Immunolocalization studies of rheumatoid tissues employing specific synovial collagenase antibody have demonstrated immunoreactive enzyme at the cartilage/pannus junction. Collagenase was not detected in chondrocytes or the cartilage matrix remote from the resorbing front, and relatively little enzyme was observed in the hypertrophied synovial membrane itself. These observations directly support the idea that synovial collagenase participates in cartilage erosion in rheumatoid arthritis.

Antibodies↗

PubMedDate not supplied

Host-mediated effectors of tumor invasion: role of mast cells in matrix degradation.

The role of collagenolytic enzymes in tumor invasion and metastasis has been emphasized, but the source of enzyme activity has remained unclear. Degradation of stromal connective tissue is a common feature of invasive neoplasia, and host-tumor cell interactions are probably important for localized collagenolysis. We have examined the role of mast cells in malignant cell invasion using cells derived from the rat mammary adenocarcinoma 13762NF. Histologic studies have shown increased numbers of mast cells at the zone of tumor invasion. Mast cell products and conditioned medium from such cells stimulated the production of collagenolytic enzymes by stromal fibroblasts as well as certain subpopulations of tumor cells in vitro. The tumor cell response to mast cell-mediated stimulation of collagenolysis appears to be related to the metastatic potential of the tumor cell. A subpopulation of host fibroblasts derived from the invading tumor zone was also found to be more responsive to mast cell factors than normal fibroblasts, as judged by collagenase production. Thus the mast cell has the potential to induce collagenolytic activity from both host fibroblasts and tumor cells.

Adenocarcinoma↗

PubMedDate not supplied

Hippocampal potentials evoked by stimulation of olfactory basal forebrain and lateral septum in the rat.

Electrophysiological characteristics of olfactory-hippocampal relations were examined because recent anatomical studies have described a substantial olfactory input to the hippocampus via the entorhinal cortex. Potentials evoked in the dorsal hippocampus of anesthetized rats by stimulation of the prepyriform cortex, pyriform cortex, diagonal band, lateral olfactory tract, anterior commissure, olfactory tubercle and anterior olfactory nucleus had similar characteristics, although latencies differed. For example, latencies were twice as long after stimulation of the obliquely oriented portion of the diagonal band than after stimulation of the prepyriform cortex. A relatively low-amplitude, initially negative wave was recorded in the subiculum, CA1 and CA2, and a relatively high-amplitude, initially positive wave was recorded in CA4 and the dentate gyrus. In CA3 negative potentials were observed at dorsal recording sites and positive potentials were recorded at more ventral sites. Peak latencies were usually two to four msec shorter for the negative than for the positive wave. Laminar distributions of responses evoked in the hippocampus by stimulation of the prepyriform cortex and diagonal band were evaluated by driving eight electrodes mounted on one carrier through the brain and were found to be strikingly similar. Maximal amplitudes of the negative wave were recorded at the level of stratum moleculare of CA1 and the subiculum, and peak amplitudes of the positive wave were associated with the hilus of the dentae gyrus. Transition from negative to positive waveforms occurred approximately at the hippocampal fissure. Although the negative and positive waves were usually elicited together, they also were separable in that only negative waves were recorded along some tracks and only positive waves along others. Also, various stimulation sites in the prepyriform cortex elicited stable high-amplitude positive waves accompanied by negative waves of varying amplitude. It is suggested that branches of the perforant path are involved in generation of the two waves and that activity in a number of olfactory structures may influence the hippocampus, probably via the perforant pathway. Thus, hippocampal potentials following prepyriform or diagnonal band stimulation were not abolished by transection of the fornix-fimbria. Dorsolateral septal stimulation evoked hippocampal responses with characteristics and distribution distinctly different from those evoked by stimulation of olfactory areas. The findings suggest that lateral septal stimulation may activate the hippocampus antidromically.

Animals↗

PubMedDate not supplied

Bronchial cartilage atrophy in chronic bronchitis: observations on chondrolytic processes.

The status of bronchial cartilage degeneration in chronic bronchitis is unclear, and little is known about the chondrolytic mechanisms involved. The potential contributions of various inflammatory cells, chondrocytes and cartilage-degrading enzymes to cartilage atrophy have been examined. Bronchial cartilage specimens were obtained at autopsy from lobar secondary bronchi from chronic bronchitics and age-matched controls; each was examined by light microscopy and immunohistology for the distributions of mast cells, macrophages, eosinophils, collagenase 1, collagenase 3, and degradation products of cartilage collagen. Most bronchitic specimens showed hypertrophic chondrocytes, some of which were immunostained for collagenase 3, and occasionally for collagenase 1. Evidence for collagen degradation products was demonstrated around the lacunae of a proportion of chondrocytes, and both collagenases were also observed in the soft inflammatory tissues in close association with the cartilage surface, together with variable distributions of mast cells and macrophages. Such observations were generally absent or very much reduced in the control, non-bronchitic specimens. Degenerative changes, atrophy and loss of bronchial cartilage were common features of most chronic bronchitic specimens, this usually being related to intrinsic changes in the chondrocyte phenotype, including proliferative and matrix-degrading properties. Mast cells and macrophages were often observed in close association with the bronchial cartilage, suggesting that inflammatory cells may also contribute to the mechanisms of bronchial cartilage degradation and loss. These observations of bronchial cartilage degeneration were generally lacking in age-matched non-bronchitic control specimens.

Atrophy↗

PubMedDate not supplied

Functional and morphologic development of brain and other organs of rats at high altitude.

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Acetylcholinesterase↗