Biomedical subjects
Publications and source records attributed to M Woodward.
Use of pressure relieving equipment can significantly help prevent the development of pressure sores. Standard setting and audit can determine not only whether patients are being accurately assessed, but whether ward practice fully reflects patients' needs.
Lysine acetyl salicylate [1.8 g t.d.s. (Aspergesic 1,000 sachet)] has been compared to 400-mg ibuprofen tablets t.d.s. in a randomized double-blind trial in patients with rheumatoid arthritis using double-dummy technique. Both drugs proved effective in relieving symptoms. Three patients experienced drug-related side-effects with Aspergesic, and one patient with ibuprofen, that necessitated early discontinuation of treatment. Aspergesic was associated with a greater number of haemoglobin values falling below the normal range than ibuprofen. At the end of the study, eight out of 10 patients who expressed a preference selected Aspergesic for improving mobility whilst 15/24 selected Aspergesic for improving pain.
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Spatial frequency difference thresholds for sinewave gratings near contrast threshold were measured using a two-alternative forced-choice technique, and the threshold frequency differences were plotted as a proportion of standard frequency for standards from 2 to 7 cycles/degree. This function shows reliable local maxima and minima, and these features are more pronounced than they are when stimuli of 30% contrast are used. This result is consistent with the notion that at low contrasts, fewer spatial frequency channels are above threshold in the area of the visual field covered by the stimulus than when the stimulus is at high contrast.
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This electron microscopic study confirms that basal lamina (BL) begins to cap the cut end of the spinal cord 15 days after spinal cord transection. BL is first seen immediately adjacent to reactive glial cells but only when there is collagen in the nearby interstitial space. This finding suggests that collagen may provide a trigger to initiate the production of BL by reactive glia. We found no direct evidence that BL in this injury area impeded the outgrowth of regenerating neurites.
Myofibroblasts were successfully grown in tissue culture from the connective tissue stroma of three human breast adenocarcinomas. These cells had slower growth kinetics than fibroblasts from normal human dermis, as did myofibroblasts from two granulating wounds. Electron microscopy of breast cancer slices and tissue cultures of these specimens confirmed the presence of myofibroblasts in both. In early passages, the specificity of carcinoma-derived myofibroblast growth kinetics is preserved. The exact role of myofibroblasts in breast cancer, whether helping or hindering tumor growth, remains undetermined.
Rat myofibroblasts from granulating wound biopsies (RGW) were successfully cultured and compared in terms of growth and morphology with fibroblasts from uninjured rat dermis (RD). Populations of early passage (P-3) RGW myofibroblasts grew significantly more slowly than RD fibroblasts. Logarithmic growth was nearly the same in late passage (P-30) populations of both cell types. Early passage RGW myofibroblasts were similar to those in vivo, as shown by well-defined microfilament bundles. RD fibroblasts contained less well defined microfilaments. Both late passage RGW myofibroblasts and RD fibroblasts displayed evidence of morphologic dedifferentiation. These data show that morphologic features of myofibroblasts and fibroblasts in vivo are maintained in vitro. Evidence is presented that cultured animal myofibroblasts maintain differentiation in early passage, whereas late passage cells suggest that these differences disappear with time.
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Ulcerated and nonulcerated skin from 5 patients with chronic radiation skin damage was examined using electron microscopy. Noticeable fibroblast disorganization was seen, with swollen and degenerating mitochondria, multiple vacuoles, and dilated irregular rough endoplasmic reticulum. Unusual crystalline inclusions were seen in some fibroblasts. In the ulcerated skin, contractile fibroblasts (myofibroblasts) were seen in 2 of 4 specimens. Stroma showed dense collagen and prominent elastosis. The microvasculature in the radiation-damaged tissue showed occasional lumen occlusion and vacuolization of endothelial cells, without consistent abnormality. These data suggest that permanent damage to fibroblasts or fibroblast stem cells may play an important role in chronic radiation skin ulceration.
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Electron microscopy of a painful fibrotic capsule around a cardiac pacemaker revealed classic myofibroblasts. These contractile fibroblasts share characteristics of both smooth muscle cells and fibroblasts and are thought to be the cellular cause of wound and scar contraction. The occurrence of pain and tenderness around a sterile pacemaker probably indicates contraction of scar tissue as the basis of the symptoms. This scar tissue is similar to that seen around other large inert implants placed in the thoracic tissue.
Skin from 19 facial rhytidectomies performed in patients with chronic solar damage was compared with postauricular skin from patients of similar age. Light microscopy demonstrated large areas of amorphous material that stained PAS positive in all 19 face-lift specimens, while none of the controls had such material. Electron microscopy of the "elastotic" material revealed large amorphous masses of granular material, with loss of the microfilament component of normal elastin. Current theories suggest that the elastotic material in solar-damaged skin is a product of radiation-damaged fibroblasts, rather than being either collagen or degenerated elastin. Such knowledge may help the plastic surgeons encourage rhytidectomy patients to protect themselves from solar radiation.
Chronic radiation skin ulcers were produced in rats with the administration of 5,000 or 8,000 rads. Electron microscopy revealed two phases of damage, the first from seven to 14 weeks and the second from 14 to 54 weeks. In the first phase, significant nuclear and cytoplasmic degeneration was prominent. During the second phase, lysosomes were common along with unusual cytoplasmic inclusions. Myofibroblasts were observed in the second phase only, suggesting that delayed would contraction in radiation ulcers was the result of the delayed onset of myofibroblast development.
Myofibroblast populations in skin scar contracture due to wound contraction and in joint contracture due to passive position were compared in male New Zealand rabbits. Active contraction was produced by removal of full thickness back skin, with healing by contraction and epithelization. Joint contracture was produced by forced knee flexion for nine weeks by means of Steinman pin fixation. Electron microscopy revealed complete absence of myofibroblasts in the contracture due to position in contrast to prominent myofibroblasts in contracted skin scars. Contracture due to position is, thus, due to collagen remodeling alone, without an active contraction process. This suggests that the potential use of drugs for biochemical control of contracture will have to take into account how the contracture formed.
Contractile fibroblasts were sought via electron microscopy in liver tissue from 12 patients with chronic alcoholic cirrhosis, and from 3 noncirrhotic patients. In 9 of the 12 cirrhotic livers, contractile fibroblasts (myofibroblasts) were seen containing the classic features of 60-80 A microfilament bundles with electron-dense bodies along with prominent microtubules. The remaining three cirrhotic liver specimens had fibroblasts containing microfilament bundles but without electron-dense bodies. Myofibroblasts were not found in any of the noncirrhotic livers. Just as in other types of scars, myofibroblasts are probably the active contractile force in the scarring and fibrosis which characterize chronic alcoholic cirrhosis.
Skin necrosis was produced in 24 male Fischer 344 rats by intradermal injection of 0.5 ml of doxorubicin (Adriamycin) at a concentration of 2 mg/ml. The resulting wounds healed slowly over 6 to 7 weeks with the reduced contraction rate paralleling the prolonged morbidity of doxorubicin ulcers in humans. Electron microscopy showed bizarre rough endoplasmic reticulum, double-walled vacuoles, and swollen mitochondria from 1 through 12 weeks after injury. Myofibroblasts with 60- to 80-A microfilaments with electron-dense bodies, intercellular connections, and prominent microtubules were seen from 4 through 12 weeks after injury. Although the appearance of myofibroblasts was delayed, their structure was normal. The delayed contraction of doxorubicin-induced skin ulcers thus appears due to persistent nonspecific cellular damage at the nuclear level rather than to specific derangement of myofibroblast function.