A generic estimate of trans-Planckian modifications to the primordial power spectrum in inflation

We derive a general expression for the power spectra of scalar and tensor fluctuations generated during inflation given an arbitrary choice of boundary condition for the mode function at a short distance. We assume that the boundary condition is specified at a short-distance cutoff at a scale $M$ which is independent of time. Using a particular prescription for the boundary condition at momentum $p = M$, we find that the modulation to the power spectra of density and gravitational wave fluctuations is of order $(H/M)$, where $H$ is the Hubble parameter during inflation, and we argue that this behavior is generic, although by no means inevitable. With fixed boundary condition, we find that the shape of the modulation to the power spectra is determined entirely by the deviation of the background spacetime from the de Sitter limit.Comment: 15 pages (RevTeX), 2 figure

Properties of the Strange Axial Mesons in the Relativized Quark Model

We studied properties of the strange axial mesons in the relativized quark model. We calculated the $K_1$ decay constant in the quark model and showed how it can be used to extract the $K_1 (^3P_1) - K_1 (^1P_1)$ mixing angle ($\theta_K$) from the weak decay $\tau \to K_1 \nu_\tau$. The ratio $BR(\tau \to \nu_\tau K_1 (1270))/BR(\tau\to \nu_\tau K_1(1400))$ is the most sensitive measurement and also the most reliable since the largest of the theoretical uncertainties factor out. However the current bounds extracted from the TPC/Two-Gamma collaboration measurements are rather weak: we typically obtain $-30^o \lesssim \theta_K \lesssim 50^o$ at 68\% C.L. We also calculated the strong OZI-allowed decays in the pseudoscalar emission model and the flux-tube breaking model and extracted a $^3P_1 - ^1P_1$ mixing angle of $\theta_K \simeq 45^o$. Our analysis also indicates that the heavy quark limit does not give a good description of the strange mesons.Comment: Revised version to be published in Phys. Rev. D. Minor changes. Latex file uses revtex version 3 and epsfig, 4 postcript figures are attached. The full postcript version with embedded figures is available at ftp://ftp.physics.carleton.ca/pub/theory/godfrey/ocipc9512.ps.

Gut microbes shape microglia and cognitive function during malnutrition

Fecal-oral contamination promotes malnutrition pathology. Lasting consequences of early life malnutrition include cognitive impairment, but the underlying pathology and influence of gut microbes remain largely unknown. Here, we utilize an established murine model combining malnutrition and iterative exposure to fecal commensals (MAL-BG). The MAL-BG model was analyzed in comparison to malnourished (MAL mice) and healthy (CON mice) controls. Malnourished mice display poor spatial memory and learning plasticity, as well as altered microglia, non-neuronal CNS cells that regulate neuroimmune responses and brain plasticity. Chronic fecal-oral exposures shaped microglial morphology and transcriptional profile, promoting phagocytic features in MAL-BG mice. Unexpectedly, these changes occurred independently from significant cytokine-induced inflammation or blood-brain barrier (BBB) disruption, key gut-brain pathways. Metabolomic profiling of the MAL-BG cortex revealed altered polyunsaturated fatty acid (PUFA) profiles and systemic lipoxidative stress. In contrast, supplementation with an ω3 PUFA/antioxidant-associated diet (PAO) mitigated cognitive deficits within the MAL-BG model. These findings provide valued insight into the malnourished gut microbiota-brain axis, highlighting PUFA metabolism as a potential therapeutic target

Quantum interference between multiple impurities in anisotropic superconductors

We study the quantum interference between impurities in d-wave superconductors within a potential scattering formalism that easily applies to multiple impurities. The evolution of the low-energy local density of states for both magnetic and nonmagnetic short-ranged scatterers are studied as a function of the spatial configuration of the impurities. Further we discuss the influence of subdominant bulk superconducting order parameters on the interference pattern from multiple impurities.Comment: 4 pages, 6 figure

Safer topical treatment for inflammation using 5α-tetrahydrocorticosterone in mouse models

Use of topical glucocorticoid for inflammatory skin conditions is limited by systemic and local side-effects. This investigation addressed the hypothesis that topical 5α-tetrahydrocorticosterone (5αTHB, a corticosterone metabolite) inhibits dermal inflammation without affecting processes responsible for skin thinning and impaired wound healing. The topical anti-inflammatory properties of 5αTHB were compared with those of corticosterone in C57Bl/6 male mice with irritant dermatitis induced by croton oil, whereas its effects on angiogenesis, inflammation, and collagen deposition were investigated by subcutaneous sponge implantation. 5αTHB decreased dermal swelling and total cell infiltration associated with dermatitis similarly to corticosterone after 24 h, although at a five fold higher dose, but in contrast did not have any effects after 6 h. Pre-treatment with the glucocorticoid receptor antagonist RU486 attenuated the effect of corticosterone on swelling at 24 h, but not that of 5αTHB. After 24 h 5αTHB reduced myeloperoxidase activity (representative of neutrophil infiltration) to a greater extent than corticosterone. At equipotent anti-inflammatory doses 5αTHB suppressed angiogenesis to a limited extent, unlike corticosterone which substantially decreased angiogenesis compared to vehicle. Furthermore, 5αTHB reduced only endothelial cell recruitment in sponges whereas corticosterone also inhibited smooth muscle cell recruitment and decreased transcripts of angiogenic and inflammatory genes. Strikingly, corticosterone, but not 5αTHB, reduced collagen deposition. However, both 5αTHB and corticosterone attenuated macrophage infiltration into sponges. In conclusion, 5αTHB displays the profile of a safer topical anti-inflammatory compound. With limited effects on angiogenesis and extracellular matrix, it is less likely to impair wound healing or cause skin thinning

Loss-of-function mutations in UDP-Glucose 6-Dehydrogenase cause recessive developmental epileptic encephalopathy

Developmental epileptic encephalopathies are devastating disorders characterized by intractable epileptic seizures and developmental delay. Here, we report an allelic series of germline recessive mutations in UGDH in 36 cases from 25 families presenting with epileptic encephalopathy with developmental delay and hypotonia. UGDH encodes an oxidoreductase that converts UDP-glucose to UDP-glucuronic acid, a key component of specific proteoglycans and glycolipids. Consistent with being loss-of-function alleles, we show using patients’ primary fibroblasts and biochemical assays, that these mutations either impair UGDH stability, oligomerization, or enzymatic activity. In vitro, patient-derived cerebral organoids are smaller with a reduced number of proliferating neuronal progenitors while mutant ugdh zebrafish do not phenocopy the human disease. Our study defines UGDH as a key player for the production of extracellular matrix components that are essential for human brain development. Based on the incidence of variants observed, UGDH mutations are likely to be a frequent cause of recessive epileptic encephalopathy