Telecommunications and radio-metric support for a manned mission to Mars

Some general characteristics of the Deep Space Network are described and related to services needed by a manned mission to Mars. Specific details of the current Network capabilities and those planned for the near future may be found in the reference

Digital demodulator-correlator

An apparatus for demodulation and correlation of a code modulated 10 MHz signal is presented. The apparatus is comprised of a sample and hold analog-to-digital converter synchronized by a frequency coherent 40 MHz pulse to obtain four evenly spaced samples of each of the signal. Each sample is added or subtracted to or from one of four accumulators to or from the separate sums. The correlation functions are then computed. As a further feature of the invention, multipliers are each multiplied by a squarewave chopper signal having a period that is long relative to the period of the received signal to foreclose contamination of the received signal by leakage from either of the other two terms of the multipliers

COMMUNICATIONS LINK FOR COMPUTERS

A system is disclosed for a computer to communicate with a selected one of a plurality of other computers through two identical communications links associated with the communicating computers. A single channel connects the two links which operate at a clock rate independent of the computers. Binary digits and clock pulses are combined and converted into a three-level signal for serial transmission over the single channel. Both control messages and data words may be transmitted. Each message and word transmitted is checked for error by the receiving link before it is accepted and the receiving computer is interrupted. If error is found, an error message is automatically transmitted to the originating computer

A Model for Sequential Decoding Overflow Due to a Noisy Carrier Reference

International Telemetering Conference Proceedings / October 15-17, 1974 / International Hotel, Los Angeles, CaliforniaAn approximate analysis of the effect of a noisy carrier reference on the performance of sequential decoding is presented. The analysis uses previously developed techniques for analyzing noisy reference performance for medium-rate uncoded communications adapted to sequential decoding for data rates of 8 to 2048 bits/s. In estimating the 10⁻⁴ deletion probability thresholds for Helios, the model agrees with experimental data to within the experimental tolerances.International Foundation for TelemeteringProceedings from the International Telemetering Conference are made available by the International Foundation for Telemetering and the University of Arizona Libraries. Visit http://www.telemetry.org/index.php/contact-us if you have questions about items in this collection

COMMUNICATIONS LINK FOR COMPUTERS

A system is disclosed for a computer to communicate with a selected one of a plurality of other computers through two identical communications links associated with the communicating computers. A single channel connects the two links which operate at a clock rate independent of the computers. Binary digits and clock pulses are combined and converted into a three-level signal for serial transmission over the single channel. Both control messages and data words may be transmitted. Each message and word transmitted is checked for error by the receiving link before it is accepted and the receiving computer is interrupted. If error is found, an error message is automatically transmitted to the originating computer

Mapping the first stages of mesoderm commitment during differentiation of human embryonic stem cells

Our understanding of how mesodermal tissue is formed has been limited by the absence of specific and reliable markers of early mesoderm commitment. We report that mesoderm commitment from human embryonic stem cells (hESCs) is initiated by epithelial-to-mesenchymal transition (EMT) as shown by gene expression profiling and by reciprocal changes in expression of the cell surface proteins, EpCAM/CD326 and NCAM/CD56. Molecular and functional assays reveal that the earliest CD326−CD56+ cells, generated from hESCs in the presence of activin A, BMP4, VEGF, and FGF2, represent a multipotent mesoderm-committed progenitor population. CD326−CD56+ progenitors are unique in their ability to generate all mesodermal lineages including hematopoietic, endothelial, mesenchymal (bone, cartilage, fat, fibroblast), smooth muscle, and cardiomyocytes, while lacking the pluripotency of hESCs. CD326−CD56+ cells are the precursors of previously reported, more lineage-restricted mesodermal progenitors. These findings present a unique approach to study how germ layer specification is regulated and offer a promising target for tissue engineering

Generation and Functional Characterization of Knock-in Mice Harboring the Cardiac Troponin I-R21C Mutation Associated with Hypertrophic Cardiomyopathy

The R21C substitution in cardiac troponin I (cTnI) is the only identified mutation within its unique N-terminal extension that is associated with hypertrophic cardiomyopathy (HCM) in man. Particularly, this mutation is located in the consensus sequence for β-adrenergic-activated protein kinase A (PKA)-mediated phosphorylation. The mechanisms by which this mutation leads to heart disease are still unclear. Therefore, we generated cTnI knock-in mouse models carrying an R21C mutation to evaluate the resultant functional consequences. Measuring the in vivo levels of incorporated mutant and WT cTnI, and their basal phosphorylation levels by top-down mass spectrometry demonstrated: 1) a dominant-negative effect such that, the R21C+/− hearts incorporated 24.9% of the mutant cTnI within the myofilament; and 2) the R21C mutation abolished the in vivo phosphorylation of Ser(23)/Ser(24) in the mutant cTnI. Adult heterozygous (R21C+/−) and homozygous (R21C+/+) mutant mice activated the fetal gene program and developed a remarkable degree of cardiac hypertrophy and fibrosis. Investigation of cardiac skinned fibers isolated from WT and heterozygous mice revealed that the WT cTnI was completely phosphorylated at Ser(23)/Ser(24) unless the mice were pre-treated with propranolol. After propranolol treatment (−PKA), the pCa-tension relationships of all three mice (i.e. WT, R21C+/−, and R21C+/+) were essentially the same. However, after treatment with propranolol and PKA, the R21C cTnI mutation reduced (R21C+/−) or abolished (R21C+/+) the well known decrease in the Ca(2+) sensitivity of tension that accompanies Ser(23)/Ser(24) cTnI phosphorylation. Altogether, the combined effects of the R21C mutation appear to contribute toward the development of HCM and suggest that another physiological role for the phosphorylation of Ser(23)/Ser(24) in cTnI is to prevent cardiac hypertrophy