The design parameters for the MICE tracker solenoid

The first superconducting magnets to be installed in the muon ionization cooling experiment (MICE) will be the tracker solenoids. The tracker solenoid module is a five coil superconducting solenoid with a 400 mm diameter warm bore that is used to provide a 4 T magnetic field for the experiment tracker module. Three of the coils are used to produce a uniform field (up to 4 T with better than 1 percent uniformity) in a region that is 300 mm in diameter and 1000 mm long. The other two coils are used to match the muon beam into the MICE cooling channel. Two 2.94-meter long superconducting tracker solenoid modules have been ordered for MICE. The tracker solenoid will be cooled using two-coolers that produce 1.5 W each at 4.2 K. The magnet system is described. The decisions that drive the magnet design will be discussed in this report. © 2007 IEEE

DOCK4, a GTPase Activator, Is Disrupted during Tumourigenesis.

We used representational difference analysis to identify homozygous genomic deletions selected during tumor progression in the mouse NF2 and TP53 tumor model. We describe a deletion targeting DOCK4, a member of the CDM gene family encoding regulators of small GTPases. DOCK4 specifically activates Rap GTPase, enhancing the formation of adherens junctions. DOCK4 mutations are present in a subset of human cancer cell lines; a recurrent missense mutant identified in human prostate and ovarian cancers encodes a protein that is defective in Rap1 activation. The engulfment defect of C. elegans mutants lacking the CDM gene ced-5 is rescued by wild-type DOCK4, but not by the mutant allele. Expression of wild-type, but not mutant, DOCK4 in mouse osteosarcoma cells with a deletion of the endogenous gene suppresses growth in soft agar and tumor invasion in vivo. DOCK4 therefore encodes a CDM family member that regulates intercellular junctions and is disrupted during tumorigenesis.</p

BACH1, a novel helicase-like protein, interacts directly with BRCA1 and contributes to its DNA repair function

BRCA1 interacts in vivo with a novel protein, BACH1, a member of the DEAH helicase family. BACH1 binds directly to the BRCT repeats of BRCA1. A BACH1 derivative, bearing a mutation in a residue that was essential for catalytic function in other helicases, interfered with normal double-strand break repair in a manner that was dependent on its BRCA1 binding function. Thus, BACH1/BRCA1 complex formation contributes to a key BRCA1 activity. In addition, germline BACH1 mutations affecting the helicase domain were detected in two early-onset breast cancer patients and not in 200 matched controls. Thus, it is conceivable that, like BRCA1, BACH1 is a target of germline cancer-inducing mutations

Carolina em Belo Horizonte

We used representational difference analysis to identify homozygous genomic deletions selected during tumor progression in the mouse NF2 and TP53 tumor model. We describe a deletion targeting DOCK4, a member of the CDM gene family encoding regulators of small GTPases. DOCK4 specifically activates Rap GTPase, enhancing the formation of adherens junctions. DOCK4 mutations are present in a subset of human cancer cell lines; a recurrent missense mutant identified in human prostate and ovarian cancers encodes a protein that is defective in Rap1 activation. The engulfment defect of C. elegans mutants lacking the CDM gene ced-5 is rescued by wild-type DOCK4, but not by the mutant allele. Expression of wild-type, but not mutant, DOCK4 in mouse osteosarcoma cells with a deletion of the endogenous gene suppresses growth in soft agar and tumor invasion in vivo. DOCK4 therefore encodes a CDM family member that regulates intercellular junctions and is disrupted during tumorigenesis

Heterozygous germ line hCHK2 mutations in Li-Fraumeni syndrome

The hCHK2 gene encodes the human homolog of the yeast Cds1 and Rad53 G 2 checkpoint kinases, whose activation in response to DNA damage prevents cellular entry into mitosis. Here, it is shown that heterozygous germ line mutations in hCHK2 occur in Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in the TP53 gene. These observations suggest that hCHK2 is a tumor suppressor gene conferring predisposition to sarcoma, breast cancer, and brain tumors, and they also provide a link between the central role of p53 inactivation in human cancer and the well-defined G 2 checkpoint in yeast. </jats:p

ALS superbend magnet system

The Lawrence Berkeley National Laboratory is preparing to upgrade the Advanced Light Source (ALS) with three superconducting dipoles (Superbends). In this paper we present the final magnet system design which incorporates R&amp;D test results and addresses the ALS operational concerns of alignment, availability, and economy. The design incorporates conduction-cooled Nb-Ti windings and HTS current leads, epoxy-glass suspension straps, and a Gifford-McMahon cryocooler to supply steady state refrigeration. We also present the current status of fabrication and testing