Error in Airspeed Measurement Due to the Static-Pressure Field Ahead of an Airplane at Transonic Speeds

The magnitude and variation of the static-pressure error for various distances ahead of sharp-nose bodies and open-nose air inlets and for a distance of 1 chord ahead of the wing tip of a swept wing are defined by a combination of experiment and theory. The mechanism of the error is discussed in some detail to show the contributing factors that make up the error. The information presented provides a useful means for choosing a proper location for measurement of static pressure for most purposes

Rifts in Spreading Wax Layers

We report experimental results on the rift formation between two freezing wax plates. The plates were pulled apart with constant velocity, while floating on the melt, in a way akin to the tectonic plates of the earth's crust. At slow spreading rates, a rift, initially perpendicular to the spreading direction, was found to be stable, while above a critical spreading rate a "spiky" rift with fracture zones almost parallel to the spreading direction developed. At yet higher spreading rates a second transition from the spiky rift to a zig-zag pattern occurred. In this regime the rift can be characterized by a single angle which was found to be dependent on the spreading rate. We show that the oblique spreading angles agree with a simple geometrical model. The coarsening of the zig-zag pattern over time and the three-dimensional structure of the solidified crust are also discussed.Comment: 4 pages, Postscript fil

A Missense Mutation in the Transcription Factor ETV5 Leads to Sterility, Increased Embryonic and Perinatal Death, Postnatal Growth Restriction, Renal Asymmetry and Polydactyly in the Mouse

ETV5 (Ets variant gene 5) is a transcription factor that is required for fertility. In this study, we demonstrate that ETV5 plays additional roles in embryonic and postnatal developmental processes in the mouse. Through a genome-wide mouse mutagenesis approach, we generated a sterile mouse line that carried a nonsense mutation in exon 12 of the Etv5 gene. The mutation led to the conversion of lysine at position 412 into a premature termination codon (PTC) within the ETS DNA binding domain of the protein. We showed that the PTC-containing allele produced a highly unstable mRNA, which in turn resulted in an undetectable level of ETV5 protein. The Etv5 mutation resulted in male and female sterility as determined by breeding experiments. Mutant males were sterile due to a progressive loss of spermatogonia, which ultimately resulted in a Sertoli cell only phenotype by 8 week-of-age. Further, the ETV5 target genes Cxcr4 and Ccl9 were significantly down-regulated in mutant neonate testes. CXCR4 and CCL9 have been implicated in the maintenance and migration of spermatogonia, respectively. Moreover, the Etv5 mutation resulted in several developmental abnormalities including an increased incidence of embryonic and perinatal lethality, postnatal growth restriction, polydactyly and renal asymmetry. Thus, our data define a physiological role for ETV5 in many aspects of development including embryonic and perinatal survival, postnatal growth, limb patterning, kidney development and fertility.This work was supported by grants the Australian Research Council (ARC) to MKO’B and CJO; the New South Wales Cancer Council, Cancer Institute New South Wales, Banque Nationale de Paris-Paribas Australia and New Zealand, RT Hall Trust, and the National Breast Cancer Foundation to CJO. DJ was a National Health and Medical Research Council (NHMRC) of Australia Peter Doherty Postdoctoral Fellow (#384297). MKO’B and CJO are NHMRC Senior Research Fellows (#545805, #481310). CCG is an NHMRC Australia Fellowship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

SOX30 is required for male fertility in mice

Male infertility is a major and growing problem and, in most cases, the specific root cause is unknown. Here we show that the transcription factor SOX30 plays a critical role in mouse spermatogenesis. Sox30-null mice are healthy and females are fertile, but males are sterile. In the absence of Sox30 meiosis initiates normally in both sexes but, in males, germ cell development arrests during the post-meiotic round spermatid period. In the mutant testis, acrosome and axoneme development are aberrant, multinucleated germ cells (symplasts) form and round spermatids unable to process beyond step 3 of spermiogenesis. No elongated spermatids nor spermatozoa are produced. Thus, Sox30 represents a rare example of a gene for which loss of function results in a complete arrest of spermatogenesis at the onset of spermiogenesis. Our results suggest that SOX30 mutations may underlie some instances of unexplained non-obstructive azoospermia in humans.Chun-Wei Allen Feng, Cassy Spiller, Donna J. Merriner, Moira K. O’Bryan, Josephine Bowles, Peter Koopma

Compendium of Current Total Ionizing Dose and Displacement Damage Results from NASA GSFC and NEPP

Total ionizing dose and displacement damage testing was performed to characterize and determine the suitability of candidate electronics for NASA space utilization. Devices tested include opto-electronics, digital, analog, linear bipolar devices, and hybrid devices

New Young Star Candidates in BRC 27 and BRC 34

We used archival Spitzer Space Telescope mid-infrared data to search for young stellar objects (YSOs) in the immediate vicinity of two bright-rimmed clouds, BRC 27 (part of CMa R1) and BRC 34 (part of the IC 1396 complex). These regions both appear to be actively forming young stars, perhaps triggered by the proximate OB stars. In BRC 27, we find clear infrared excesses around 22 of the 26 YSOs or YSO candidates identified in the literature, and identify 16 new YSO candidates that appear to have IR excesses. In BRC 34, the one literature-identified YSO has an IR excess, and we suggest 13 new YSO candidates in this region, including a new Class I object. Considering the entire ensemble, both BRCs are likely of comparable ages, within the uncertainties of small number statistics and without spectroscopy to confirm or refute the YSO candidates. Similarly, no clear conclusions can yet be drawn about any possible age gradients that may be present across the BRCs.Comment: 54 pages, 19 figures, accepted by A

NASA Goddard Space Flight Center's Compendium of Recent Total Ionizing Dose and Displacement Damage Dose Results

Total ionizing dose and displacement damage dose testing were performed to characterize and determine the suitability of candidate electronics for NASA spacecraft and program use

RBM5 Is a Male Germ Cell Splicing Factor and Is Required for Spermatid Differentiation and Male Fertility

Alternative splicing of precursor messenger RNA (pre-mRNA) is common in mammalian cells and enables the production of multiple gene products from a single gene, thus increasing transcriptome and proteome diversity. Disturbance of splicing regulation is associated with many human diseases; however, key splicing factors that control tissue-specific alternative splicing remain largely undefined. In an unbiased genetic screen for essential male fertility genes in the mouse, we identified the RNA binding protein RBM5 (RNA binding motif 5) as an essential regulator of haploid male germ cell pre-mRNA splicing and fertility. Mice carrying a missense mutation (R263P) in the second RNA recognition motif (RRM) of RBM5 exhibited spermatid differentiation arrest, germ cell sloughing and apoptosis, which ultimately led to azoospermia (no sperm in the ejaculate) and male sterility. Molecular modelling suggested that the R263P mutation resulted in compromised mRNA binding. Within the adult mouse testis, RBM5 localises to somatic and germ cells including spermatogonia, spermatocytes and round spermatids. Through the use of RNA pull down coupled with microarrays, we identified 11 round spermatid-expressed mRNAs as putative RBM5 targets. Importantly, the R263P mutation affected pre-mRNA splicing and resulted in a shift in the isoform ratios, or the production of novel spliced transcripts, of most targets. Microarray analysis of isolated round spermatids suggests that altered splicing of RBM5 target pre-mRNAs affected expression of genes in several pathways, including those implicated in germ cell adhesion, spermatid head shaping, and acrosome and tail formation. In summary, our findings reveal a critical role for RBM5 as a pre-mRNA splicing regulator in round spermatids and male fertility. Our findings also suggest that the second RRM of RBM5 is pivotal for appropriate pre-mRNA splicing.This work was supported by grants from the National Health and Medical Research Council (NHMRC) to DJ (#606503); the Australian Research Council (ARC) to MKO and CJO; the New South Wales Cancer Council, Cancer Institute New South Wales, Banque Nationale de Paris-Paribas Australia and New Zealand, RT Hall Trust, and the National Breast Cancer Foundation to CJO. DJ was an NHMRC Peter Doherty Postdoctoral Fellow (#384297). MKO and CJO are NHMRC Senior Research Fellows (#545805, #481310). CCG is an NHMRC Australia Fellowship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

RAB-Like 2 Has an Essential Role in Male Fertility, Sperm Intra-Flagellar Transport, and Tail Assembly

A significant percentage of young men are infertile and, for the majority, the underlying cause remains unknown. Male infertility is, however, frequently associated with defective sperm motility, wherein the sperm tail is a modified flagella/cilia. Conversely, a greater understanding of essential mechanisms involved in tail formation may offer contraceptive opportunities, or more broadly, therapeutic strategies for global cilia defects. Here we have identified Rab-like 2 (RABL2) as an essential requirement for sperm tail assembly and function. RABL2 is a member of a poorly characterized clade of the RAS GTPase superfamily. RABL2 is highly enriched within developing male germ cells, where it localizes to the mid-piece of the sperm tail. Lesser amounts of Rabl2 mRNA were observed in other tissues containing motile cilia. Using a co-immunoprecipitation approach and RABL2 affinity columns followed by immunochemistry, we demonstrated that within developing haploid germ cells RABL2 interacts with intra-flagella transport (IFT) proteins and delivers a specific set of effector (cargo) proteins, including key members of the glycolytic pathway, to the sperm tail. RABL2 binding to effector proteins is regulated by GTP. Perturbed RABL2 function, as exemplified by the Mot mouse line that contains a mutation in a critical protein-protein interaction domain, results in male sterility characterized by reduced sperm output, and sperm with aberrant motility and short tails. Our data demonstrate a novel function for the RABL protein family, an essential role for RABL2 in male fertility and a previously uncharacterised mechanism for protein delivery to the flagellum.This work was supported by grants from the NHMRC to MKO (#606445) and CJO, the Australian Research Council (MKO, RJA, and CJO), the New South Wales Cancer Council (CJO), Cancer Institute New South Wales (CJO), Banque Nationale de Paris-Paribas Australia and New Zealand (CJO), RT Hall Trust (CJO), and the National Breast Cancer Foundation (CJO). JCYL is the recipient of a NHMRC PhD scholarship. MKO and CJO are the recipients of NHMRC Senior Research Fellowships (#545805 and #481310). CCG is the recipient an NHMRC Australia Fellowship. JCW is the recipient of an Australian Research Council Federation Fellowship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript