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Remobilization does not fully restore immobilization induced articular cartilage atrophy.

The recovery of articular cartilage from immobilization induced atrophy was studied. The right hind limbs of 29-week-old beagle dogs were immobilized for 11 weeks and then remobilized for 50 weeks. Cartilage from the immobilized knee was compared with tissue from age matched control animals. After the immobilization period, uncalcified articular cartilage glycosaminoglycan concentration was reduced by 20% to 23%, the reduction being largest (44%) in the superficial zone. The collagen fibril network showed no significant changes, but the amount of collagen crosslinks was reduced (13.5%) during immobilization. After remobilization, glycosaminoglycan concentration was restored at most sites, except for in the upper parts of uncalcified cartilage in the medial femoral and tibial condyles (9% to 17% less glycosaminoglycans than in controls). The incorporation of 35SO4 was not changed, and remobilization also did not alter the birefringence of collagen fibrils. Remobilization restored the proportion of collagen crosslinks to the control level. The changes induced by joint unloading were reversible at most sites investigated, but full restoration of articular cartilage glycosaminoglycan concentration was not obtained in all sites, even after remobilization for 50 weeks. This suggests that lengthy immobilization of a joint can cause long lasting articular cartilage proteoglycan alterations at the same time as collagen organization remains largely unchanged. Because proteoglycans exert strong influence on the biomechanical properties of cartilage, lengthy immobilization may jeopardize the well being of articular cartilage.

Amino Acids↗

[Clonal proliferation index and its changes in malignant transformation of tissues].

The microspectrometric investigation used 5- and 8 microns-thick histological specimens, stained after Feulgen, and the following equipment: scanning integrating microspectrophotometer (1,080); TV-image analyzer (70). Interphase nuclei of normal growth tissue, mild and moderate dysplasia, atypical proliferation and carcinoma were investigated using bioptical material from the larynx, cervix uteri, endometrium, stomach, large bowel, prostate and breast. The weighted mean index of DNA accumulation in nuclei as well as the "index of clonal proliferation" (ICP)--ratio of average DNA index for carcinogenesis stage in question and normal tissue index--suggested by the author, were measured. Malignant transformation was characterized by the following ICP values: mild and moderate dysplasia--less than 1.4; intraepithelial neoplasia--2.2 and carcinoma and adenocarcinoma--3.3 and higher. Microspectrophotometric analysis of Feulgen-DNA yields reliable data on ICP in malignant tissue which can be used for clinical purposes in treatment and prognosis of malignant disease.

Carcinoma↗

Deuterium oxide (heavy water) arrests the cell cycle of PtK2 cells during interphase.

Deuterium oxide (D2O, heavy water) exerts an antiproliferative effect on a variety of cells in vitro and on some organisms. This effect is mainly ascribed to a tubulin-mediated antimitotic action. We evaluated the morphology, the mitotic activity, and the dynamics of the cell cycle of PtK2 cells grown in vitro in the presence of 75% D2O for up to eight weeks by microspectrophotometric DNA measurements as well as flow cytometric analysis and a determination of mitotic indices. Substitution of heavy water for water in the culture medium initially increased the mitotic index by a (pro-) metaphase block but after 2 to 3 days of incubation no mitotic figures were seen. Analysis of cells grown for 6 days in medium containing 75% D2O revealed accumulation of cells in S/G2-phase. Extended treatment stabilized the high level of cells in this specific phase, when compared to normal growing cells. Cells grown for 1 to 6 weeks in the presence of D2O remained non-proliferating, nevertheless, they were able to divide again after recovery in non-deuterated medium. The time needed for resumption of the mitotic activity was proportional to the duration of deuterium oxide exposure. Cells incubated for 8 weeks in 75% D2O did not recommence mitotic activity. Light and electron microscopic examination revealed characteristic morphological changes of size and ciliation in PtK2 cells subjected to prolonged deuteration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Histamine H1 receptor-mediated Ca2+ signaling in cultured bovine corneal endothelial cells.

The corneal endothelium pumps ions and water from the stroma to the aqueous humor, maintaining corneal transparency. This report investigates the possibility that cultured corneal endothelial cells express neurohormonal Ca2+ signaling pathways employed by other epithelia to regulate transport or other cellular functions. Agonist-stimulated changes in intracellular calcium ([Ca2+]i) in single bovine corneal endothelial cells (BCEC) derived from confluent cultures were measured by microspectrofluorimetry using the Ca(2+)-sensitive probe, fura 2. Mean resting [Ca2+]i in BCEC was 46 +/- 2 nM (n = 124). The muscarinic cholinergic agonist, carbachol, did not mobilize Ca2+, whereas histamine induced a rapid increase in [Ca2+]i to initial peak levels of 549 +/- 22 nM (n = 46) at maximally stimulating doses. The initial rise in [Ca2+]i in response to histamine was dose dependent, with a minimum effective dose of 50 nM, EC50 = 0.84 mumol/l, and a maximum effective dose of 10 mumol/l. [Ca2+]i decreased from the initial peak, but then stabilized to form an agonist-dependent sustained elevation or abruptly fell back to baseline to begin oscillatory fluctuations. The initial peak was insensitive to removal of extracellular calcium (Ca2+o), whereas subsequent elevations in [Ca2+]i or sustained [Ca2+]i oscillations required Ca2+o. The amplitude of the oscillations in [Ca2+]i increased with an increase in [histamine]. However, frequency was independent of [histamine] (mean = 0.62 spikes min-1 +/- 0.06, n = 33). Histamine-induced Ca2+ mobilization was inhibited by the H1 receptor antagonist triprolidine, but was unaffected by ranitidine (H2 antagonist) or thioperamide (H3 antagonist).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of light activation method on flexural properties of dental composites.

PURPOSE: To determine if irradiating composites in a laboratory tungsten-halogen light-curing unit produced equal flexural properties to stepwise hand-curing with a tungsten-halogen lamp. METHODS: Bars (n = 10) of nine commercial composites were formed by light-curing in square glass tubes (2 x 2 x 25 mm). Flexure strength (FS, MPa) and flexure modulus (FM, GPa) were tested in three-point bending after aging specimens in water at 37 degrees C for 1 day. Two methods were used to irradiate the composites: a) Triad II (Dentsply) using 40-second exposures from top and bottom; and b) Optilux 400 (Demetron; 600 mW/cm2) using 3 x 40 seconds overlapping exposures from the top only. Filler wt% was determined by thermal gravimetric analysis. The degree of conversion (DC) of each composite cured with the two techniques was evaluated by micro-FTIR. T-tests were performed for FS and FM to compare Triad II vs Optilux for each composite (alpha < 0.05). RESULTS: There was a trend for Optilux to produce greater FS (significant for A110, Herculite and P60) and FM (significant for all but Clearfil, Esthet-X and Z250), but differences averaged less than 10%. There was no difference in DC between the irradiation modes for any composite.

Acrylic Resins↗