PubMed · 1546431
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
K A Hanash. 1992. Transrectal prostatic core biopsy: a simplified method.. https://doi.org/10.1016/0090-4295(92)90313-l
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
CCND1 amplification results in cyclin D1 overexpression. However, other unidentified genetic mechanisms contribute to enhanced gene expression. In the present study, 32 squamous cell carcinoma of the head and neck (SCCHN) were investigated regarding chromosomal abnormalities involving 11q13 by cytogenetic analysis, genomic CCND1 amplification by differential PCR and FISH, and cyclin D1 expression on the mRNA and protein level by differential RT-PCR and immunohistochemistry, respectively. CCND1 amplification, observed in 11 of 32 (34%) tumours, resulted in overexpression of cyclin D1 on the mRNA and/or protein level, in 3 cases in association with chromosomal translocations. In cytogenetic analysis, 4 tumours had hsr(11)(q13), all of which showed CCND1 amplification and cyclin D1 overexpression. Overexpression of cyclin D1 was detected at the mRNA level in 23 tumours (72%) and on the protein level in 25 tumours (78%). In one case a translocation was seen together with cyclin D1 overexpression on the mRNA level, without any cytogenetic or molecular signs of amplification. Furthermore, cases with cyclin D1 overexpression were frequently observed in the absence of any genomic rearrangement. We conclude that, besides amplifications, chromosomal translocations and other transcriptional or translational regulatory mechanisms are involved in CCND1 deregulation.
OBJECTIVES: To evaluate the diagnostic accuracy of transvaginal sonography (TVS) in detecting uterine cavity abnormalities in infertile patients, with reference to hysteroscopy as the gold standard method. STUDY DESIGN: At the Institute of Obstetrics and Gynaecology, University of Bari, 134 infertile women were investigated with both TVS and hysteroscopy. In all cases endometrial biopsy was performed. Sensitivity, specificity, and positive and negative predictive values were calculated for TVS, considering hysteroscopic diagnosis as the gold standard. Statistical analysis was performed by using McNemar test. RESULTS: There was one failed insertion of hysteroscope. Hysteroscopy diagnosed pathological findings in 58 out of 133 cases (44%). TVS was in agreement with 50 of the 58 (86%) of the pathological findings diagnosed at hysteroscopy. As a test for the detection of uterine cavity abnormalities, TVS in comparison with hysteroscopy had 84.5% sensitivity and 98.7% specificity, 98.0% positive predictive value and 89.2% negative predictive value. CONCLUSIONS: TVS is able to diagnose polyps, septum and submucous fibroids with quite significant accuracy, while hysteroscopy is indicated for their confirmation and removal. Thus, hysteroscopy provides both diagnostic and therapeutic capabilities, but TVS permits to proceed directly to operative hysteroscopy avoiding the need for a separate diagnostic procedure.
There is no consensus regarding the results from in vivo and in vitro studies on the impact of chronic high insulin and/or high glucose exposure on acute insulin stimulation of glycogen synthase (GS) kinetic parameters in human skeletal muscle. The aim of this study was to evaluate the kinetic parameters of glycogen synthase activity in human myotube cultures at conditions of chronic high insulin combined or not with high glucose exposure, before and after a subsequent acute insulin stimulation. Acute insulin stimulation significantly increased the fractional activity (FV(0.1)) of GS, increased the sensitivity of GS to the allosteric activator glucose 6-phosphate (A(0.5)) and increased the sensitivity of GS to its substrate UDPG (K(m(0.1))) when myotubes were precultured at low insulin with/without high glucose conditions. However, this effect of acute insulin stimulation was abolished in myotubes precultured at high insulin with or without high glucose. Furthermore, we found significant correlations between the fractional velocities FV(0.1) of GS and K(m(0.1)) (rho=-0.72, P<0.0001), between FV(0.1) and A(0.5) (rho=-0.82, P<0.0001) and between K(m(0.1)) and A(0.5) values (rho=0.71, P<0.0001). Our results show that chronic exposure of human myotubes to high insulin with or without high glucose did not affect the basal kinetic parameters but abolished the reactivity of GS to acute insulin stimulation. We suggest that insulin induced insulin resistance of GS is caused by a failure of acute insulin stimulation to decrease A(0.5) and K(m(0.1)) in human skeletal muscle.