Minimum cycle and homology bases of surface embedded graphs

We study the problems of finding a minimum cycle basis (a minimum weight set of cycles that form a basis for the cycle space) and a minimum homology basis (a minimum weight set of cycles that generates the $1$-dimensional ($\mathbb{Z}_2$)-homology classes) of an undirected graph embedded on a surface. The problems are closely related, because the minimum cycle basis of a graph contains its minimum homology basis, and the minimum homology basis of the $1$-skeleton of any graph is exactly its minimum cycle basis. For the minimum cycle basis problem, we give a deterministic $O(n^\omega+2^{2g}n^2+m)$-time algorithm for graphs embedded on an orientable surface of genus $g$. The best known existing algorithms for surface embedded graphs are those for general graphs: an $O(m^\omega)$ time Monte Carlo algorithm and a deterministic $O(nm^2/\log n + n^2 m)$ time algorithm. For the minimum homology basis problem, we give a deterministic $O((g+b)^3 n \log n + m)$-time algorithm for graphs embedded on an orientable or non-orientable surface of genus $g$ with $b$ boundary components, assuming shortest paths are unique, improving on existing algorithms for many values of $g$ and $n$. The assumption of unique shortest paths can be avoided with high probability using randomization or deterministically by increasing the running time of the homology basis algorithm by a factor of $O(\log n)$.Comment: A preliminary version of this work was presented at the 32nd Annual International Symposium on Computational Geometr

OctubaFest 2013, KSU Tuba and Euphonium Ensemble

KSU School of Music presents OctubaFest 2013, KSU Tuba and Euphonium Ensemble.https://digitalcommons.kennesaw.edu/musicprograms/1291/thumbnail.jp

Delayed Endovascular Coil Extrusion following Internal Carotid Artery Embolization

Internal carotid artery injury is a rare and devastating complication of endoscopic sinus and skull base surgery that has an associated mortality rate of 15%. This case describes a patient who developed massive epistaxis following routine sinus surgery and was eventually diagnosed with a pseudoaneurysm of the cavernous internal carotid artery. Endovascular coiling and Onyx (Covidien, Irvine, California, United States) liquid embolization were ultimately used to completely occlude the internal carotid artery with resolution of bleeding; however, the patient had an unexpected late complication of coil extrusion through the pseudoaneurysm sac into the sphenoid sinus and nasal cavity. The endoscopic skull base team safely excised the coils endoscopically without recurrent bleeding. We describe the multidisciplinary operative management of this case of endovascular coil extrusion to increase awareness of this potentially life-threatening complication

Tumor Microenvironment-Induced Immunometabolic Reprogramming of Natural Killer Cells

Energy metabolism is key to the promotion of tumor growth, development, and metastasis. At the same time, cellular metabolism also mediates immune cell survival, proliferation and cytotoxic responses within the tumor microenvironment. The ability of natural killer cells to eradicate tumors relies on their ability to functionally persist for the duration of their anti-tumor effector activity. However, a tumor's altered metabolic requirements lead to compromised functional responses of cytokine-activated natural killer cells, which result in decreased effectiveness of adoptive cell-based immunotherapies. Tumors exert these immunosuppressive effects through a number of mechanisms, a key driver of which is hypoxia. Hypoxia also fuels the generation of adenosine from the cancer-associated ectoenzymes CD39 and CD73. Adenosine's immunosuppression manifests in decreased proliferation and impaired anti-tumor function, with adenosinergic signaling emerging as an immunometabolic checkpoint blockade target. Understanding such immunometabolic suppression is critical in directing the engineering of a new generation of natural killer cell-based immunotherapies that have the ability to more effectively target difficult-to-treat solid tumors

Mixed Chamber Ensembles

Kennesaw State University School of Music presents Mixed Chamber Ensembles, 10:00 a.m. performance.https://digitalcommons.kennesaw.edu/musicprograms/1395/thumbnail.jp

Myocardial Lipin 1 knockout in mice approximates cardiac effects of human LPIN1 mutations

Lipin 1 is a bifunctional protein that is a transcriptional regulator and has phosphatidic acid (PA) phosphohydrolase activity, which dephosphorylates PA to generate diacylglycerol. Human lipin 1 mutations lead to episodic rhabdomyolysis, and some affected patients exhibit cardiac abnormalities, including exercise-induced cardiac dysfunction and cardiac triglyceride accumulation. Furthermore, lipin 1 expression is deactivated in failing heart, but the effects of lipin 1 deactivation in myocardium are incompletely understood. We generated mice with cardiac-specific lipin 1 KO (cs-Lpin1-/-) to examine the intrinsic effects of lipin 1 in the myocardium. Cs-Lpin1-/- mice had normal systolic cardiac function but mild cardiac hypertrophy. Compared with littermate control mice, PA content was higher in cs-Lpin1-/- hearts, which also had an unexpected increase in diacylglycerol and triglyceride content. Cs-Lpin1-/- mice exhibited diminished cardiac cardiolipin content and impaired mitochondrial respiration rates when provided with pyruvate or succinate as metabolic substrates. After transverse aortic constriction-induced pressure overload, loss of lipin 1 did not exacerbate cardiac hypertrophy or dysfunction. However, loss of lipin 1 dampened the cardiac ionotropic response to dobutamine and exercise endurance in association with reduced protein kinase A signaling. These data suggest that loss of lipin 1 impairs cardiac functional reserve, likely due to effects on glycerolipid homeostasis, mitochondrial function, and protein kinase A signaling

The Time-Domain Spectroscopic Survey: Understanding the Optically Variable Sky with SEQUELS in SDSS-III

The Time-Domain Spectroscopic Survey (TDSS) is an SDSS-IV eBOSS subproject primarily aimed at obtaining identification spectra of ~220,000 optically-variable objects systematically selected from SDSS/Pan-STARRS1 multi-epoch imaging. We present a preview of the science enabled by TDSS, based on TDSS spectra taken over ~320 deg^2 of sky as part of the SEQUELS survey in SDSS-III, which is in part a pilot survey for eBOSS in SDSS-IV. Using the 15,746 TDSS-selected single-epoch spectra of photometrically variable objects in SEQUELS, we determine the demographics of our variability-selected sample, and investigate the unique spectral characteristics inherent in samples selected by variability. We show that variability-based selection of quasars complements color-based selection by selecting additional redder quasars, and mitigates redshift biases to produce a smooth quasar redshift distribution over a wide range of redshifts. The resulting quasar sample contains systematically higher fractions of blazars and broad absorption line quasars than from color-selected samples. Similarly, we show that M-dwarfs in the TDSS-selected stellar sample have systematically higher chromospheric active fractions than the underlying M-dwarf population, based on their H-alpha emission. TDSS also contains a large number of RR Lyrae and eclipsing binary stars with main-sequence colors, including a few composite-spectrum binaries. Finally, our visual inspection of TDSS spectra uncovers a significant number of peculiar spectra, and we highlight a few cases of these interesting objects. With a factor of ~15 more spectra, the main TDSS survey in SDSS-IV will leverage the lessons learned from these early results for a variety of time-domain science applications.Comment: 17 pages, 14 figures, submitted to Ap

Adenosinergic Signaling Alters Natural Killer Cell Functional Responses

Adenosine is a potent immunosuppressive purine metabolite contributing to the pathogenesis of solid tumors. Extracellular adenosine signals on tumor-infiltrating NK cells to inhibit their proliferation, maturation, and cytotoxic function. Cytokine priming imparts upon NK cells distinct activation statuses, which modulate NK anti-tumor immunity and responses to purinergic metabolism. Here, for the first time, we investigated human NK cell responses to adenosinergic signaling in the context of distinct cytokine priming programs. NK cells were shown to be hyper-responsive to adenosine when primed with IL-12 and IL-15 compared to IL-2, exhibiting enhanced IFN-γ expression from CD56bright and CD56dim subsets while modulating the expression of activation marker NKG2D. These responses resulted in signaling that was dependent on mTOR. Adenosine induced upregulation of transcriptional signatures for genes involved in immune responses while downregulating cellular metabolism and other protein synthesis functions that correlate to inhibited oxidative phosphorylation and glycolysis. Overall, our findings show that adenosine acts on specific cellular pathways rather than inducing a broad inhibition of NK cell functions. These responses are dependent on cytokine priming signatures and are important in designing therapeutic interventions that can reprogram NK cell immunometabolism for improved immunotherapies of solid tumors