Green tea polyphenols attenuate deterioration of bone microarchitecture in female rats with systemic chronic inflammation.

UNLABELLED: Green tea polyphenols (GTP) are promising agents for preventing bone loss. GTP supplementation sustained microarchitecture and improved bone quality via a decrease in inflammation. Findings suggest a significant role for GTP in skeletal health of patients with chronic inflammation. INTRODUCTION: This study evaluated whether GTP can restore bone microstructure along with a molecular mechanism in rats with chronic inflammation. A 2 [placebo vs. lipopolysaccharide (LPS)]× 2 [no GTP vs. 0.5% GTP (w/v) in drinking water] factorial design was employed. METHODS: Female rats were assigned to four groups: placebo, LPS, placebo + GTP, and LPS + GTP for 12 weeks. Efficacy was evaluated by examining changes in bone microarchitecture using histomorphometric and microcomputed tomographic analyses and by bone strength using the three-point bending test. A possible mechanism was studied by assessing the difference in tumor necrosis factor-α (TNF-α) expression in tibia using immunohistochemistry. RESULTS: LPS lowered trabecular volume fraction, thickness, and bone formation in proximal tibia while increasing osteoclast number and surface perimeter in proximal tibia and eroded surface in endocortical tibial shafts. GTP increased trabecular volume fraction and number in both femur and tibia and periosteal bone formation rate in tibial shafts while decreasing trabecular separation in proximal tibia and eroded surface in endocortical tibial shafts. There was an interaction between LPS and GTP in trabecular number, separation, bone formation, and osteoclast number in proximal tibia, and trabecular thickness and number in femur. GTP improved the strength of femur, while suppressing TNF-α expression in tibia. CONCLUSION: In conclusion, GTP supplementation mitigated deterioration of bone microarchitecture and improved bone integrity in rats with chronic inflammation by suppressing bone erosion and modulating cancellous and endocortical bone compartments, resulting in a larger net bone volume. Such a protective role of GTP may be due to a suppression of TNF-α.

Leiomyosarcoma of the urinary bladder presenting as life threatening gross hematuria.

Leiomyosarcomas are a relatively rare tumor entity encountered within the urinary bladder. There are just over 100 cases reported in the medical literature. Herein, we describe a case of leiomyosarcoma presenting initially as a urinary tract infection with lower abdominal pain. A life threatening episode of gross hematuria guided to the final diagnosis and treatment. Due to the rarity of this malignancy, we present this case including a review of the existing literature relative to the diagnosis and treatment.

Transitional cell carcinoma due to chronic UroLume stent irritation.

UroLume stents have been used for >15 years to improve the voiding dynamics in patients with benign prostatic hyperplasia and urethral stricture disease. Common complications include stent migration, stricture within the stent, and urothelial hyperplasia, any of which could require stent removal, which itself carries morbidity. We report a case of high-grade urothelial carcinoma associated with chronic UroLume application.

Insulin-like growth factor 1 is required for G2 progression in the estradiol-induced mitotic cycle.

Insulin-like growth factor 1 (IGF1) has been proposed as a "G1-progression factor" and as a mediator of estradiol's (E2) mitogenic effects on the uterus. To test these hypotheses, we compared E2's mitogenic effects on the uteri of Igf1-targeted gene deletion (null) and wild-type littermate mice. The proportion of uterine cells involved in the cell cycle and G1- and S-phase kinetics were not significantly different in wild-type and Igf1-null mice. However, the appearance of E2-induced mitotic figures and cell number increases were profoundly retarded in Igf1-null uterine tissue. There was a significant increase in nuclear DNA concentration in Igf1-null cells, consistent with a G2 arrest. Interestingly, apoptotic cells were also significantly reduced in abundance, and the normal massive apoptotic response to E2 withdrawal was absent in the Igf1-null uterus. These data show that Igf1 is an essential mediator of E2's mitogenic effects, with a critical role not in G1 progression but in G2 progression.

Fibroblast growth factors 1 and 2 in the primate uterus.

Fibroblast growth factors (FGF) 1 and 2 are paracrine effectors of proliferation and angiogenesis in many tissues. To elucidate potential roles for these growth factors in uterine plasticity, we used in situ hybridization histochemistry to identify the cellular sources of FGF-1 and -2 production, and immunohistochemistry to identify the cellular and extracellular deposition sites of the peptides in the primate uterus. To evaluate the effects of estradiol on uterine FGFs, uteri from ovariectomized rhesus monkeys treated with estradiol- or vehicle-containing pellets were investigated. FGF-1 and -2 mRNAs were both expressed in uterine epithelial and myometrial cells. Quantitative comparison of their mRNA levels using computerized grain counting showed no significant difference between estradiol- and vehicle-treated animals. FGF-1 immunoreactivity was detected in scattered epithelial, vascular, and myometrial cells in the vehicle-treated animals but found to be significantly more intense and widespread in estradiol-treated animals. In both conditions, FGF-1 immunostaining was predominantly nuclear. FGF-2 immunoreactivity was concentrated extracellularly in the basal lamina of both glandular and surface epithelium and was abundant and diffusely distributed within myometrial and vascular cells in both cytoplasm and nucleus. There was no apparent difference in the pattern or intensity of FGF-2 immunostaining related to estradiol treatment. These data demonstrate that major uterine cell types synthesize both FGF-1 and -2, and that the two peptides are differentially localized in uterine cellular and extracellular compartments and differentially sensitive to regulation by estradiol.