In vivo autofluorescence. Measurements of human crystalline lenses with cataract and normal findings after excitation with monochromatic light]

In 25 eyes with nuclear cataract, 18 eyes with posterior subcapsular cataract, 25 eyes with cortical cataract, and 23 eyes without any pathological lens changes, the maximal fluorescence intensity was determined after excitation with monochromatic light at 365 nm, 405 nm, 436 nm, and 485 nm. The coefficient of variation was smaller than 5%. All eyes with cataract underwent cataract surgery a few days after the fluorescence measurements. The fluorescence spectrometer, especially constructed for in vivo measurements, consists of a modified slit lamp (Zeiss 75 SL) and an optical multichannel analyser (OMA) for gauging the data. The clinical trial was undertaken to determine whether, considering the influence of age, there is a difference between the fluorescence intensities in eyes with the above named cataracts and noncataractous eyes. The data were analyzed to determine the effect of age upon fluorescence intensity for all excitation wavelengths in both cataractous and noncataractous eyes. Age had an influence on the fluorescence intensities for all four excitation wavelengths. Assuming that the influence of age was not dependent on the state of the lens, it was quantified for all measurements and an "age-corrected" fluorescence intensity was calculated. The statistical analyses of these "age-corrected" fluorescence intensities revealed a significant difference (P < 0.001) for all of the types of cataracts examined and for normal eyes. The cataract types examined and the normal eyes showed differences in their fluorescence feature. To assess the fluorescence intensities obtained after excitation with the wavelengths mentioned above, one must take into consideration the influence of age on the measurements.     

Smad7 dependent expression signature highlights BMP2 and HK2 signaling in HSC transdifferentiation

AIM: To analyse the influence of Smad7, antagonist of transforming growth factor (TGF)-β canonical signaling pathways on hepatic stellate cell (HSC) transdifferentia-tion in detail. METHODS: We systematically analysed genes regulated by TGF-β/Smad7 in activated HSCs by microarray analy-sis and validated the results using real time polymerase chain reaction and Western blotting analysis. RESULTS: We identif ied 100 known and unknown tar-gets underlying the regulation of Smad7 expression and delineated 8 gene...     

Väter und ihre Bedeutung für die psychische Gesundheit ihrer Kinder

The article points out that despite socio-historic changes, fathers or father-related issues are not involved in the psychotherapeutic work to the same extent as mothers or mother-specific issues are involved. Subsequently, the significance of fathers for their children’s development is elaborated on the background of current research on fathers, developmental psychology, and attachment theory, and, finally, embedded in the psychodramatic development theory.     

Glucocorticoids activate TGF-β induced PAI-1 and CTGF expression in rat hepatocytes

Background  

In addition to the activation of hepatic stellate cells TGF-β govern apoptosis and growth control of hepatocytes in liver injury. In non-parenchymal cells, TGF-β induces plasminogen activator inhibitor 1 (PAI-1) and connective tissue growth factor (CTGF) expression, which are involved in extra cellular matrix formation. Both genes were also regulated by glucocorticoids, which in certain cases showed antagonistic effects to the TGF-β-Smad 3 pathway. The purpose of our work was to investigate the influence of TGF-β and dexamethasone on PAI-1 and CTGF expression and secretion in primary hepatocytes.     

Id1 is a critical mediator in TGF-beta-induced transdifferentiation of rat hepatic stellate cells

Transforming growth factor (TGF)-beta is critically involved in the activation of hepatic stellate cells (HSCs) that occurs during the process of liver damage, for example, by alcohol, hepatotoxic viruses, or aflatoxins. Overexpression of the TGF-beta antagonist Smad7 inhibits transdifferentiation and arrests HSCs in a quiescent stage. Additionally, bile duct ligation (BDL)-induced fibrosis is ameliorated by introducing adenoviruses expressing Smad7 with down-regulated collagen and alpha-smooth muscle actin (alpha-SMA) expression. The aim of this study was to further characterize the molecular details of TGF-beta pathways that control the transdifferentiation process. In an attempt to elucidate TGF-beta target genes responsible for fibrogenesis, an analysis of Smad7-dependent mRNA expression profiles in HSCs was performed, resulting in the identification of the inhibitor of differentiation 1 (Id1) gene. Ectopic Smad7 expression in HSCs strongly reduced Id1 mRNA and protein expression. Conversely, Id1 overexpression in HSCs enhanced cell activation and circumvented Smad7-dependent inhibition of transdifferentiation. Moreover, knock-down of Id1 in HSCs interfered with alpha-SMA fiber formation, indicating a pivotal role of Id1 for fibrogenesis. Treatment of HSCs with TGF-beta1 led to increased Id1 protein expression, which was not directly mediated by the ALK5/Smad2/3, but the ALK1/Smad1 pathway. In vivo, Id1 expression and Smad1 phosphorylation were co-induced during fibrogenesis. In conclusion, Id1 is identified as TGF-beta/ALK1/Smad1 target gene in HSCs and represents a critical mediator of transdifferentiation that might be involved in hepatic fibrogenesis. Supplementary material for this article can be found on the HEPATOLOGY website (http://interscience.wiley.com/jpages/0270-9139/suppmat/index.html).