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Subsequent Repair (subsequent + repair)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Recurrent Clear Cell Hidradenoma of the Foot

DERMATOLOGIC SURGERY, Issue 7 2000
Ryan Will BA
Background. Clear cell hidradenoma is an uncommon neoplasm without established optimal treatment. Objective. Using Mohs micrographic surgery, a recurrent clear cell hidradenoma of the right foot was treated. Methods. Case report and literature review. Results. Two stages of Mohs micrographic surgery and subsequent repair successfully treated the recurrent clear cell hidradenoma. No recurrence of the neoplasm has been observed at 11 months follow-up. Conclusion Optimal treatment of clear cell hidradenoma is unestablished. Adequate primary local excision is essential. Mohs micrographic surgery should be considered for treatment, especially on recurrent tumors in critical locations. [source]

Anti-disialosyl antibodies mediate selective neuronal or Schwann cell injury at mouse neuromuscular junctions

GLIA, Issue 3 2005
Susan K. Halstead
Abstract The human paralytic neuropathy, Miller Fisher syndrome (MFS) is associated with autoantibodies specific for disialosyl epitopes on gangliosides GQ1b, GT1a, and GD3. Since these gangliosides are enriched in synaptic membranes, anti-ganglioside antibodies may target neuromuscular junctions (NMJs), thereby contributing to disease symptoms. We have shown previously that at murine NMJs, anti-disialosyl antibodies induce an ,-latrotoxin-like effect, electrophysiologically characterized by transient massive increase of spontaneous neurotransmitter release followed by block of evoked release, resulting in paralysis of the muscle preparation. Morphologically, motor nerve terminal damage, as well as perisynaptic Schwann cell (pSC) death is observed. The relative contributions of neuronal and pSC injury to the paralytic effect and subsequent repair are unknown. In this study, we have examined the ability of subsets of anti-disialosyl antibodies to discriminate between the neuronal and glial elements of the NMJ and thereby induce either neuronal injury or pSC death. Most antibodies reactive with GD3 induced pSC death, whereas antibody reactivity with GT1a correlated with the extent of nerve terminal injury. Motor nerve terminal injury resulted in massive uncontrolled exocytosis with paralysis. However, pSC ablation induced no acute (within 1 h) electrophysiological or morphological changes to the underlying nerve terminal. These data suggest that at mammalian NMJs, acute pSC injury or ablation has no major deleterious influence on synapse function. Our studies provide evidence for highly selective targeting of mammalian NMJ membranes, based on ganglioside composition, that can be exploited for examining axonal,glial interactions both in disease states and in normal NMJ homeostasis. © 2005 Wiley-Liss, Inc. [source]

Recovery of touch after median nerve lesion and subsequent repair

MICROSURGERY, Issue 1 2003
M.F. Meek M.D., Ph.D.
Many techniques have been developed for the evaluation of peripheral nerve function. Consequently, physicians use different techniques in the clinic. This study describes the evaluation of touch after median nerve lesions in the forearm and repair. In order to evaluate touch, 25 patients, aged 11,51 years (mean, 29 years), were evaluated 3,10.5 years (mean, 5 years) after median nerve repair. The evaluation included the moving two-point discrimination test and Semmes-Weinstein monofilaments. We showed that 32% good,excellent results can be obtained with difficult nerve lesions. The results could have been improved if a sensory reeducation regime had been applied. © 2003 Wiley-Liss, Inc. MICROSURGERY 23:2,5 2003 [source]

The accumulation of intracellular ITEGE and DIPEN neoepitopes in bovine articular chondrocytes is mediated by CD44 internalization of hyaluronan

ARTHRITIS & RHEUMATISM, Issue 2 2006
Jennifer J. Embry Flory
Objective A dramatic loss of aggrecan proteoglycan from cartilage is associated with osteoarthritis. The fate of residual G1 domains of aggrecan is unknown, but inefficient turnover of these domains may impede subsequent repair and retention of newly synthesized aggrecan. Thus, the objective of this study was to determine whether ITEGE- and DIPEN-containing G1 domains, generated in situ, are internalized by articular chondrocytes, and whether these events are dependent on hyaluronan (HA) and its receptor, CD44. Methods ITEGE and DIPEN neoepitopes were detected by immunofluorescence staining of bovine articular cartilage chondrocytes treated with or without interleukin-1, (IL-1,). Additionally, purified ITEGE- or DIPEN-containing G1 domains were aggregated with HA and then added to articular chondrocytes, articular chondrocytes transfected with CD44,67, or COS-7 cells transfected with or without full-length CD44. Internalized epitopes were distinguished by their resistance to extensive trypsinization of the cell surface. Results Both ITEGE and DIPEN were visualized within the extracellular cell-associated matrix of chondrocytes as well as within intracellular vesicles. Following trypsinization, the intracellular accumulation of both epitopes was clearly visible. IL-1 treatment increased extracellular as well as intracellular ITEGE epitope accumulation. Once internalized, the ITEGE neoepitope became localized within the nucleus and displayed little colocalization with HA, DIPEN, or other G1 domain epitopes. The internalization of both ITEGE and DIPEN G1 domains was dependent on the presence of HA and CD44. Conclusion One important mechanism for the elimination of residual G1 domains following extracellular degradation of aggrecan is CD44-mediated co-internalization with HA. [source]