Increased gene expression of plasminogen activators and inhibitors in left ventricular hypertrophy

In the early stages of left ventricular hypertrophy (LVH) acute adaptive changes occur in the coronary vasculature as it remodels. Plasminogen activators (PAs) and inhibitors (PAIs) have the potential effects of proteolytic degradation that is relevant to tissue remodeling and angiogenesis. Our study focused on the possible roles of PAI-1, PAI-2, uPA and tPA in myocyte hypertrophy and angiogenesis in the early and late stages of pressure overload induced left ventricular hypertrophy (LVH). We divided seventeen adult swine, weighing 24.2 ± 6.5 kg, into four groups: control, sham-operated, early LVH and late heart failure LVH group. At surgery we placed a fixed constrictor on the ascending aorta immediately above the aortic valve. This increased LV systolic pressure from 133 ± 15 to 193 ± 24 mm Hg after the surgery. We subdivided the early group into groups of 3 animals each that we euthanized at 8, 24 and 72 h after operation and obtained heart samples for analysis. In the late heart failure group individual animals were euthanized at 55, 59, 62 and 72 days after the detection of congestive heart failure. We also obtained tissue samples from the control and sham-operated swine. Sections for histologic analysis were fixed in 10% buffered formalin. We isolated RNA, size fractionated it using 1% formaldehyde-agarose gel electrophoresis and then did Northern blots. The mRNAs from both PAI-1 and PAI-2 showed a remarkable increase at 8 and 24 h after acute aortic constriction and returned to control by 72 h. Regional differences showed that most of the increases were in the endocardium. Three animals in the late heart failure LVH group were determined to be in congestive heart failure at about 2 months after the onset of aortic constriction. In these animals PAI-1 and PAI-2 were increased in both the left and right ventricles but remained low in an animal of the same elevation in aortic pressure seen by the LV who did not have congestive failure. These data suggest that PA and PAI gene expressions change before morphologic changes occur in the early stages of developing LVH. Also at the time of onset of congestive heart failure this increased expression reappears. PAs and PA inhibitors mRNA levels vary in the different regions of the heart reflecting changing wall stresses. Thus, the PAs and PA inhibitors may play an important role in angiogenesis that occurs during the early stages of LVH. The increased expression in the late stage of LVH may reflect further changes in wall stresses since these animals also showed overt clinical signs of heart failure.     

Anaerobic degradation of cyclohexane-1,2-diol by a new Azoarcus species

A bacterium, strain 22Lin, was isolated on cyclohexane-1,2-diol as sole electron donor and carbon source and nitrate as electron acceptor. Cells are motile rods and are facultatively anaerobic. A phylogenetic comparison based on the total 16S rRNA gene sequence allowed the assignment of the isolate to the genus Azoarcus. Cyclohexanol, cyclohexanone, cyclohexane-1,3-diol, and cyclohexane-1,3-dione, which are oxidized by a different denitrifying strain, did not support denitrifying growth of isolate 22Lin. On the contrary, cyclohexanol (I₅₀ = 37 μM) and cyclohexanone (I₅₀ = 28 μM) inhibited growth on cyclohexane-1,2-diol, but not on acetate. NAD was reduced by crude extracts of strain 22Lin in the presence of cyclohexane-1,2-dione, but not in the presence of cyclohexanone or cyclohexane-1,3-dione. The formation of 6-oxohexanoate from cyclohexane-1,2-dione and of adipate during NAD reduction suggests that strain 22Lin possesses a carbon–carbon hydrolase that transforms cyclohexane-1,2-dione into 6-oxohexanoate. This pathway was once observed in an aerobic pseudomonad that was lost and could not be reisolated. Here, the application of strictly anoxic enrichment conditions enabled the reisolation of another strain (22Lin) that uses this pathway. Received: 3 February 1997 / Accepted: 12 May 1997     

Detection of 6q deletions in breast carcinoma cell lines by fluorescence in situ hybridization

Dual-color fluorescence in situ hybridization was performed to detect the frequency and extent of 6q deletions in ten breast carcinoma cell lines. In five cell lines, the 6q deletions involved large regions extending from 6q12–q16 to 6q27, and in one the deletion extended from the region distal to YAC 751G10 at 6q25.1 to 6q27. In two cell lines, 6q deletions occurred only in cells with polysomy 6, indicating that such deletions might be secondary chromosomal aberrations and reflect late genetic changes in breast carcinomas. In addition, an overrepresentation of 6q21–q22.2 was detected in one cell line. Received: 17 July 1998 / Accepted: 28 September 1998     

Adenylate Energy Charge in Escherichia coli During Growth and Starvation

The value of the adenylate energy charge, [(adenosine triphosphate) + (1/2) (adenosine diphosphate)]/[(adenosine triphosphate) + (adenosine diphosphate) + (adenosine monophosphate)], in Escherichia coli cells during growth is about 0.8. During the stationary phase after cessation of growth, or during starvation in carbon-limited cultures, the energy charge declines slowly to a value of about 0.5, and then falls more rapidly. During the slow decline in energy charge, all the cells are capable of forming colonies, but a rapid fall in viability coincides with the steep drop in energy charge. These results suggest that growth can occur only at energy charge values above about 0.8, that viability is maintained at values between 0.8 and 0.5, and that cells die at values below 0.5. Tabulation of adenylate concentrations previously reported for various organisms and tissues supports the prediction, based on enzyme kinetic observations in vitro, that the energy charge is stabilized near 0.85 in intact metabolizing cells of a wide variety of types.     

Über den Einfluss der Tageslänge nach der photoperiodischen Induktion auf die Infloreszenzen vonKalanchoë Blossfeldiana

Zusammenfassung Den Pflanzen wurde ein Blühimpuls durch verschieden lange Behandlung mit 9stündigem Kurztag (während 2, 8 und 16 Tagen) gegeben und die Entwicklung der Infloreszenzen im anschließenden 12-, 18- und 24stündigen Tag beobachtet. Sie war je nach der Tageslänge sehr verschieden. Die Belichtungsdauer während der Entwicklung der Blüten übt also einen starken Einfluß auf das Blühergebnis aus. Zwischen 18- und 24stündigem Langtag war aber kein statistisch zu sichernder Einfluß feststellbar; beide wirkten gleich stark verzögernd gegenüber 12stündigem Tag, wobei die für das Blühen sehr viel günstigere Wirkung des 12-Std-Tages aber daher kommt, daß er fürKalanchoë Bloßfeldiana noch blühfördernde Kurztagswirkung hat.Mit 6 Textabbildungen. Wilhelm Ruhland zum 75. Geburtstag.     

Über die untere kritische Tageslänge bei der Kurztagspflanze Kalanchoë Blossfeldiana

Zusammenfassung Der Kurztag wurde fürKalanchoë Bloßfeldiana auf 2 Stunden bis hinab zu 1 Sek. abgekürzt. Bei Anwendung von natürlichem Tageslicht oder elektrischem Licht von 60–80 000 Lux bei Zimmertemperatur kamen die Pflanzen bei allen diesen Tageslängen zum Blühen.Man kann die Pflanzen also täglich 23 Stunden, 59 Min. und 59 Sek. im Dunkeln halten und braucht sie nur 1 Sek. zu belichten, um die Blütenbildung herbeizuführen.Alle Blütenstände waren völlig normal ausgebildet, unverlaubt und relativ reichblütig.Mit abnehmender Belichtungszeit ging die Blütenzahl zurück, und der Zeitpunkt des ersten Sichtbarwerdens der Infloreszenzen sowie des Aufblühens der Knospen wurde hinausgeschoben. Von 20 Min. abwärts trat diese Abnahme des Blühimpulses aber nicht mehr klar ein, so daß bei den längeren Belichtungszeiten wohl auch die Menge der Assimilate — die bei den sehr kurzen Zeiten überall wohl als gleich unbedeutend angesehen werden darf—mit eine Rolle spielte.Mit 3 Textabbildungen.