Directional solidification and physical properties measurements of the zinc-aluminum eutectic alloy

Zn-5wt% Al eutectic alloy was directionally solidified with different growth rates (5.32–250.0 μm/s) at a constant temperature gradient of 8.50 K/mm using a Bridgman-type growth apparatus. The values of eutectic spacing were measured from transverse sections of the samples. The dependences of the eutectic spacing and undercooling on growth rate are determined as λ=9.21V-0.53 and ΔT=0.0245V0.53, respectively. The results obtained in this work were compared with the Jackson-Hunt eutectic theory and the similar experimental results in the literature. Microhardness of directionally solidified samples was also measured by using a microhardness test device. The dependency of the microhardness on growth rate is found as Hv=115.64V0.13. Afterwards, the electrical resistivity (r) of the casting alloy changes from 40×10-9 to 108×10-9 Ω·m with the temperature rising in the range of 300–630 K. The enthalpy of fusion (ΔH) and specific heat (C_p) for the Zn-Al eutectic alloy are calculated to be 113.37 J/g and 0.309 J/(g·K), respectively by means of differential scanning calorimetry (DSC) from heating trace during the transformation from liquid to solid.     

Key role of ERK1/2 molecular scaffolds in heart pathology

The ability of cardiomyocytes to detect mechanical and humoral stimuli is critical for adaptation of the myocardium in response to new conditions and for sustaining the increased workload during stress. While certain stimuli mediate a beneficial adaptation to stress conditions, others result in maladaptive remodelling, ultimately leading to heart failure. Specific signalling pathways activating either adaptive or maladaptive cardiac remodelling have been identified. Paradoxically, however, in a number of cases, the transduction pathways involved in such opposing responses engage the same signalling proteins. A notable example is the Raf–MEK1/2–ERK1/2 signalling pathway that can control both adaptive and maladaptive remodelling. ERK1/2 signalling requires a signalosome complex where a scaffold protein drives the assembly of these three kinases into a linear pathway to facilitate their sequential phosphorylation, ultimately targeting specific effector molecules. Interestingly, a number of different Raf–MEK1/2–ERK1/2 scaffold proteins have been identified, and their role in determining the adaptive or maladaptive cardiac remodelling is a promising field of investigation for the development of therapeutic strategies capable of selectively potentiating the adaptive response.     

Glycerol effect on the loss of solid constituents from hepatocytes isolated in a potassium chelating fluid

Riassunto Epatociti isolati mediante dispersione meccanica dopo incubazione del tessuto epatico in un mezzo acquoso contenente tetrafenilborato di Na, un agente chelante il K, perdono circa il 30% del loro contenuto in sostanze solide. L'aggiunta al mezzo di incubazione di glicerolo riduce tale perdita.

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This work was supported by a grant of the Consiglio Nazionale delle Ricerche.     

Cytology of experimental teratomas and teratocarcinomas

Zusammenfassung Von bei Mäusen erzeugten Teratomen und Teratocarcinomen entstehen in der Hälfte der Fälle ungefähr gleich häufig bösartige wie gutartige Mischtumoren. Bei der Punktion und der nachfolgenden cytologischen Untersuchung war es jedoch nicht möglich, aus den Abstrichen maligne und benigne Tumoren zu trennen.

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This work was supported by grants from the Yugoslav federal science Foundation No. 813/3 and the council for Scientific Affairs of SR Croatia, NIH PL 480 Research Agreement No. 02-038-1 and No. CA-10815 from the National Cancer Institute. One of us (DS) was supported by a Damon Runyon Cancer Research Fellowship.     

SIRT6 is a histone H3 lysine 9 deacetylase that modulates telomeric chromatin

The Sir2 deacetylase regulates chromatin silencing and lifespan in Saccharomyces cerevisiae. In mice, deficiency for the Sir2 family member SIRT6 leads to a shortened lifespan and a premature ageing-like phenotype. However, the molecular mechanisms of SIRT6 function are unclear. SIRT6 is a chromatin-associated protein, but no enzymatic activity of SIRT6 at chromatin has yet been detected, and the identity of physiological SIRT6 substrates is unknown. Here we show that the human SIRT6 protein is an NAD+-dependent, histone H3 lysine 9 (H3K9) deacetylase that modulates telomeric chromatin. SIRT6 associates specifically with telomeres, and SIRT6 depletion leads to telomere dysfunction with end-to-end chromosomal fusions and premature cellular senescence. Moreover, SIRT6-depleted cells exhibit abnormal telomere structures that resemble defects observed in Werner syndrome, a premature ageing disorder. At telomeric chromatin, SIRT6 deacetylates H3K9 and is required for the stable association of WRN, the factor that is mutated in Werner syndrome. We propose that SIRT6 contributes to the propagation of a specialized chromatin state at mammalian telomeres, which in turn is required for proper telomere metabolism and function. Our findings constitute the first identification of a physiological enzymatic activity of SIRT6, and link chromatin regulation by SIRT6 to telomere maintenance and a human premature ageing syndrome.