Bacterial growth and primary production along a north-south transect of the Atlantic Ocean

The oceanic carbon cycle is mainly determined by the combined activities of bacteria and phytoplankton, but the interdependence of climate, the carbon cycle and the microbes is not well understood. To elucidate this interdependence, we performed high-frequency sampling of sea water along a north-south transect of the Atlantic Ocean. Here we report that the interaction of bacteria and phytoplankton is closely related to the meridional profile of water temperature, a variable directly dependent on climate. Water temperature was positively correlated with the ratio of bacterial production to primary production, and, more strongly, with the ratio of bacterial carbon demand to primary production. In warm latitudes (25 degrees N to 30 degrees S), we observed alternating patches of predominantly heterotrophic and autotrophic community metabolism. The calculated regression lines (for data north and south of the Equator) between temperature and the ratio of bacterial production to primary production give a maximum value for this ratio of 40% in the oligotrophic equatorial regions. Taking into account a bacterial growth efficiency of 30%, the resulting area of net heterotrophy (where the bacterial carbon demand for growth plus respiration exceeds phytoplankton carbon fixation) expands from 8 degrees N (27 degrees C) to 20 degrees S (23 degrees C). This suggests an output of CO2 from parts of the ocean to the atmosphere.     

An unwelcome discovery: The pole effect in the electric arc, a threat to early 20th century precision spectrometry

In late 1912, Fritz Goos at the Hamburg Physikalisches Staatslaboratorium discovered a systematic dependency of arc-spectra wavelengths on the length of the electric arc used and on its electric parameters, such as, for instance, the current employed. In early 1913, at Heinrich Kayser's better-equipped physical laboratory in Bonn, Goos was able to confirm these effects using a large concave Rowland grating. He was able to establish that variations of between 3 mm and 10 mm in the length of the arc produced wavelength differences of up to 0.02 Å violet shift and -0.007 Å redshift respectively. Further inquiry also revealed a dependency of the wavelength on the region of the arc selected for spectrometric observation. All these surprising effects were soon collectively named pole effect.As is shown in this paper, the pole effect threatened the validity of the results of the entire research tradition of high-precision spectroscopy which, around 1910, had excelled in establishing several internally coherent systems of wavelength assignments. These wavelength catalogues had been established by spectroscopists such as Heinrich Kayser, Paul Eversheim and their co-workers in Bonn, by August Herman Pfund in Baltimore, and by Charles Fabry and Henri Buisson in Marseille under the aegis of the International Union for Co-Operation in Solar Research. They had all produced locally consistent, homogeneous systems of wavelengths with estimated errors sometimes smaller than 0.001 Å. However, long before 1913, strange non-local inconsistencies had emerged between these systems that were of much greater magnitude than the estimated error. The discovery of the pole effect opened up the possibility that variations in the arc parameters used in the measurements, which the different teams had hitherto not specified, were responsible for the systematic differences, in their respective sets of measurements, coming to up to 0.025 Å.This paper explores the interrelations between local knowledge production, the strategies for the establishment of local coherence, and the ways in which the community of physicists and spectroscopists handled a possible threat to this coherence after 1913. Around 1930, a general agreement was reached about the physical cause of the pole effect, namely Stark effects, caused in turn by intermolecular electric fields of ions in the arc. Much before 1930, however, the community had already succeeded in standardizing the instrumentation used in high-precision spectrometry and had conformed its research practice to such an extent that from 1917 on the pole effect could be routinely circumvented in high-precision spectrometry and interferometry. Thus, experimentation along with its instrumentation, indeed had a life of its own, independent of the many unsuccessful efforts to explain the pole effect theoretically.     

Senescence surveillance of pre-malignant hepatocytes limits liver cancer development

Upon the aberrant activation of oncogenes, normal cells can enter the cellular senescence program, a state of stable cell-cycle arrest, which represents an important barrier against tumour development in vivo. Senescent cells communicate with their environment by secreting various cytokines and growth factors, and it was reported that this 'secretory phenotype' can have pro- as well as anti-tumorigenic effects. Here we show that oncogene-induced senescence occurs in otherwise normal murine hepatocytes in vivo. Pre-malignant senescent hepatocytes secrete chemo- and cytokines and are subject to immune-mediated clearance (designated as 'senescence surveillance'), which depends on an intact CD4(+) T-cell-mediated adaptive immune response. Impaired immune surveillance of pre-malignant senescent hepatocytes results in the development of murine hepatocellular carcinomas (HCCs), thus showing that senescence surveillance is important for tumour suppression in vivo. In accordance with these observations, ras-specific Th1 lymphocytes could be detected in mice, in which oncogene-induced senescence had been triggered by hepatic expression of Nras(G12V). We also found that CD4(+) T cells require monocytes/macrophages to execute the clearance of senescent hepatocytes. Our study indicates that senescence surveillance represents an important extrinsic component of the senescence anti-tumour barrier, and illustrates how the cellular senescence program is involved in tumour immune surveillance by mounting specific immune responses against antigens expressed in pre-malignant senescent cells.     

Zur Differenzierbarkeit stetiger Funktionen — Ampère's Beweis und seine Folgen

Ohne Zusammenfassung Vorgelegt von C. Truesdell     

Acquisition of a multifunctional IgA+ plasma cell phenotype in the gut

The largest mucosal surface in the body is in the gastrointestinal tract, a location that is heavily colonized by microbes that are normally harmless. A key mechanism required for maintaining a homeostatic balance between this microbial burden and the lymphocytes that densely populate the gastrointestinal tract is the production and transepithelial transport of poly-reactive IgA (ref. 1). Within the mucosal tissues, B cells respond to cytokines, sometimes in the absence of T-cell help, undergo class switch recombination of their immunoglobulin receptor to IgA, and differentiate to become plasma cells. However, IgA-secreting plasma cells probably have additional attributes that are needed for coping with the tremendous bacterial load in the gastrointestinal tract. Here we report that mouse IgA(+) plasma cells also produce the antimicrobial mediators tumour-necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS), and express many molecules that are commonly associated with monocyte/granulocytic cell types. The development of iNOS-producing IgA(+) plasma cells can be recapitulated in vitro in the presence of gut stroma, and the acquisition of this multifunctional phenotype in vivo and in vitro relies on microbial co-stimulation. Deletion of TNF-α and iNOS in B-lineage cells resulted in a reduction in IgA production, altered diversification of the gut microbiota and poor clearance of a gut-tropic pathogen. These findings reveal a novel adaptation to maintaining homeostasis in the gut, and extend the repertoire of protective responses exhibited by some B-lineage cells.     

用分子束外延技术按样定制半导体微观结构

在按样定制的半导体微观结构中,通过把异质结精确地植入晶体内即可定域地确定所期望的势能差。分子束外延技术用于以一个原子接一个原子的构建晶体薄膜,从而可以在微观惊工内精确地“裁剪”人工层状晶体。在ＧａＡｓ／ＡｌｘＧａ１－ｘＡｓ超晶格中各组分的周期性调制产生了新颖的电子性质,它开辟了崭新的技术用途。     

Ablation of cyclase-associated protein 2 (CAP2) leads to cardiomyopathy

Cyclase-associated proteins are highly conserved proteins that have a role in the regulation of actin dynamics. Higher eukaryotes have two isoforms, CAP1 and CAP2. To study the in vivo function of CAP2, we generated mice in which the CAP2 gene was inactivated by a gene-trap approach. Mutant mice showed a decrease in body weight and had a decreased survival rate. Further, they developed a severe cardiac defect marked by dilated cardiomyopathy (DCM) associated with drastic reduction in basal heart rate and prolongations in atrial and ventricular conduction times. Moreover, CAP2-deficient myofibrils exhibited reduced cooperativity of calcium-regulated force development. At the microscopic level, we observed disarrayed sarcomeres with development of fibrosis. We analyzed CAP2’s role in actin assembly and found that it sequesters G-actin and efficiently fragments filaments. This activity resides completely in its WASP homology domain. Thus CAP2 is an essential component of the myocardial sarcomere and is essential for physiological functioning of the cardiac system, and a deficiency leads to DCM and various cardiac defects.