CPT Violation Implies Violation of Lorentz Invariance

An interacting theory that violates CPT invariance necessarily violates Lorentz invariance. On the other hand, CPT invariance is not sufficient for out-of-cone Lorentz invariance. Theories that violate CPT by having different particle and antiparticle masses must be nonlocal.Comment: Minor changes in the published versio

Leading-twist pion and kaon distribution amplitudes in the gauge-invariant nonlocal chiral quark model from the instanton vacuum

We investigate the leading-twist light-cone distribution amplitudes for the pion and kaon based on the gauge-invariant nonlocal chiral quark model from the instanton vacuum in the presence of external axial-vector currents. We find that the nonlocal contribution from the gauge invariance has much effects on the pion distribution amplitudes, while it changes mildly the kaon ones. We also study the Gegenbauer moments of the distribution amplitudes and compare them with the empirical analysis of the CLEO data.Comment: 14 pages, 10 figure

Ectopic A-lattice seams destabilize microtubules

Natural microtubules typically include one A-lattice seam within an otherwise helically symmetric B-lattice tube. It is currently unclear how A-lattice seams influence microtubule dynamic instability. Here we find that including extra A-lattice seams in GMPCPP microtubules, structural analogues of the GTP caps of dynamic microtubules, destabilizes them, enhancing their median shrinkage rate by >20-fold. Dynamic microtubules nucleated by seeds containing extra A-lattice seams have growth rates similar to microtubules nucleated by B-lattice seeds, yet have increased catastrophe frequencies at both ends. Furthermore, binding B-lattice GDP microtubules to a rigor kinesin surface stabilizes them against shrinkage, whereas microtubules with extra A-lattice seams are stabilized only slightly. Our data suggest that introducing extra A-lattice seams into dynamic microtubules destabilizes them by destabilizing their GTP caps. On this basis, we propose that the single A-lattice seam of natural B-lattice MTs may act as a trigger point, and potentially a regulation point, for catastrophe

Genesis of the Antarctic Slope Current in West Antarctica

The stability of the West Antarctic Ice Sheet (WAIS) depends on ocean heat transport toward its base and remains a source of uncertainty in sea level rise prediction. The Antarctic Slope Current (ASC), a major boundary current of the ocean's global circulation, serves as a dynamic gateway for heat transport toward Antarctica. Here, we use observations collected from the Bellingshausen Sea to propose a mechanistic explanation for the initiation of the westward‐flowing ASC. Waters modified throughout the Bellingshausen Sea by ocean‐sea‐ice and ocean‐ice‐shelf interactions are exported to the continental slope in a narrow, topographically steered western boundary current. This focused outflow produces a localized front at the shelf break that supports the emerging ASC. This mechanism emphasizes the importance of buoyancy forcing, integrated over the continental shelf, as opposed to local wind forcing, in the generation mechanism and suggests the potential for remote control of melt rates of WAIS' largest ice shelves

Bone mass and microarchitecture of irradiated and bone marrow-transplanted mice: influences of the donor strain

Summary Total body irradiation and bone marrow transplantation induced dramatic trabecular bone loss and cortical thickening in mice. Transplanted cells were engrafted in bone marrow, along trabeculae, and in periosteal and endosteal envelopes. None of the osteocytes were of donor origin. Bone microarchitecture of transplanted mice changed to tend toward the donor phenotype. Introduction Osteopenia and osteoporosis are complications of bone marrow transplants (BMT) attributed to related chemotherapy. However, the specific influence of total body irradiation (TBI) is unknown. Methods We investigated the effects of TBI and BMT on bone mass and microarchitecture by micro-CT. Eighteen C57Bl/6 (B6) mice receiving lethal TBI had a BMT with marrow cells from green fluorescent protein--transgenic-C57Bl/6 (GFP) mice. Transplanted (TGFPB6), B6, and GFP mice were euthanized 1, 3, and 6 months after BMT or at a related age. Results TGFPB6 presented a dramatic bone loss compared with B6 and did not restore their trabecular bone mass over time, despite a cortical thickening 6 months after BMT. Serum testosterone levels were not significantly reduced after BMT. During aging, GFP mice have less trabeculae, thicker cortices, but a narrower femoral shaft than B6 mice. From 3 months after BMT, cortical characteristics of TGFPB6 mice differed statistically from B6 mice and were identical to those of GFP mice. GFP+ cells were located along trabecular surfaces and in periosteal and endosteal envelopes, but none of the osteocytes expressed GFP. Conclusion Our findings suggest that engrafted cells did not restore the irradiation-induced trabecular bone loss, but reconstituted a marrow microenvironment and bone remodeling similar to those of the donor. The effects of irradiation and graft on bone remodeling differed between cortical and trabecular bone

Hearing-Related Quality of Life in 75 Patients With a Percutaneous Bone Conduction Device

Objective: To evaluate long-term hearing-related quality of life (HRQoL) and device use in bone conduction (BCD) users. Furthermore, to assess differences between indications and changes in HRQoL over time. Study design: Prospective questionnaire survey. Setting: Tertiary referral center. Patients: Seventy-five patients with a percutaneous BCD. Main outcome measures: Glasgow Benefit Inventory (GBI) at 3 and 12 months postoperatively, Glasgow Health Status Inventory (GHSI) preoperatively, and 6 and 36 months postoperatively, device use at 6, 12, and 36 months. Changes over time were assessed and outcomes were compared between indications. Results: After implantation, 97% of all patients reported a positive benefit on the GBI total. The GHSI total had improved with median 15 points (Interquartile range [IQR] 12). At 36 months, median device use was 15 hours/day (IQR 10) and one nonuser was reported. Patients with bilateral hearing loss (BHL) showed greater improvement on the GHSI total (median 18 vs 14, p &lt; 0.0001) and used their devices more frequently (median 16 vs 8 h/day, p &lt; 0.0001) than patients with unilateral HL (UHL). Postoperative GHSI and GBI scores were consistent over time, in the entire patient population and for every indication. Between 6 and 36 months, device use was stable over time, except for patients with single-sided deafness (SSD; median -6.4 h/day, p = 0.009). Conclusion: The BCD improves HRQoL in patients with BHL, in patients with unilateral conductive/mixed hearing loss and in patients with SSD. Patients with BHL experienced a greater improvement in hearing status compared to patients with UHL. Although use decreased over time in SSD patients, device use was high for every indication.</p

Wind-driven transport of fresh shelf water into the upper 30m of the Labrador Sea

The Labrador Sea is one of a small number of deep convection sites in the North Atlantic that contribute to the meridional overturning circulation. Buoyancy is lost from surface waters during winter, allowing the formation of dense deep water. During the last few decades, mass loss from the Greenland ice sheet has accelerated, releasing freshwater into the high-latitude North Atlantic. This and the enhanced Arctic freshwater export in recent years have the potential to add buoyancy to surface waters, slowing or suppressing convection in the Labrador Sea. However, the impact of freshwater on convection is dependent on whether or not it can escape the shallow, topographically trapped boundary currents encircling the Labrador Sea. Previous studies have estimated the transport of freshwater into the central Labrador Sea by focusing on the role of eddies. Here, we use a Lagrangian approach by tracking particles in a global, eddy-permitting (1∕12°) ocean model to examine where and when freshwater in the surface 30m enters the Labrador Sea basin. We find that 60% of the total freshwater in the top 100m enters the basin in the top 30m along the eastern side. The year-to-year variability in freshwater transport from the shelves to the central Labrador Sea, as found by the model trajectories in the top 30m, is dominated by wind-driven Ekman transport rather than eddies transporting freshwater into the basin along the northeast

Mitochondrial activities in human cultured skin fibroblasts contaminated by Mycoplasma hyorhinis

BACKGROUND: Mycoplasma contaminations are a recurrent problem in the use of cultured cells, including human cells, especially as it has been shown to impede cell cycle, triggering cell death under various conditions. More specific consequences on cell metabolism are poorly known. RESULTS: Here we report the lack of significant consequence of a heavy contamination by the frequently encountered mycoplasma strain, M. hyorhinis, on the determination of respiratory chain activities, but the potential interference when assaying citrate synthase. Contamination by M. hyorhinis was detected by fluorescent imaging and further quantified by the determination of the mycoplasma-specific phosphate acetyltransferase activity. Noticeably, this latter activity was not found equally distributed in various mycoplasma types, being exceptionally high in M. hyorhinis. CONCLUSION: While we observed a trend for respiration reduction in heavily contaminated cells, no significant and specific targeting of any respiratory chain components could be identified. This suggested a potential interference with cell metabolism rather than direct interaction with respiratory chain components

Translational evidence for two distinct patterns of neuroaxonal injury in sepsis: a longitudinal, prospective translational study

Background Brain homeostasis deteriorates in sepsis, giving rise to a mostly reversible sepsis-associated encephalopathy (SAE). Some survivors experience chronic cognitive dysfunction thought to be caused by permanent brain injury. In this study, we investigated neuroaxonal pathology in sepsis. Methods We conducted a longitudinal, prospective translational study involving (1) experimental sepsis in an animal model; (2) postmortem studies of brain from patients with sepsis; and (3) a prospective, longitudinal human sepsis cohort study at university laboratory and intensive care units (ICUs). Thirteen ICU patients with septic shock, five ICU patients who died as a result of sepsis, fourteen fluid-resuscitated Wistar rats with fecal peritonitis, eleven sham-operated rats, and three human and four rat control subjects were included. Immunohistologic and protein biomarker analysis were performed on rat brain tissue at baseline and 24, 48, and 72 h after sepsis induction and in sham-treated rats. Immunohistochemistry was performed on human brain tissue from sepsis nonsurvivors and in control patients without sepsis. The clinical diagnostics of SAE comprised longitudinal clinical data collection and magnetic resonance imaging (MRI) and electroencephalographic assessments. Statistical analyses were performed using SAS software (version 9.4; SAS Institute, Inc., Cary, NC, USA). Because of non-Gaussian distribution, the nonparametric Wilcoxon test general linear models and the Spearman correlation coefficient were used. Results In postmortem rat and human brain samples, neurofilament phosphoform, β-amyloid precursor protein, β-tubulin, and H&E stains distinguished scattered ischemic lesions from diffuse neuroaxonal injury in septic animals, which were absent in controls. These two patterns of neuroaxonal damage were consistently found in septic but not control human postmortem brains. In experimental sepsis, the time from sepsis onset correlated with tissue neurofilament levels (R = 0.53, p = 0.045) but not glial fibrillary acidic protein. Of 13 patients with sepsis who had clinical features of SAE, MRI detected diffuse axonal injury in 9 and ischemia in 3 patients. Conclusions Ischemic and diffuse neuroaxonal injury to the brain in experimental sepsis, human postmortem brains, and in vivo MRI suggest these two distinct lesion types to be relevant. Future studies should be focused on body fluid biomarkers to detect and monitor brain injury in sepsis. The relationship of neurofilament levels with time from sepsis onset may be of prognostic value