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Biomedical subjects

J J Van Rybroek

Publications and source records attributed to J J Van Rybroek.

5 recordsLinked to original sources

Congenital angiomatoid malignant fibrous histiocytoma. A light-microscopic, immunopathologic, and electron-microscopic study.

We present a case of a congenital angiomatoid malignant fibrous histiocytoma. This rapidly growing lesion, which was located in the subcutis of the left upper arm, was excised at the age of 8 1/2 months. The patient, a girl, was well and free of disease 10 months after surgical removal of the tumor. The tumor appeared grossly encapsulated. The gray-tan tissue contained cystic spaces filled with recent and organizing hemorrhages. Microscopically, the tumor was composed of solid masses of histiocyte- and fibroblast-like cells, inflammatory infiltrate, and multifocal irregular blood-filled spaces, which were predominantly devoid of endothelial cells. The tumor was studied immunohistochemically with antibodies specific for FVIII-related antigen, S-100 protein, epithelial membrane antigen, vimentin, desmin, alpha-1-antitrypsin, muramidase, laminin, and collagen type IV. Ulex europaeus lectin-I was also utilized. These studies, along with our ultrastructural findings, suggest that: (a) the tumor is composed of a mixture of mesenchymal cells; (b) an imperfect angiogenesis may be taking place, resulting in a wide spectrum of vascular structures; and (c) the cell of origin may be a pluripotent mesenchymal cell.

Blood Vessels↗

Intercellular junctions in the developing arachnoid membrane in the chick.

The arachnoid membrane of chick embryos was prepared for electron microscopic study by means of thin sections and freeze-fracture replicas. Particular attention was given to the relationships among junctional complexes during arachnoid maturation. By 14 days of incubation, the arachnoid had differentiated into morphologically distinct inner and outer zones. Both desmosomes and gap junctions were present among the cells of both layers at this time. Desmosomes were most numerous in the inner arachnoid layer and their structure remained constant. Gap junctions showed a great variation in structure. The large gap junctions contained a particle packing pattern in which rows of intramembranous particles were separated by particle-free zones. Arched gap junctions were also present. Smaller arrays of gap junctions exhibited a variety of configurations on the membrane P-face. The first tight-junctional stands clearly identifiable in freeze-fractured preparations appeared at 15-17 days. These were closely associated with the particles of gap junctions and consisted of single stands on the P-face. By hatching age (21 days) a "mature" pattern of tight-junctional strands was interwoven in several layers. In the interim, more complex arrangements of tight-junctional strands were in intimate relation with gap junctions.

Animals↗

Surface coat material associated with the cells of the developing lens vesicle in the chick embryo.

Ruthenium red (RR) and cetylpyridinium chloride (CPC) were used to demonstrate the distribution of cell surface coat material (SCM) on the free epithelial surface of the developing lens vesicle in stages 14-17 (50-64 hours) chick embryos. Observations were made by light microscopy and transmission. (TEM) and scanning (SEM) electron microscopy. A progressive increase in SCM is observed on cellular apices within the epithelium of the lens vesicle by means of RR staining, particularly at the margins of the aperture which are the sites of presumptive fusion. In contrast, a relatively thin layer of SCM persist on the adjacent surface ectoderm. Ruthenium red-positive SCM extends across the aperture of the lens vesicle prior to initial contact between the advancing epithelial surfaces. The presence of abundant SCM is interpreted as a possible significant prerequisite to invagination and to epithelial adhesion and fusion prior to detachment of the lens from surface ectoderm. When CPC is added to the fixative, a flocculent precipitate over the aperture of the lens vesicle and an associated band of modified surface ectoderm which extends ventrally from its lower margin are observed. The modified ectoderm and associated SCM likely represent a presumptive region of active coordinated cellular migration.

Animals↗

Correlated scanning and transmission electron microscopy of developing lens vesicle in the chick.

Cells within the lens placode undergo transient surface modifications during the course of invagination. At stage 13, cellular apices bulge outward and display decreased surface diameters when compared to adjacent surface ectoderm. The lens vesicle is well invaginated by stage 14. An area of modified cells can be recognized ventral to the lens vesicle aperture. These cells present a smaller surface area and increased pleomorphism. Normal surface ectoderm extends to the dorsal and lateral edges of the aperture. The apical surfaces of cells which line the lumen of the lens vesicle display a complex topography such that individual cell boundaries are not easily distinguished. At stage 17, cellular processes which partially occlude the closing aperture of the lens vesicle may assist in reestablishing ectoderm over the newly formed lens. Preliminary results of cytochalasin B exposure on the invaginating lens vesicle suggest that the contractile action of microfilaments influences the complex cellular topography.

Animals↗

White cell fragmentation after therapeutic leukapheresis for acute leukemia.

A 70-year-old woman with newly diagnosed acute nonlymphocytic leukemia (FAB M5) underwent therapeutic leukapheresis because of a white cell count (WBC) of 144 X 10(9) per I and clinical evidence of leukostasis. A peripheral blood film taken immediately after leukapheresis showed numerous cytoplasmic and nuclear fragments. The patient's clinical course thereafter was significantly compromised by disseminated intravascular coagulation with a severe bleeding diathesis, renal failure, and respiratory failure that led to her death. This case illustrates that therapeutic leukapheresis for elevated WBC in patients with acute leukemia may result in leukocyte fragmentation and possible intravascular coagulation.

Acute Disease↗