[Determination of the size of bladder-neck adenoma using ultrasonics].
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Biomedical subjects
Publications and source records attributed to M Sobel.
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Laminin, a major basement membrane component, arrested the migration of MCF-7/AZ human breast adenocarcinoma cells that were not invasive in vitro. Migration of invasive MCF-7/6 cells was not affected by laminin. Both cell types expressed the 67 kD laminin receptor, at both mRNA and protein level, but did not express the alpha 6 subunit of the VLA-6 integrin-type laminin receptor. The presence of YIGSR peptides (100 micrograms/ml), reported to block the interaction between laminin and its 67 kD receptor, did not change the migratory response of MCF-7/AZ or MCF-7/6 cells when meeting laminin lanes. In addition, the migration of these cell types was not affected by the presence of 17-beta-estradiol (10(-6) M) or all-trans retinoic acid (10(-6) M), which were both reported to increase the number of 67 kD receptors. We could therefore not assign an involvement of the 67 kD receptors in migration of MCF-7 cells on laminin, nor did we find evidence that conditioned medium of MCF-7/6 cells contains factors that are able to initiate migration of MCF-7/AZ cells on laminin.
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The microvascular anatomy of the sesamoid complex was investigated in 15 cadaver specimens using histology and tissue clearing (Spalteholz) techniques. It was found that both sesamoids appeared equally well vascularized and the vascular supply to each sesamoid originated from two major sources (proximal and plantar) and one minor source (distal). Proximally, vessels originating from the first plantar metatarsal artery enter the sesamoid at its attachment to the flexor hallucis brevis. In addition, vessels enter the plantar surface of the sesamoid near the midline and arborize throughout the bone, anastamosing with the proximal vessels. The distal vascular supply to the sesamoids originates from its distal capsular attachment and appears to contribute minimally to the overall vascular scheme. The lateral attachments of the sesamoids to the plantar plate and joint capsule were relatively avascular. In two bipartite specimens examined, the major blood supply originated from the proximal and distal poles of the sesamoid. No vessels were observed entering the plantar surface of these specimens. The results of this study suggest that injury to the proximal or plantar aspects of the sesamoids could disrupt the vascular supply to these bones. These areas should, therefore, be avoided during the surgical approach to the sesamoids.
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The role of the competent superior peroneal retinaculum (SPR) as a primary restraint to peroneal tendon subluxation and mechanical attritional wear is clear. Injury to the SPR has classically been described as a dorsiflexion eversion movement of the ankle coupled with a forceful peroneal tendon reflex contraction. This mechanism, however, does not cause injury to the lateral collateral ligaments of the ankle and does not explain the coexistent findings of lateral ankle instability, laxity of the SPR, and concurrent peroneal tendon pathology. Anatomic studies reveal a parallel alignment of the calcaneal band of the SPR and the calcaneofibular ligament. A cadaveric model of ankle instability created by serial sectioning of the lateral collateral ligaments revealed increasing visual strain on the SPR with increasing degrees of ankle instability. These findings suggest the SPR serves as a secondary restraint to ankle inversion stress and that the force or forces that result in chronic ankle instability can also injure and attenuate the superior peroneal retinaculum.