Extracorporeal shock wave therapy for calcifying tendinitis of the shoulder.

We prospectively studied extracorporeal shock wave therapy (ESWT) for calcific tendinitis of the shoulder in 46 consecutive patients. All patients were randomly divided into 2 groups: treatment and control. The 33 patients in the treatment group received 2 courses of ESWT at the energy density of 0.55 mJ/mm(2) (1000 impulses). The control group underwent sham treatment with a dummy electrode (13 patients). Evaluation included the Constant score, pain scale, and radiographs. The ESWT results were good to excellent in 87.9% of shoulders (29/33) and fair in 12.1% (4/33), and the control results were fair in 69.2% (9/13) and poor in 30.1% (4/13). Among ESWT patients, calcium deposits were completely eliminated in 7 cases (21.2%), partially eliminated in 11 (36.3%), and unchanged in 15 (45.4%). In contrast, elimination was partial in 2 control patients (15.3%) and unchanged in 11 (84.7%). There was no significant difference between Gärtner type I and type II groups in the Constant score (P > .05). ESWT shows promise for pain relief and functional restoration of calcific tendinitis with negligible complications.

Soft-tissue osteoma of the hand: case report.

A soft-tissue osteoma is rare. Only 1 previous case involving the hand has been published. We report a 66-year-old man with a soft-tissue osteoma of the palm that was treated by marginal excision.

A modified cell culture method for autologous chondrocyte transplantation.

Autologous chondrocyte transplantation (ACT) is a promising method to treat chondral and osteochondral defects. This study introduced a modified method for cell culture in ACT. Porcine chondrocytes were cultured for 3 weeks under low hydrostatic pressure at 250 Pa. The results showed that the dry weight of the cartilage-like membrane in the loading group was 3.0 times more than the control group (no loading) (p < 0.01), and cell numbers were significantly increased by 3.1 times (p < 0.01) after a 3-week culture. Compared with the fresh tissue sample, the mRNA expression of collagen II was not statistically different and the mRNA of aggrecan was only slightly decreased by 19%. These data suggest that the hydrostatic pressure at this level significantly increased the cell numbers and biosynthesis of cultured chondrocytes.

Effects of ellagic acid by oral administration on distribution and metabolism of 2-aminofluorene in Sprague-Dawley rats.

The effects of ellagic acid on the in vivo N-acetylation and metabolism of 2-aminofluorene (2-AF) were investigated in bladder, blood, colon, kidney, liver, feces and urine samples from male Sprague-Dawley rats. Major metabolites such as 1-OH-2-AAF, 8-OH-2-AAF and 9-OH-2-AAF were found in bladder tissues, 1-OH-2-AAF, 5-OH-2-AAF and 8-OH-2-AAF were found in blood samples, 1-OH-2-AAF, 3-OH-2-AAF, 5-OH-2-AAF, 8-OH-2-AAF and 9-OH-2-AAF were found in colon tissues, 1-OH-2-AAF, 3-OH-2-AAF and 9-OH-2-AAF were found in kidney tissues, 1-OH-2-AAF, 3-OH-2-AAF and 8-OH-2-AAF were found in liver tissues, 1-OH-2-AAF, 3-OH-2-AAF, 5-OH-2-AAF and 8-OH-2-AAF were found in feces samples and 1-OH-2-AAF, 3-OH-2-AAF, 5-OH-2-AAF and 8-OH-2-AAF were also found in urine samples after rats had been orally treated with 2-AF (50 mg/kg) for 24 h. Pretreatment of male rats with ellagic acid (10 mg/kg) 24 h prior to the administration of 2-AF (50 mg/kg) resulted in absence of 8-OH-2-AAF in bladder tissues, and there were significant decreases of 8-OH-2-AAF in blood and urine samples. In blood samples, amounts of 2-AAF and 8-OH-2-AAF were significantly decreased; in colon tissues, amounts of 2-AF, 1-OH-2-AAF and 3-OH-2-AAF, in liver tissues, amounts of 2-AAF, 1-OH-2-AAF and 3-OH-2-AAF, and in urine samples, amounts of 2-AF and 8-OH-2-AAF were significantly decreased in 24-h ellagic acid (EA)-treated rats before 2-AF was added to the diet. However, significantly increased 1-OH-2-AAF concentrations were found in urine samples in 24-h EA-treated rats before 2-AF was administered. In the EA and 2-AF rats, in the same time treated groups, bladder, colon and liver tissues, and feces and urine samples showed significant differences when compared to the ones without EA co-treatment. We saw significant decreases of the amounts of 2-AF and 1-OH-2-AAF in colon tissues. The feces samples showed increased amounts of 2-AAF in EA- and in 2-AF- treated rats in the same time groups, but urine samples showed a decreased amount of 8-OH-2-AAF in both EA-treated groups. The total amounts of 2-AF metabolites in bladder, blood, kidney and liver tissues showed significant difference between control and the group which was EA-treated 24 h before 2-AF was added. The total amounts of 2-AF metabolites in the liver, feces and urine showed significant decreases between control and EA-treated at the same time with 2-AF groups. This is the first report of EA affecting the N-acetylation and metabolism of 2-AF in rat tissues in vivo.

The combined regulation of estrogen and cyclic tension on fibroblast biosynthesis derived from anterior cruciate ligament.

Female athletes are two to eight times more likely to suffer a knee or ankle ligament injury than male athletes, and sex hormones have been considered to play an important role in the injury. Because ligaments are always under mechanical loading during sports, mechanical force is also a critical factor in ligament injuries. In this study, the effects of estrogen and mechanical loading on the gene expression of three major components of ligament--collagen type I, type III, and biglycan--in primary cultured porcine anterior cruciate ligament (ACL) fibroblasts were investigated individually and collectively using reverse transcript-polymerase chain reaction (RT-PCR). The results revealed that cyclic tensile loading alone increased the messenger RNA expression of collagen I but did not affect that of collagen III and biglycan, and estrogen alone increased the gene expression of collagen I and III but not of biglycan. However, combined administration of estrogen and cyclic loading inhibited the mRNA expression of all the three genes. These results suggested that the inhibition of the gene expression of major extracellular matrix component molecules caused by the combined effects of estrogen and mechanical loading, unique to females, might be responsible for the increased incidence of ligaments injury in female athletes.

Tensile forces attenuate estrogen-stimulated collagen synthesis in the ACL.

The purpose of this study was to examine whether mechanical tensile forces affect estrogen regulation of collagen synthesis of anterior cruciate ligament fibroblasts at the mRNA level. Estrogen was studied at three physiologic levels, 10(-11), 10(-10), and 10(-9)M. The results revealed that estrogen alone stimulated Type I and III collagen synthesis at the mRNA level, and application of mechanical force decreased the expression of collagen Type I and III genes at all tested estrogen levels. These findings suggest that estrogen may directly regulate ligament structure and function by alteration of Type I and III collagen synthesis. This regulation is dependent on mechanical loading.

PCR and flow cytometric analysis of paclitaxel-inhibited arylamine N-acetyltransferase activity and gene expression in human osteogenic sarcoma cells (U-2 OS).

Human epidemiological studies suggest an association between N-acetyltransferase (NAT) activity and the incidence of bladder and colorectal cancers. In this study, paclitaxel was selected to examine the inhibition of arylamine NAT activity, gene expression and 2-aminofluorene-DNA adduct formation in a human osteogenic sarcoma cell line (U-2 OS). The activity of NAT was determined by high performance liquid chromatography (HPLC) assay for the amounts of acetylated 2-aminofluorene (AF) and p-aminobenzoic acid (PABA) and nonacetylated AF and PABA. Human osteogenic sarcoma cell cytosols and intact cells were used to examine the NAT activity, gene expression and AF-DNA adduct formation. The results demonstrated that NAT activity percent of NAT in examined cells, gene expression (NAT1 mRNA) and AF-DNA adduct formation in human osteogenic sarcoma cells were inhibited and decreased by paclitaxel in a dose-dependent manner. The results also demonstrated that paclitaxel decreased the apparent values of Km and Vmax from intact human osteogenic sarcoma cells (U-2 OS). Thus, paclitaxel is an uncompetitive inhibitor of the NAT enzyme.

Effects of tamoxifen on DNA adduct formation and arylamines N-acetyltransferase activity in human breast cancer cells.

Tamoxifen was used to determine the effects of N-acetyltransferase(NAT) activity and 2-aminofluorene (2-AF)-DNA adduct formation in human breast cancer cells. Breast cancer cells were categorized into two groups based on the status of estrogen receptor, ER (+) and ER (-). 2-AF-DNA adduct formations in breast cancer cells are 2.58 +/- 0.39 pmol adduct/mg DNA for ER (+) and 2.74 +/- 0.46 pmol adduct/mg DNA for ER (-), respectively. Co-treatment with 1 microM tamoxifen inhibited DNA-adduct formations up to 65% in ER (+) and 61% in ER (-), respectively. The inhibition of Tamoxifen on DNA adduct formation between ER (+) and ER (-) cell was not significantly different. The results of the N-acetyltransferase activity in human breast cancer cells were inhibited by tamoxifen in a dose dependent manner. Tamoxifen inhibited 50.0% and 42.8% of Km in ER (+) and ER (-), 58.2% and 35.6% of Vmax, respectively. Based on the kinetic study of N-acetyltransferase activity, tamoxifen plays a non-competitive role in the acetylation reaction. This study demonstrates that tamoxifen inhibited not only NAT activity but also DNA-adduct formation in human breast cancer cells, regardless of the status of estrogen receptor. These findings could provide a clue that tamoxifen has chemoprevention effects in breast cancer.

Hydrocortisone affects the N-acetylation of 2-aminofluorene and DNA-2-aminofluorene adduct formation in Sprague-Dawley rats.

The effects of hydrocortisone on the in vivo acetylation of 2-aminofluorene (AF) and AF-DNA adducts in Sprague-Dawley rats were investigated. Pretreatment with hydrocortisone (50 mg/kg) 48 hours prior to the administration of AF (50 mg/kg) resulted in a 61% and 30% increase, respectively, in the urinary and fecal recovery of N-acetyl-2-aminofluorene (AAF) and a 36% increase in the metabolic clearance of AF to AAF. Hydrocortisone did not affect Michael's-Menten parameters for N-acetyltransferase (NAT) activity in blood, liver, lung and bladder. Similarly, the apparent value of Km for AF in the examined tissues was not affected by hydrocortisone. However, the apparent value of Vmax for liver NAT activity was significantly increased after hydrocortisone pretreatment. Following exposure of rats to AF with and without pretreatment with hydrocortisone, DNA-AF adducts were examined in the target tissue of liver and bladder and also in non-target tissue of lung and circulating leukocytes. The DNA-AF adducts in liver, bladder, lung and leukocytes were increased by pretreatment with hydrocortisone.