The 1998 November 14 Occultation of GSC 0622-00345 by Saturn. II. Stratospheric Thermal Profile, Power Spectrum, and Gravity Waves

On 1998 November 14, Saturn and its rings occulted the star GSC 0622-00345. The occultation latitude was 55.5 degrees S. This paper analyzes the 2.3 {\mu}m light curve derived by Harrington & French. A fixed-baseline isothermal fit to the light curve has a temperature of 140 +/- 3 K, assuming a mean molecular mass of 2.35 AMU. The thermal profile obtained by numerical inversion is valid between 1 and 60 {\mu}bar. The vertical temperature gradient is >0.2 K/km more stable than the adiabatic lapse rate, but it still shows the alternating-rounded-spiked features seen in many temperature gradient profiles from other atmospheric occultations and usually attributed to breaking gravity (buoyancy) waves. We conduct a wavelet analysis of the thermal profile, and show that, even with our low level of noise, scintillation due to turbulence in Earth's atmosphere can produce large temperature swings in light-curve inversions. Spurious periodic features in the "reliable" region of a wavelet amplitude spectrum can exceed 0.3 K in our data. We also show that gravity-wave model fits to noisy isothermal light curves can lead to convincing wave "detections". We provide new significance tests for localized wavelet amplitudes, wave model fits, and global power spectra of inverted occultation light curves by assessing the effects of pre- and post-occultation noise on these parameters. Based on these tests, we detect several significant ridges and isolated peaks in wavelet amplitude, to which we fit a gravity wave model. We also strongly detect the global power spectrum of thermal fluctuations in Saturn's atmosphere, which resembles the "universal" (modified Desaubies) curve associated with saturated spectra of propagating gravity waves on Earth and Jupiter.Comment: LaTeX/emulateapj, 13 pages, 7 figure

Embedding spanning bounded degree graphs in randomly perturbed graphs

We study the model G 8 G(n; p) of randomly perturbed dense graphs, where G is any n-vertex graph with minimum degree at least n and G(n; p) is the binomial random graph. We introduce a general approach for studying the appearance of spanning subgraphs in this model using absorption. This approach yields simpler proofs of several known results. We also use it to derive the following two new results. For every > 0 and C 5, and every n-vertex graph F with maximum degree at most , we show that if p = !(n−2~(+1)) then G 8 G(n; p) with high probability contains a copy of F. The bound used for p here is lower by a log-factor in comparison to the conjectured threshold for the general appearance of such subgraphs in G(n; p) alone, a typical feature of previous results concerning randomly perturbed dense graphs. We also give the rst example of graphs where the appearance threshold in G 8 G(n; p) is lower than the appearance threshold in G(n; p) by substantially more than a log-factor. We prove that, for every k C 2 and > 0, there is some > 0 for which the kth power of a Hamilton cycle with high probability appears in G 8 G(n; p) when p = !(n−1~k−). The appearance threshold of the kth power of a Hamilton cycle in G(n; p) alone is known to be n−1~k, up to a log-term when k = 2, and exactly for k > 2

The Mission Accessible Near-Earth Objects Survey: Four years of photometry

Over 4.5 years, the Mission Accessible Near-Earth Object Survey (MANOS) assembled 228 Near-Earth Object (NEO) lightcurves. We report rotational lightcurves for 82 NEOs, constraints on amplitudes and periods for 21 NEOs, lightcurves with no detected variability within the image signal to noise and length of our observing block for 30 NEOs, and 10 tumblers. We uncovered 2 ultra-rapid rotators with periods below 20s; 2016MA with a potential rotational periodicity of 18.4s, and 2017QG$_{18}$ rotating in 11.9s, and estimate the fraction of fast/ultra-rapid rotators undetected in our project plus the percentage of NEOs with a moderate/long periodicity undetectable during our typical observing blocks. We summarize the findings of a simple model of synthetic NEOs to infer the object morphologies distribution using the measured distribution of lightcurve amplitudes. This model suggests a uniform distribution of axis ratio can reproduce the observed sample. This suggests that the quantity of spherical NEOs (e.g., Bennu) is almost equivalent to the quantity of highly elongated objects (e.g., Itokawa), a result that can be directly tested thanks to shape models from Doppler delay radar imaging analysis. Finally, we fully characterized 2 NEOs as appropriate targets for a potential robotic/human mission: 2013YS$_{2}$ and 2014FA$_{7}$ due to their moderate spin periods and low $\Delta v$.Comment: Accepted for Publication, The Astrophysical Journal Supplement Serie

Management and Population Status of Kihansi Spray Toad Nectophrynoides asperginis in Captive Breeding Facilities in Tanzania

Kihansi spray toad Nectophrynoides asperginis was discovered in 1996 in Kihansi gorge. The toad was declared extinct in the wild in 2009 due to habitat alteration. Before its extinction, 499 individuals were flown to the United States of America zoos in 2000 for captive breeding. In 2010, the University of Dar es Salaam, and in 2011 the Kihansi captive breeding facilities were established in Tanzania. The intention was to breed, and reintroduce the toad back to the natural environment in the gorge. The founder populations for the two facilities were sourced from the USA zoos. This study addresses captive management practices, and population status of the toad at the two facilities from 2013 to 2019. Toad counts were carried out once every two months. There was a significant increase in the number of toads over the years. The increase was associated with suitable management practices. Success in captive breeding at the facilities led to the removal of 3,236 individuals from the University for restocking the Kihansi facility and for reintroduction, and 1,273 individuals from Kihansi facility for reintroduction. The establishment of the two facilities played a major role in both the ex-situ and in-situ conservation of the toadKeywords: Kihansi spray toad; extinction; captive breeding; population; reintroduction

Lymphoid Enhancer Factor-1 Links Two Hereditary Leukemia Syndromes through Core-binding Factor α Regulation of ELA2

Two hereditary human leukemia syndromes are severe congenital neutropenia (SCN), caused by mutations in the gene ELA2, encoding the protease neutrophil elastase, and familial platelet disorder with acute myelogenous leukemia (AML), caused by mutations in the gene AML1, encoding the transcription factor core-binding factor α (CBFα). In mice, CBFα regulates the expression of ELA2, suggesting a common link for both diseases. However, gene-targeted mouse models have failed to reproduce either human disease, thus prohibiting further in vivo studies in mice. Here we investigate CBFα regulation of the human ELA2 promoter, taking advantage of bone marrow obtained from patients with either illness. In particular, we have identified novel ELA2 promoter substitutions (-199 C to A) within a potential motif for lymphoid enhancer factor-1 (LEF-1), a transcriptional mediator of Wnt/β-catenin signaling, in SCN patients. The LEF-1 motif lies adjacent to a potential CBFα binding site that is in a different position in human compared with mouse ELA2. We find that LEF-1 and CBFα co-activate ELA2 expression. In vitro, the high mobility group domain of LEF-1 interacts with the runt DNA binding and proline-, serine-, threonine-rich activation domains of CBFα. ELA2 transcript levels are up-regulated in bone marrow of an SCN patient with the -199 C to A substitution. Conversely, a mutation of the CBFα activation domain, found in a patient with familial platelet disorder with AML, fails to stimulate the ELA2 promoter in vitro, and bone marrow correspondingly demonstrates reduced ELA2 transcript. Observations in these complementary patients indicate that LEF-1 cooperates with CBFα to activate ELA2 in vivo and also suggest the possibility that up-regulating promoter mutations can contribute to SCN. Two hereditary AML predisposition syndromes may therefore intersect via LEF-1, potentially linking them to more generalized cancer mechanisms

Mutations in KCNK4 that Affect Gating Cause a Recognizable Neurodevelopmental Syndrome

Aberrant activation or inhibition of potassium (K+) currents across the plasma membrane of cells has been causally linked to altered neurotransmission, cardiac arrhythmias, endocrine dysfunction, and (more rarely) perturbed developmental processes. The K+ channel subfamily K member 4 (KCNK4), also known as TRAAK (TWIK-related arachidonic acid-stimulated K+ channel), belongs to the mechano-gated ion channels of the TRAAK/TREK subfamily of two-pore-domain (K2P) K+ channels. While K2P channels are well known to contribute to the resting membrane potential and cellular excitability, their involvement in pathophysiological processes remains largely uncharacterized. We report that de novo missense mutations in KCNK4 cause a recognizable syndrome with a distinctive facial gestalt, for which we propose the acronym FHEIG (facial dysmorphism, hypertrichosis, epilepsy, intellectual disability/developmental delay, and gingival overgrowth). Patch-clamp analyses documented a significant gain of function of the identified KCNK4 channel mutants basally and impaired sensitivity to mechanical stimulation and arachidonic acid. Co-expression experiments indicated a dominant behavior of the disease-causing mutations. Molecular dynamics simulations consistently indicated that mutations favor sealing of the lateral intramembrane fenestration that has been proposed to negatively control K+ flow by allowing lipid access to the central cavity of the channel. Overall, our findings illustrate the pleiotropic effect of dysregulated KCNK4 function and provide support to the hypothesis of a gating mechanism based on the lateral fenestrations of K2P channels

Loss-of-function mutations in Lysyl-tRNA synthetase cause various leukoencephalopathy phenotypes

Objective: To expand the clinical spectrum of lysyl-tRNA synthetase (KARS) gene–related diseases, which so far includes Charcot-Marie-Tooth disease, congenital visual impairment and microcephaly, and nonsyndromic hearing impairment. Methods: Whole-exome sequencing was performed on index patients from 4 unrelated families with leukoencephalopathy. Candidate pathogenic variants and their cosegregation were confirmed by Sanger sequencing. Effects of mutations on KARS protein function were examined by aminoacylation assays and yeast complementation assays. Results: Common clinical features of the patients in this study included impaired cognitive ability, seizure, hypotonia, ataxia, and abnormal brain imaging, suggesting that the CNS involvement is the main clinical presentation. Six previously unreported and 1 known KARS mutations were identified and cosegregated in these families. Two patients are compound heterozygous for missense mutations, 1 patient is homozygous for a missense mutation, and 1 patient harbored an insertion mutation and a missense mutation. Functional and structural analyses revealed that these mutations impair aminoacylation activity of lysyl-tRNA synthetase, indicating that de- fective KARS function is responsible for the phenotypes in these individuals. Conclusions: Our results demonstrate that patients with loss-of-function KARS mutations can manifest CNS disorders, thus broadening the phenotypic spectrum associated with KARS-related disease

The Emerging Story of Disability Associated with Lymphatic Filariasis: A Critical Review

Globally, 40 million people live with the chronic effects of lymphatic filariasis (LF), making it the second leading cause of disability in the world. Despite this, there is limited research into the experiences of people living with the disease. This review summarises the research on the experiences of people living with LF disability. The review highlights the widespread social stigma and oppressive psychological issues that face most people living with LF-related disability. Physical manifestations of LF make daily activities and participation in community life difficult. The findings confirm the need for the Global Programme to Eliminate Lymphatic Filariasis (GPELF) to support morbidity management activities that address the complex biopsychosocial issues that people living with LF-related disability face