PubMed · 6059361
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G Wolff, H Schwarz. 1967. [Is gastritis diffuse?].. https://pubmed.ncbi.nlm.nih.gov/6059361/
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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.
Airway epithelium represents the first line of defense against toxic inhalants. In some subjects, cigarette smoking causes airway inflammation, hypersecretion of mucus, and poorly reversible airflow limitation through mechanisms that are still largely unknown. Likewise, it is unclear why only some smokers develop chronic obstructive pulmonary disease (COPD). Two cell types consistently result in relation to chronic airflow limitation in COPD: neutrophils and CD8(+) cells. Neutrophils are compartmentalized in the mucosal surface of the airways and air spaces, that is, the epithelium and lumen, whereas CD8(+) cells exhibit a more extensive distribution along the subepithelial zone of the airways and lung parenchyma, including alveolar walls and arteries. This pattern of inflammatory cell distribution is observed in mild or moderate COPD, and in patients who have developed COPD, it is not modified by smoking cessation. The number of neutrophils further increases in the submucosa of patients with severe COPD, suggesting a role for these cells in the progression of the disease. Hypersecretion of mucus is a major manifestation in COPD. Mucus is produced by bronchial glands and goblet cells lining the airway epithelium. Unlike mucous gland enlargement, greater mucosal inflammation is associated with sputum production. Whereas neutrophil infiltration of submucosal glands occurs only in smokers with COPD, goblet cell hyperplasia in peripheral airways occurs both in smokers with or without COPD, suggesting that the major determinant of goblet cell hyperplasia is cigarette smoke itself.