'Designer atoms' for quantum metrology

Entanglement is recognized as a key resource for quantum computation and quantum cryptography. For quantum metrology, the use of entangled states has been discussed and demonstrated as a means of improving the signal-to-noise ratio. In addition, entangled states have been used in experiments for efficient quantum state detection and for the measurement of scattering lengths. In quantum information processing, manipulation of individual quantum bits allows for the tailored design of specific states that are insensitive to the detrimental influences of an environment. Such 'decoherence-free subspaces' (ref. 10) protect quantum information and yield significantly enhanced coherence times. Here we use a decoherence-free subspace with specifically designed entangled states to demonstrate precision spectroscopy of a pair of trapped Ca+ ions; we obtain the electric quadrupole moment, which is of use for frequency standard applications. We find that entangled states are not only useful for enhancing the signal-to-noise ratio in frequency measurements--a suitably designed pair of atoms also allows clock measurements in the presence of strong technical noise. Our technique makes explicit use of non-locality as an entanglement property and provides an approach for 'designed' quantum metrology.     

Abnormal lipid composition of microsomes from cirrhotic rat liver—does it contribute to decreased microsomal function?

We determined to what extent a change in the lipid composition of the smooth endoplasmic reticulum contributes to altered microsomal function in cirrhosis. Rats were rendered cirrhotic either by chronic exposure to phenobarbital/CCl₄ (MCIR) or by bile duct ligation (BCIR). Microsomal function was tested in vivo by the aminopyrine breath test (ABT), then microsomes were prepared and their phospholipid and cholesterol composition analysed. ABT was reduced by 35 and 41% in BCIR and MCIR, respectively. Cholesterol in microsomes was increased in both cirrhotic groups. (BCIR +154%, MCIR +75%) while total phospholipid content was not affected. As shown in other membrane systems, the phospholipid/cholesterol (PL/XOL) ratio showed an excellent inverse correlation with fluorescence anisotropy determined by diphenylhexatriene fluorescence polarization (r=–0.896). The PL/XOL ratio was significantly correlated with aminopyrine N-demethylation in vivo (r=0.649). Alterations in the composition of phospholipid groups (an increase in sphingomyelin in both cirrhotic groups, and a decrease in phosphatidylcholine and an increase in phosphatidylethanolamine in BCIR) also contributed to increased membrane rigidity. We conclude that altered membrane fluidity contributes to diminished microsomal function but that other factors must also be involved since the PL/XOL ratio explained only 42% of the variance in aminopyrine N-demethylation.     

Abnormal lipid composition of microsomes from cirrhotic rat liver--does it contribute to decreased microsomal function?

We determined to what extent a change in the lipid composition of the smooth endoplasmic reticulum contributes to altered microsomal function in cirrhosis. Rats were rendered cirrhotic either by chronic exposure to phenobarbital/CCl4 (MCIR) or by bile duct ligation (BCIR). Microsomal function was tested in vivo by the aminopyrine breath test (ABT), then microsomes were prepared and their phospholipid and cholesterol composition analysed. ABT was reduced by 35 and 41% in BCIR and MCIR, respectively. Cholesterol in microsomes was increased in both cirrhotic groups. (BCIR + 154%, MCIR + 75%) while total phospholipid content was not affected. As shown in other membrane systems, the phospholipid/cholesterol (PL/XOL) ratio showed an excellent inverse correlation with fluorescence anisotropy determined by diphenylhexatriene fluorescence polarization (r = -0.896). The PL/XOL ratio was significantly correlated with aminopyrine N-demethylation in vivo (r = 0.649). Alterations in the composition of phospholipid groups (an increase in sphingomyelin in both cirrhotic groups, and a decrease in phosphatidylcholine and an increase in phosphatidylethanolamine in BCIR) also contributed to increased membrane rigidity. We conclude that altered membrane fluidity contributes to diminished microsomal function but that other factors must also be involved since the PL/XOL ratio explained only 42% of the variance in aminopyrine N-demethylation.     

Elektronenoptische Beobachtungen bei Speicherkrankheiten

Summary Ultrastructural changes in spleen and liver in a case ofMorbus Gaucher andNiemann-Pick are discussed.The results are: (1) The Ultrastructure shows a distinct differentiation between the two diseases. (2) It seems that storage begins in mitochondria. (3) In the case ofMorbus Niemann-Pick, all Mitochondria of storage cells show an abnormal ultrastructure (diminuation in size, increased osmiophilia, disorder in the arrangement of cristae and membranes).

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Die Arbeit erscheint ausführlich an anderer Stelle.     

Structures of complement component C3 provide insights into the function and evolution of immunity

The mammalian complement system is a phylogenetically ancient cascade system that has a major role in innate and adaptive immunity. Activation of component C3 (1,641 residues) is central to the three complement pathways and results in inflammation and elimination of self and non-self targets. Here we present crystal structures of native C3 and its final major proteolytic fragment C3c. The structures reveal thirteen domains, nine of which were unpredicted, and suggest that the proteins of the alpha2-macroglobulin family evolved from a core of eight homologous domains. A double mechanism prevents hydrolysis of the thioester group, essential for covalent attachment of activated C3 to target surfaces. Marked conformational changes in the alpha-chain, including movement of a critical interaction site through a ring formed by the domains of the beta-chain, indicate an unprecedented, conformation-dependent mechanism of activation, regulation and biological function of C3.     

STIM1 is a Ca2+ sensor that activates CRAC channels and migrates from the Ca2+ store to the plasma membrane

As the sole Ca2+ entry mechanism in a variety of non-excitable cells, store-operated calcium (SOC) influx is important in Ca2+ signalling and many other cellular processes. A calcium-release-activated calcium (CRAC) channel in T lymphocytes is the best-characterized SOC influx channel and is essential to the immune response, sustained activity of CRAC channels being required for gene expression and proliferation. The molecular identity and the gating mechanism of SOC and CRAC channels have remained elusive. Previously we identified Stim and the mammalian homologue STIM1 as essential components of CRAC channel activation in Drosophila S2 cells and human T lymphocytes. Here we show that the expression of EF-hand mutants of Stim or STIM1 activates CRAC channels constitutively without changing Ca2+ store content. By immunofluorescence, EM localization and surface biotinylation we show that STIM1 migrates from endoplasmic-reticulum-like sites to the plasma membrane upon depletion of the Ca2+ store. We propose that STIM1 functions as the missing link between Ca2+ store depletion and SOC influx, serving as a Ca2+ sensor that translocates upon store depletion to the plasma membrane to activate CRAC channels.     

Increased level of 5-hydroxyindoleacetic acid in cerebrospinal fluid from infantile hydrocephalus

Zusammenfassung Die Konzentration der 5-Hydroxyindolessigsäure wurde in der Cerebrospinalflüssigkeit hydrocephalischer Kleinkinder (bis 1 Jahr) bestimmt. Die Werte waren deutlich erhöht. In einigen Fällen wurde die Konzentration an Homovanillinsäure, die ebenfalls erhöht war, bestimmt.