes draining skin allografts.

Histological, histochemical, ultrastructural, and radiolabeling characteristics of the microvasculature in regional nodes draining skin allograft sites are described. From 12 to 48 hours after grafting, these nodes show increased vascular permeability and altered lymphocyte traffic pattern. The rapid rise in lymphocyte migration indices and the apparent plugging of intermediate sinuses by lymphocytes suggest that both increased entry and decreased egress of recirculating cells contribute in "lymphocyte trapping." This is followed by redistribution of cortical capillary arcades as existing germinal centers dissolve and proliferating lymphocytes infiltrate the cortex. Normal microvascular patterns reappeared at 7 to 14 days as primary and secondary nodules form in the enlarged nodes. Increased length and arborization of high endothelial venules resulted from focal proliferation of endothelial cells in transition zones from high to low endothelium. In stimulated nodes, high endothelial cells exhibit increased cytoplasmic basophilia and acid hydrolase activities which correlate with the appearance of numerous polyribosomes, RER cisternae, and lysosomes in their cytoplasm. These "activated" endothelial cells phagocytose microthrombi within venular lumens.

Experimental papillary necrosis of the kidney. 3. Effects of reserpine and other pharmacologic agents on the lesion.

Reserpine is able to exert a pronounced inhibitory effect on the development of papillary necrosis following the administration of bromoethylamine hydrobromide to the rat. This inhibitory effect has been observed using light microscopy, histochemistry, indigo carmine excretion and urine output. These observations suggest that vasoconstriction may play a significant role in the pathogenesis of papillary necrosis, but the evidence for this is incomplete.

Experimental papillary necrosis of the kidney. II. Electron microscopic and histochemical studies.

Renal papillary necrosis was induced in rats by bromoethylamine hydrobromide and studied electron microscopically and histochemically. Morphologic changes appear to develop in vessels and tubules simultaneously, rather than tubular lesions preceding and leading to vascular lesions, or vice versa. Abnormalities are recognized as early as 3 hours, but platelets do not make their appearance until 12 hours, eliminating primary vascular thrombosis as the source of papillary injury.

Experimental papillary necrosis of the kidney. I. Morphologic and functional data.

Papillary necrosis was produced in rats by a single intravenous injection of bromoethylamine hydrobromide (BEA). The earliest changes as seen by light microscopy were necroses of the limbs of Henle and eosinophilic droplets in collecting ducts. Complete necrosis of the papilla took place between 4 and 7 days and the dead papilla was usually sequestered completely by 21 days. Cortical changes occurred secondary to papillary necrosis. Tubular atrophy and loss was greatest in the deeper parts of the central cortex, the more superficial nephrons frequently being spared. The perihilar cortex was the least involved. This distribution was considered to be related to the respective lengths of the limbs of Henle, nephrons with limbs extending into the papilla being those undergoing change. Increased urine output occurred during the first day and continued thereafter. There was a profound defect in concentrating ability.