PURE JUMP SHOCK MODELS IN DISCRETE TIME CASE

A device is subject to damage caused by environmental shocks.Shocks occur randomly indiscrete time according to a properly defined family of independent random variables.Theincremental damage caused by a shock depends on the magnitude of the shock.The device has athreshold τ and it fails once the damage exceeds the threshold.The first failure time T of the deviceand its failure rate are examined.If τ is random,under mild conditions we show that the lifedistribution properties of the random threshold are inherited by the first failure time T.For fixed τ,the conditions for the failure rate to increase or to have an increasing average are also found.Finally,as an application of the main results,the additive deterioration models are briefly discussed.     

A study on the pharmacokinetics in mouse of adenine-9-beta-D-arabinofuranoside 5-monophosphate conjugated with lactosaminated albumin

In plasma of mice injected with adenine-9-beta-D-arabinofuranoside monophosphate (ara-AMP) coupled to human lactosaminated serum albumin (L-HSA) some of the ara-AMP molecules are enzymatically released, whereas others remain linked to L-HSA. Evidence has been obtained that ara-AMP is not deaminated when it is conjugated to L-HSA, in contrast to the free drug which is rapidly metabolized to its hypoxanthine derivative.     

HNPCC-like cancer predisposition in mice through simultaneous loss of Msh3 and Msh6 mismatch-repair protein functions.

Cancer predisposition in hereditary non-polyposis colon cancer (HNPCC) is caused by defects in DNA mismatch repair (MMR). Mismatch recognition is attributed to two heterodimeric protein complexes: MutSalpha (refs 2, 3, 4, 5), a dimer of MutS homologues MSH2 and MSH6; and MutSbeta (refs 2,7), a dimer of MSH2 and MSH3. These complexes have specific and redundant mismatch recognition capacity. Whereas MSH2 deficiency ablates the activity of both dimers, causing strong cancer predisposition in mice and men, loss of MSH3 or MSH6 (also known as GTBP) function causes a partial MMR defect. This may explain the rarity of MSH6 and absence of MSH3 germline mutations in HNPCC families. To test this, we have inactivated the mouse genes Msh3 (formerly Rep3 ) and Msh6 (formerly Gtmbp). Msh6-deficient mice were prone to cancer; most animals developed lymphomas or epithelial tumours originating from the skin and uterus but only rarely from the intestine. Msh3 deficiency did not cause cancer predisposition, but in an Msh6 -deficient background, loss of Msh3 accelerated intestinal tumorigenesis. Lymphomagenesis was not affected. Furthermore, mismatch-directed anti-recombination and sensitivity to methylating agents required Msh2 and Msh6, but not Msh3. Thus, loss of MMR functions specific to Msh2/Msh6 is sufficient for lymphoma development in mice, whereas predisposition to intestinal cancer requires loss of function of both Msh2/Msh6 and Msh2/Msh3.     

Cytogenetic and biochemical comparison of Mus musculus and Mus hortulanus

Two chromosome markers of Mus hortulanus are described: a dotted Y chromosome exceeding half of the length of autosome 19, and the 'domesticus' type of C-banding in the X chromosome. In Mus musculus from distant regions of the USSR (more than 200 specimens of various subspecies), the Y chromosome is equal to autosome 19, and the X chromosome is of the 'molossinus' type. Specific biochemical characteristics of house mice of the USSR are shown.     

The effect of moderate hemodilution with fluosol-DA or normal saline on acetaminophen disposition in the rat

Hemodilution with 40 ml/kg of Fluosol or saline reduced the acetaminophen Vd and the acetaminophen sulfate ClM at 48 or 72 h, respectively. Fluosol hemodilution increased the acetaminophen renal excretion at 24 and 72 h. But at 48 h, Fluosol hemodilution either inhibited the renal secretion of acetaminophen or enhanced its reabsorption.     

证明压强为洛伦兹不变量的新方法

用一种新的方法证明了热力学体系压强是洛伦兹不变量.