Atmospheric neutrons

Contributions to fast neutron measurements in the atmosphere are outlined. The results of a calculation to determine the production, distribution and final disappearance of atmospheric neutrons over the entire spectrum are presented. An attempt is made to answer questions that relate to processes such as neutron escape from the atmosphere and C-14 production. In addition, since variations of secondary neutrons can be related to variations in the primary radiation, comment on the modulation of both radiation components is made

Depleted Energy Charge and Increased Pulmonary Endothelial Permeability Induced by Mitochondrial Complex I inhibition are Mitigated by Coenzyme Q\u3csub\u3e1\u3c/sub\u3e in the Isolated Perfused Rat Lung

Mitochondrial dysfunction is associated with various forms of lung injury and disease that also involve alterations in pulmonary endothelial permeability, but the relationship, if any, between the two is not well understood. This question was addressed by perfusing isolated intact rat lung with a buffered physiological saline solution in the absence or presence of the mitochondrial complex I inhibitor rotenone (20 μM). Compared to control, rotenone depressed whole lung tissue ATP from 5.66±0.46 (SEM) to 2.34±0.15 µmol·g−1 dry lung, with concomitant increases in the ADP:ATP and AMP:ATP ratios. Rotenone also increased lung perfusate lactate (from 12.36±1.64 to 38.62±3.14 µmol·15 min−1 perfusion·g−1 dry lung) and the lactate:pyruvate ratio, but had no detectable impact on lung tissue GSH:GSSG redox status. The amphipathic quinone coenzyme Q1 (CoQ1; 50 μM) mitigated the impact of rotenone on the adenine nucleotide balance, wherein mitigation was blocked by NAD(P)H-quinone oxidoreductase 1 or mitochondrial complex III inhibitors. In separate studies, rotenone increased the pulmonary vascular endothelial filtration coefficient (Kf) from 0.043±0.010 to 0.156±0.037 ml·min−1·cm H2O−1·g−1 dry lung, and CoQ1 protected against the effect of rotenone on Kf. A second complex I inhibitor, piericidin A, qualitatively reproduced the impact of rotenone on Kf and the lactate:pyruvate ratio. Taken together, the observations imply that pulmonary endothelial barrier integrity depends on mitochondrial bioenergetics as reflected in lung tissue ATP levels and that compensatory activation of whole lung glycolysis cannot protect against pulmonary endothelial hyperpermeability in response to mitochondrial blockade. The study further suggests that low-molecular-weight amphipathic quinones may have therapeutic utility in protecting lung barrier function in mitochondrial insufficiency

Living IoT: A Flying Wireless Platform on Live Insects

Sensor networks with devices capable of moving could enable applications ranging from precision irrigation to environmental sensing. Using mechanical drones to move sensors, however, severely limits operation time since flight time is limited by the energy density of current battery technology. We explore an alternative, biology-based solution: integrate sensing, computing and communication functionalities onto live flying insects to create a mobile IoT platform. Such an approach takes advantage of these tiny, highly efficient biological insects which are ubiquitous in many outdoor ecosystems, to essentially provide mobility for free. Doing so however requires addressing key technical challenges of power, size, weight and self-localization in order for the insects to perform location-dependent sensing operations as they carry our IoT payload through the environment. We develop and deploy our platform on bumblebees which includes backscatter communication, low-power self-localization hardware, sensors, and a power source. We show that our platform is capable of sensing, backscattering data at 1 kbps when the insects are back at the hive, and localizing itself up to distances of 80 m from the access points, all within a total weight budget of 102 mg.Comment: Co-primary authors: Vikram Iyer, Rajalakshmi Nandakumar, Anran Wang, In Proceedings of Mobicom. ACM, New York, NY, USA, 15 pages, 201

Effective algebraic degeneracy

We prove that any nonconstant entire holomorphic curve from the complex line C into a projective algebraic hypersurface X = X^n in P^{n+1}(C) of arbitrary dimension n (at least 2) must be algebraically degenerate provided X is generic if its degree d = deg(X) satisfies the effective lower bound: d larger than or equal to n^{{(n+1)}^{n+5}}

A Neuropsychoanalytical approach to the hard problem of consciousness

A neuropsychoanalytical approach to the ‘hard problem’ of consciousness revolves around the distinction between the subject and objects of consciousness. In contrast to the mainstream of cognitive science, neuropsychoanalysis prioritises the subject. The subject of consciousness is the indispensable page upon which its objects are inscribed. This has implications for our conception of the mental. The subjective being of consciousness is not registered in the classical exteroceptive modalities; it is not a cognitive representation, not a memory trace. Cognitive representations are ‘mental solids,’ embedded within subjective consciousness, and their tangible and visible (etc.) properties are projected onto reality. It is important to recognise that mental solids (e.g. the body-as-object) are no more real than the subjective being they are represented in (the body-as-subject). Moreover, pure subjectivity is not without content or quality. This aspect of consciousness is conventionally described quantitatively as the level of consciousness, ‘wakefulness’. But it feels like something to be awake. The primary modality of this aspect of consciousness is affect. Some implications of this frame of reference are discussed here, in broad brush strokes. This is an electronic version of an article published as Journal of Integrative Neuroscience, Volume 13, Issue 2, 2014, pp. 173-185. DOI: http://dx.doi.org/10.1142/S0219635214400032, © World Scientific Publishing Company, http://www.worldscientific.com/worldscinet/jin

Mutations in LRRC50 Predispose Zebrafish and Humans to Seminomas

Seminoma is a subclass of human testicular germ cell tumors (TGCT), the most frequently observed cancer in young men with a rising incidence. Here we describe the identification of a novel gene predisposing specifically to seminoma formation in a vertebrate model organism. Zebrafish carrying a heterozygous nonsense mutation in Leucine-Rich Repeat Containing protein 50 (lrrc50 also called dnaaf1), associated previously with ciliary function, are found to be highly susceptible to the formation of seminomas. Genotyping of these zebrafish tumors shows loss of heterozygosity (LOH) of the wild-type lrrc50 allele in 44.4% of tumor samples, correlating with tumor progression. In humans we identified heterozygous germline LRRC50 mutations in two different pedigrees with a family history of seminomas, resulting in a nonsense Arg488* change and a missense Thr590Met change, which show reduced expression of the wild-type allele in seminomas. Zebrafish in vivo complementation studies indicate the Thr590Met to be a loss-of-function mutation. Moreover, we show that a pathogenic Gln307Glu change is significantly enriched in individuals with seminoma tumors (13% of our cohort). Together, our study introduces an animal model for seminoma and suggests LRRC50 to be a novel tumor suppressor implicated in human seminoma pathogenesis