Thyroid carcino-sarcoma in a dog.
Enzymatically isolated osteoarthritic (OA) chondrocytes were cultured in alginate beads in a well defined culture medium for 12 days. The DNA content was measured according to a fluorimetric method and cell proliferation was determined by the incorporation of 3H-thymidine in the newly synthesized DNA. Interleukin 6 (IL-6) and IL-8, stromelysin [matrix metalloproteinase-3 (MMP-3)], and aggrecan (AGG) production were assayed by specific enzyme amplified sensitivity immunoassays, and prostaglandin E2 (PGE2) production by specific radioimmunoassay. All NSAID were tested at the mean peak plasma concentration (Cmax) obtained after oral administration of a therapeutic dose.
To compare the effects of dexamethasone (Dex) and celecoxib (Cel) on F-isoprostane, prostacyclin (PGI2), and thromboxane A2 (TxA2) following hyperoxia, and hyperoxia followed by recovery in room air (RA), newborn rabbits were exposed to hyperoxia (80-100% oxygen) for 4 days, during which they were treated with saline (Sal, i.m.), Dex (i.m.), vehicle (Veh, PO), or Cel (PO, n = 12 per group). Six animals in each group were sacrificed immediately following hyperoxia, and the remainder allowed to recover in RA for 5 days. The control litters were treated simultaneously in RA with all conditions other than atmospheric oxygen being identical. Blood samples were assayed for 8-epi-prostaglandin F2alpha (8-epi-PGF2alpha), 6-keto prostaglandin F1alpha (6-ketoPGF1alpha), and TxB2. Dex and Cel decreased 8-epi-PGF2alpha during hyperoxia and the recovery period. Dex increased 6-ketoPGF2alpha following hyperoxia, while similar increments were noted during recovery with Cel. Although TxB2 was decreased only during the recovery period, TxB2/6-ketoPGF1alpha ratio was lower during hyperoxia and recovery in both treated groups. The effect of Cel on 8-epi-PGF2. and TxA2/PGI2 ratio confirm the formation of a COX-derived F2-isoprostane that is possibly linked to TxA2 receptors. Further studies are required to examine whether Cel can be used as a therapeutic alternative to Dex for oxygen-induced injury in the newborn.
AA-861 treatment decreased fracture-bridging time, significantly increased early callus cartilage (5.6-fold; p < 0.001) and bone formation (4.2-fold; p = 0.015), and significantly increased callus mechanical properties compared with the vehicle-treated rat fractures. Callus cell proliferation rate was increased by AA-861 treatment, compared with vehicle, at day 2 after fracture (3.68% compared with 2.08%; p < 0.001; 95% confidence interval, -2.81 to -0.039) but was reduced by celecoxib treatment at day 4 after fracture (4.22% compared with 1.84%; p < 0.001; 95% confidence interval, 2.27 to 4.07). At day 10 after fracture, AA-861 and celecoxib treatment increased Type-II collagen mRNA levels (16.0-fold and 6.1-fold, respectively; p < 0.001 for both), but only AA-861 treatment caused an increase in Type-X collagen mRNA (6.3-fold; p < 0.001). AA-861 treatment significantly increased cyclooxygenase-2 (4.0-fold at day 10; p < 0.001) and osteopontin mRNA levels (3.6-fold at day 7; p = 0.024), while decreasing 5-lipoxygenase mRNA levels (5.6-fold at day 4; p < 0.001).
A series of 90 rats underwent a duodenoesophageal reflux surgery were divided into 2 groups: the control group was given a commercial chow and the celecoxib group experimental chow containing celecoxib. The animals were sacrificed sequentially every 10 weeks after surgery. In the control group, esophagitis, columnar-lined epithelium (CLE) and adenocarcinoma (ADC) were first observed at the 10th, 20th, and 30th week, respectively, and their incidences sequentially increased and reached 100%, 89% and 47% at the 40th week, respectively. In the celecoxib group, the esophagitis was mild and the incidence of CLE was significantly lower at each week compared with the control group. ADC was not observed in the celecoxib group throughout the experiment. Celecoxib suppressed esophagitis and subsequent CLE and ADC in rats.
COX-2 was detected by immunohistochemistry in both uterine fibroids and uterine smooth muscle, with higher immunoreactivity in uterine fibroids; the positive index of the smooth muscle cells was 11.90 and the positive index of uterine fibroids cells was 46.50 (P<0.05). The expression of COX-2 mRNA in uterine fibroids was higher (0.122±0.062) than in normal smooth muscle tissue (0.025±0.009; P<0.05). Also, the western blot results showed that COX-2 expression was significantly higher in uterine fibroid cases, as compared to the expression in uterine smooth muscle. Immunofluorescence showed that the occurrence of COX-2 was obviously higher in smooth muscle cells of uterine fibroids than in the healthy smooth muscle cells. NS-398 or celecoxib significantly inhibited the proliferation of smooth muscle cells of uterine fibroids, but did not inhibit the proliferation of healthy smooth muscle cells. Accordingly, NS-398 or celecoxib significantly reduced the expression of the downstream metabolite of COX-2, PGE2, in the smooth muscle cells of uterine fibroids, but not in healthy smooth muscle cells.