Suppression of matter density growth at scales exceeding the cosmic screening length

One of the main objectives of modern cosmology is to explain the origin and evolution of cosmic structures at different scales. The principal force responsible for the formation of such structures is gravity. In a general relativistic framework, we have shown that matter density contrasts do not grow over time at scales exceeding the cosmic screening length, which corresponds to a cosmological scale of the order of two to three gigaparsecs at the present time, at which gravitational interactions exhibit an exponential cut-off. This is a purely relativistic effect. To demonstrate the suppression of density growth, we have performed N-body simulations in a box with a comoving size of $5.632\,{\rm Gpc}/h$ and obtained the power spectrum of the mass density contrast. We have shown that it becomes independent of time for scales beyond the cosmic screening length as a clear manifestation of the cosmic screening effect.Comment: 7 pages, 3 figure

Mass density vs. energy density at cosmological scales

In the presence of the gravitational field, the energy density of matter no longer coincides with its mass density. A discrepancy exists, of course, also between the associated power spectra. Within the $\Lambda$CDM model, we derive a formula that relates the power spectrum of the energy density to that of the mass density and test it with the help of N-body simulations run in comoving boxes of 2.816 Gpc/$h$. The results confirm the validity of the derived formula and simultaneously show that the power spectra diverge significantly from one another at large cosmological scales.Comment: 10 pages, 4 figure

Distributed Deep Joint Source-Channel Coding with Decoder-Only Side Information

We consider low-latency image transmission over a noisy wireless channel when correlated side information is present only at the receiver side (the Wyner-Ziv scenario). In particular, we are interested in developing practical schemes using a data-driven joint source-channel coding (JSCC) approach, which has been previously shown to outperform conventional separation-based approaches in the practical finite blocklength regimes, and to provide graceful degradation with channel quality. We propose a novel neural network architecture that incorporates the decoder-only side information at multiple stages at the receiver side. Our results demonstrate that the proposed method succeeds in integrating the side information, yielding improved performance at all channel noise levels in terms of the various distortion criteria considered here, especially at low channel signal-to-noise ratios (SNRs) and small bandwidth ratios (BRs). We also provide the source code of the proposed method to enable further research and reproducibility of the results.Comment: 7 pages, 4 figure

Median Distance Model for Likert-Type Items in Contingency Table Analysis

Likert-type items (questions) are a widely used scale in questionnaire design. The “neutral” or “undecided” option may lead to misinterpretation and confusion about the results. This paper proposes two novel log-linear models to measure how much accumulation of the neutral option over the contingency tables at any question levels. These models also test the odds that a respondent’s level how far from the median. These models will help the researchers how to incorporate the neutral option in conceptual frameworks

Case report of radiation-induced lung injury with trastuzumab emtansine: the lung also matters

With an increase in the number of agents used concurrently with radiotherapy (RT), a new research area has emerged regarding toxicity. Here, we present a case of a 47-year-old woman presenting with radiation-induced lung injury (RILI) that occurred six months after the end of RT with concomitant and sequential use of trastuzumab-emtansine (T-DM1) with RT. The patient’s T-DM1 treatment was discontinued because of RILI. Antibiotic and methylprednisolone treatments were started. The steroid dose was gradually tapered and completely discontinued after full recovery. If new agents are used concurrently with RT, the toxicity profile of new agents should be kept in mind

Detection of CRISPR-Cas9-Mediated Mutations Using a Carbon Nanotube-Modified Electrochemical Genosensor.

The CRISPR-Cas9 system has facilitated the genetic modification of various model organisms and cell lines. The outcomes of any CRISPR-Cas9 assay should be investigated to ensure/improve the precision of genome engineering. In this study, carbon nanotube-modified disposable pencil graphite electrodes (CNT/PGEs) were used to develop a label-free electrochemical nanogenosensor for the detection of point mutations generated in the genome by using the CRISPR-Cas9 system. Carbodiimide chemistry was used to immobilize the 5'-aminohexyl-linked inosine-substituted probe on the surface of the sensor. After hybridization between the target sequence and probe at the sensor surface, guanine oxidation signals were monitored using differential pulse voltammetry (DPV). Optimization of the sensitivity of the nanogenoassay resulted in a lower detection limit of 213.7 nM. The nanogenosensor was highly specific for the detection of the precisely edited DNA sequence. This method allows for a rapid and easy investigation of the products of CRISPR-based gene editing and can be further developed to an array system for multiplex detection of different-gene editing outcomes

Autosomal recessive variants in TUBGCP2 alter the γ-tubulin ring complex leading to neurodevelopmental disease.

Microtubules help building the cytoskeleton of neurons and other cells. Several components of the gamma-tubulin (γ-tubulin) complex have been previously reported in human neurodevelopmental diseases. We describe two siblings from a consanguineous Turkish family with dysmorphic features, developmental delay, brain malformation, and epilepsy carrying a homozygous mutation (p.Glu311Lys) in TUBGCP2 encoding the γ-tubulin complex 2 (GCP2) protein. This variant is predicted to disrupt the electrostatic interaction of GCP2 with GCP3. In primary fibroblasts carrying the variant, we observed a faint delocalization of γ-tubulin during the cell cycle but normal GCP2 protein levels. Through mass spectrometry, we observed dysregulation of multiple proteins involved in the assembly and organization of the cytoskeleton and the extracellular matrix, controlling cellular adhesion and of proteins crucial for neuronal homeostasis including axon guidance. In summary, our functional and proteomic studies link TUBGCP2 and the γ-tubulin complex to the development of the central nervous system in humans

Post-intervention Status in Patients With Refractory Myasthenia Gravis Treated With Eculizumab During REGAIN and Its Open-Label Extension

OBJECTIVE: To evaluate whether eculizumab helps patients with anti-acetylcholine receptor-positive (AChR+) refractory generalized myasthenia gravis (gMG) achieve the Myasthenia Gravis Foundation of America (MGFA) post-intervention status of minimal manifestations (MM), we assessed patients' status throughout REGAIN (Safety and Efficacy of Eculizumab in AChR+ Refractory Generalized Myasthenia Gravis) and its open-label extension. METHODS: Patients who completed the REGAIN randomized controlled trial and continued into the open-label extension were included in this tertiary endpoint analysis. Patients were assessed for the MGFA post-intervention status of improved, unchanged, worse, MM, and pharmacologic remission at defined time points during REGAIN and through week 130 of the open-label study. RESULTS: A total of 117 patients completed REGAIN and continued into the open-label study (eculizumab/eculizumab: 56; placebo/eculizumab: 61). At week 26 of REGAIN, more eculizumab-treated patients than placebo-treated patients achieved a status of improved (60.7% vs 41.7%) or MM (25.0% vs 13.3%; common OR: 2.3; 95% CI: 1.1-4.5). After 130 weeks of eculizumab treatment, 88.0% of patients achieved improved status and 57.3% of patients achieved MM status. The safety profile of eculizumab was consistent with its known profile and no new safety signals were detected. CONCLUSION: Eculizumab led to rapid and sustained achievement of MM in patients with AChR+ refractory gMG. These findings support the use of eculizumab in this previously difficult-to-treat patient population. CLINICALTRIALSGOV IDENTIFIER: REGAIN, NCT01997229; REGAIN open-label extension, NCT02301624. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that, after 26 weeks of eculizumab treatment, 25.0% of adults with AChR+ refractory gMG achieved MM, compared with 13.3% who received placebo

Minimal Symptom Expression' in Patients With Acetylcholine Receptor Antibody-Positive Refractory Generalized Myasthenia Gravis Treated With Eculizumab

The efficacy and tolerability of eculizumab were assessed in REGAIN, a 26-week, phase 3, randomized, double-blind, placebo-controlled study in anti-acetylcholine receptor antibody-positive (AChR+) refractory generalized myasthenia gravis (gMG), and its open-label extension