Counting BPS Operators in Gauge Theories: Quivers, Syzygies and Plethystics

We develop a systematic and efficient method of counting single-trace and multi-trace BPS operators with two supercharges, for world-volume gauge theories of $N$ D-brane probes for both $N \to \infty$ and finite $N$. The techniques are applicable to generic singularities, orbifold, toric, non-toric, complete intersections, et cetera, even to geometries whose precise field theory duals are not yet known. The so-called ``Plethystic Exponential'' provides a simple bridge between (1) the defining equation of the Calabi-Yau, (2) the generating function of single-trace BPS operators and (3) the generating function of multi-trace operators. Mathematically, fascinating and intricate inter-relations between gauge theory, algebraic geometry, combinatorics and number theory exhibit themselves in the form of plethystics and syzygies.Comment: 59+1 pages, 7 Figure

Cytochrome c lysine acetylation regulates cellular respiration and cell death in ischemic skeletal muscle

Skeletal muscle is more resilient to ischemia-reperfusion injury than other organs. Tissue specific post-translational modifications of cytochrome c (Cytc) are involved in ischemia-reperfusion injury by regulating mitochondrial respiration and apoptosis. Here, we describe an acetylation site of Cytc, lysine 39 (K39), which was mapped in ischemic porcine skeletal muscle and removed by sirtuin5 in vitro. Using purified protein and cellular double knockout models, we show that K39 acetylation and acetylmimetic K39Q replacement increases cytochrome c oxidase (COX) activity and ROS scavenging while inhibiting apoptosis via decreased binding to Apaf-1, caspase cleavage and activity, and cardiolipin peroxidase activity. These results are discussed with X-ray crystallography structures of K39 acetylated (1.50 Å) and acetylmimetic K39Q Cytc (1.36 Å) and NMR dynamics. We propose that K39 acetylation is an adaptive response that controls electron transport chain flux, allowing skeletal muscle to meet heightened energy demand while simultaneously providing the tissue with robust resilience to ischemia-reperfusion injury.National Institutes of Health R01 GM116807, R01 NS120322Ministerio de Ciencia e Innovación PGC2018-096049-B-I00, PID2021-126663NB-I00Junta de Andalucía BIO-198, US-1254317, US-1257019, P18-FR-3487, P18HO-409

Intraoperative non invasive intracranial pressure monitoring during pneumoperitoneum: a case report and a review of the published cases and case report series.

Non-invasive measurement of ICP (nICP) can be warranted in patients at risk for developing increased ICP during pneumoperitoneum (PP). Our aim was to assess available data on the application of nICP monitoring during these procedures and to present a patient assessed with an innovative combination of noninvasive tools. Literature review of nICP assessment during PP did not find any studies comparing different methods intraprocedurally and only few studies of any nICP monitoring were available: transcranial Doppler (TCD) studies used the pulsatility index (PI) as an estimator of ICP and failed to detect a significant ICP increase during PP, whereas two out of three optic nerve sheath diameter (ONSD) studies detected a statistically significant ICP increase. In the case study, we describe a 52 year old man with a high grade thalamic glioma who underwent urgent laparoscopic cholecystectomy. Considering the high intraoperative risk of developing intracranial hypertension, he was monitored through parallel ONSD ultrasound measurement and TCD derived formulae (flow velocity diastolic formula, FVdnICP, and PI). ONSD and FVdnICP methods indicated a significant ICP increase during PP, whereas PI was not significantly increased. Our experience, combined with the literature review, seems to suggest that PI might not detect ICP changes in this context, however we indicate a possible interest of nICP monitoring during PP by means of ONSD and of TCD derived FVdNICP, especially for patients at risk for increased ICP.D.C. and M.C. are partially supported by NIHR Brain Injury Healthcare Technology Co-operative, Cambridge, UK