Results of the August 1977 Soviet and American meterological rocketsonde intercomparison held at Wallops Island, Virginia

A coordinated program of rocketsonde investigations along about 60 deg E and 70 deg W between the United States and U.S.S.R. is discussed. The rocketsonde instruments used by the U.S. and U.S.S.R. were compared and the results are presented. The U.S. Super Loki Datasonde and the U.S.S.R. M100B rocketsonde are discussed. Results indicate that the U.S/U.S.S.R. rocketsonde measurement agreement improved since the 1973 intercomparisons. It was learned that the mean of the differences of the temperatures compare to within 6 C at about 60 km and to within 2 C near 50 km. Wind measurements were also found to agree

The In Vivo Role of the RP-Mdm2-p53 Pathway in Signaling Oncogenic Stress Induced by pRb Inactivation and Ras Overexpression

The Mdm2-p53 tumor suppression pathway plays a vital role in regulating cellular homeostasis by integrating a variety of stressors and eliciting effects on cell growth and proliferation. Recent studies have demonstrated an in vivo signaling pathway mediated by ribosomal protein (RP)-Mdm2 interaction that responds to ribosome biogenesis stress and evokes a protective p53 reaction. It has been shown that mice harboring a Cys-to-Phe mutation in the zinc finger of Mdm2 that specifically disrupts RP L11-Mdm2 binding are prone to accelerated lymphomagenesis in an oncogenic c-Myc driven mouse model of Burkitt's lymphoma. Because most oncogenes when upregulated simultaneously promote both cellular growth and proliferation, it therefore stands to reason that the RP-Mdm2-p53 pathway might also be essential in response to oncogenes other than c-Myc. Using genetically engineered mice, we now show that disruption of the RP-Mdm2-p53 pathway by an Mdm2C305F mutation does not accelerate prostatic tumorigenesis induced by inactivation of the pRb family proteins (pRb/p107/p130). In contrast, loss of p19Arf greatly accelerates the progression of prostate cancer induced by inhibition of pRb family proteins. Moreover, using ectopically expressed oncogenic H-Ras we demonstrate that p53 response remains intact in the Mdm2C305F mutant MEF cells. Thus, unlike the p19Arf-Mdm2-p53 pathway, which is considered a general oncogenic response pathway, the RP-Mdm2-p53 pathway appears to specifically suppress tumorigenesis induced by oncogenic c-Myc

Sticking of particulate matter on airborne pollen

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