Operating SIRTF for maximum lifetime

The instruments of the Space Infrared Telescope Facility (SIRTF) are cooled directly by liquid helium, while the optical system is cooled by helium vapor. The greater the power dissipation into the liquid helium, the more vapor is produced, and the colder the telescope. Observations at shorter wavelengths do not require telescope temperatures as low as those required at shorter wavelengths. By taking advantage of this, it may be possible to extend the helium and mission lifetime by 10% or even 20%

Operating SIRTF for maximum lifetime

The instruments of the Space Infrared Telescope Facility (SIRTF) are cooled directly by liquid helium, while the optical system is cooled by helium vapor. The greater the power dissipation into the liquid helium, the more vapor is produced, and the colder the telescope. Observations at shorter wavelengths do not require telescope temperatures as low as those required at shorter wavelengths. By taking advantage of this, it may be possible to extend the helium and mission lifetime by 10% or even 20%

TET2 regulates mast cell differentiation and proliferation through catalytic and non-catalytic activities

Dioxygenases of the TET family impact genomefunctions by converting 5-methylcytosine (5mC) inDNA to 5-hydroxymethylcytosine (5hmC). Here, we identified TET2 as a crucial regulator of mast cell differentiation and proliferation. In the absence of TET2,mast cells showed disrupted gene expression and altered genome-wide 5hmC deposition, especially at enhancers and in the proximity of down regulated genes. Impaired differentiation of Tet2-ablated cells could be relieved or further exacerbated by modulating the activity of other TET family members, and mechanistically it could be linked to the dysregulated expression of C/EBP family transcription factors.Conversely, the marked increase in proliferation induced by the loss of TET2 could be rescued exclu-sively by re-expression of wild-type or catalytically inactive TET2. Our data indicate that, in the absence of TET2, mast cell differentiation is under the control of compensatory mechanisms mediated by other TET family members, while proliferation is strictly dependent on TET2 expression