An efficient channel model for evaluating wireless NoC architectures

Wireless Networks-on-Chip (WiNoCs) have emerged to solve the scalability and performance bottleneck of conventional wired NoC architectures. However unlike communication in the macro-world, on-chip communication poses several constraints, hence there is the need for simulation and design tools that consider the effect of the wireless channel at the nanotechnology level. In this paper, we present a parameterizable channel model for WiNoCs which takes into account practical issues and constraints of the propagation medium, such as transmission frequency, operating temperature, ambient pressure and distance between the on-chip antennas. The proposed channel model demonstrates that total path loss of the wireless channel in WiNoCs suffers from not only dielectric propagation loss (DPL) but also molecular absorption attenuation (MAA) which reduces the reliability of the syste

Non-orthogonal multiple access schemes with partial relay selection

In this paper, non-orthogonal multiple access (NOMA) in amplify-and-forward relay systems with partial relay selection (PRS) is investigated. More specifically, new exact closed-form expressions for the outage probabilities at two users are derived, based on which an asymptotic analysis at high signal- to-noise ratio (SNR) is carried out. Additionally, in order to investigate the performance gap between the NOMA and orthogonal multiple access (OMA) schemes, a closed-form approximate expression at high SNR for the sum rate is derived. Furthermore, relying on our results, the impact of the PRS on the sum rate and outage probability of the proposed NOMA scheme is examined. In particular, the derived asymptotic expressions show that the proposed scheme can improve over the traditional OMA not only the sum rate but also the user fairness. Finally, simulation results are presented to corroborate the analytical results

Topsoil Selling - extreme anthropogenic erosion and its consequences for paddy soil quality (Mekong Delta, Vietnam)

Increasing urbanization and industrialization leads to rising demands for construction material, particularly in low-income countries. Thus, agricultural topsoil is sometimes removed and used as raw material e.g. for brick production. Topsoil selling (TSS) is practiced around the world from America, Europe, and Afrika to Asia. In the Mekong, Delta farmers sell the topsoil from their paddy fields to contractors. The temporal effects of topsoil removal on soil quality are not yet fully understood. We hypothesized that after soil removal, soil quality is significantly lower compared to the original topsoil. To test this hypothesis, we sampled paddy soil chronosequences in two different provinces, ranging between 1 and 8 years after TSS. Soil organic carbon (Corg) stocks at TSS sites were up to 20 t/ha lower than at control sites (control: 50 t/ha) in Sóc Trăng and up to 15 t/ha lower in Trà Vinh (control: 30 t/ha). The C/N ratio was nearly constant around 10. Analysis of inorganic nutrients (e.g. P, K, Na, S, Zn, Cu) showed that changes are variable in space, time and among nutrients. Annual average changes ranged from less than a kg per hectare and year for micronutrients (e.g. Cu, Zn) to several tens and hundreds of kg for macronutrients (e.g. P, S). The so far available data revealed that TSS induces mainly a dramatic loss of soil organic matter. It was ongoing up to the 8th year of the chronosequences but was not necessarily accompanied by losses in inorganic nutrients. As a result, there appears to be a chance for farmers in the Mekong Delta to overcome risks of soil quality decline after topsoil removal. Within the next months, we will receive the results from P- and S fractionation and also results from lignin analysis (lignin-derived phenols) will complement to the available data. Thus, we will gain further insights into soil evolution after topsoil selling shortly

Loss of the tumor suppressor, Tp53, enhances the androgen receptor-mediated oncogenic transformation and tumor development in the mouse prostate.

Recent genome analysis of human prostate cancers demonstrated that both AR gene amplification and TP53 mutation are among the most frequently observed alterations in advanced prostate cancer. However, the biological role of these dual genetic alterations in prostate tumorigenesis is largely unknown. In addition, there are no biologically relevant models that can be used to assess the molecular mechanisms for these genetic abnormalities. Here, we report a novel mouse model, in which elevated transgenic AR expression and Trp53 deletion occur simultaneously in mouse prostatic epithelium to mimic human prostate cancer cells. These compound mice developed an earlier onset of high-grade prostatic intraepithelial neoplasia and accelerated prostate tumors in comparison with mice harboring only the AR transgene. Histological analysis showed prostatic sarcomatoid and basaloid carcinomas with massive squamous differentiation in the above compound mice. RNA-sequencing analyses identified a robust enrichment of the signature genes for human prostatic basal cell carcinomas in the above prostate tumors. Master regulator analysis revealed SOX2 as a transcriptional regulator in prostatic basal cell tumors. Elevated expression of SOX2 and its downstream target genes were detected in prostatic tumors of the compound mice. Chromatin immunoprecipitation analyses implicate a coregulatory role of AR and SOX2 in the expression of prostatic basal cell signature genes. Our data demonstrate a critical role of SOX2 in prostate tumorigenesis and provide mechanistic insight into prostate tumor aggressiveness and progression mediated by aberrant AR and p53 signaling pathways

Nuclear localization of the mitochondrial factor HIGD1A during metabolic stress.

Cellular stress responses are frequently governed by the subcellular localization of critical effector proteins. Apoptosis-inducing Factor (AIF) or Glyceraldehyde 3-Phosphate Dehydrogenase (GAPDH), for example, can translocate from mitochondria to the nucleus, where they modulate apoptotic death pathways. Hypoxia-inducible gene domain 1A (HIGD1A) is a mitochondrial protein regulated by Hypoxia-inducible Factor-1α (HIF1α). Here we show that while HIGD1A resides in mitochondria during physiological hypoxia, severe metabolic stress, such as glucose starvation coupled with hypoxia, in addition to DNA damage induced by etoposide, triggers its nuclear accumulation. We show that nuclear localization of HIGD1A overlaps with that of AIF, and is dependent on the presence of BAX and BAK. Furthermore, we show that AIF and HIGD1A physically interact. Additionally, we demonstrate that nuclear HIGD1A is a potential marker of metabolic stress in vivo, frequently observed in diverse pathological states such as myocardial infarction, hypoxic-ischemic encephalopathy (HIE), and different types of cancer. In summary, we demonstrate a novel nuclear localization of HIGD1A that is commonly observed in human disease processes in vivo

Neonatal Cerebral Hypoxia-Ischemia Impairs Plasticity in Rat Visual Cortex

Ocular dominance plasticity (ODP) following monocular deprivation (MD) is a model of activity-dependent neural plasticity that is restricted to an early critical period regulated by maturation of inhibition. Unique developmental plasticity mechanisms may improve outcomes following early brain injury. Our objective was to determine the effects of neonatal cerebral hypoxia–ischemia (HI) on ODP. The rationale extends from observations that neonatal HI results in death of subplate neurons, a transient population known to influence development of inhibition. In rodents subjected to neonatal HI and controls, maps of visual response were derived from optical imaging during the critical period for ODP and changes in the balance of eye-specific response following MD were measured. In controls, MD results in a shift of the ocular dominance index (ODI) from a baseline of 0.15 to −0.10 (p < 0.001). Neonatal HI with moderate cortical injury impairs this shift, ODI = 0.14 (p < 0.01). Plasticity was intact in animals with mild injury and in those exposed to hypoxia alone. Neonatal HI resulted in decreased parvalbumin expression in hemispheres receiving HI compared with hypoxia alone: 23.4 versus 35.0 cells/high-power field (p = 0.01), with no change in other markers of inhibitory or excitatory neurons. Despite abnormal inhibitory neuron phenotype, spontaneous activity of single units and development of orientation selective responses were intact following neonatal HI, while overall visual responses were reduced. Our data suggest that specific plasticity mechanisms are impaired following early brain injury and that the impairment is associated with altered inhibitory neuronal development and cortical activation

The S_3 flavor symmetry in 3-3-1 models

We propose two 3-3-1 models (with either neutral fermions or right-handed neutrinos) based on S_3 flavor symmetry responsible for fermion masses and mixings. The models can be distinguished upon the new charge embedding (\mathcal{L}) relevant to lepton number. The neutrino small masses can be given via a cooperation of type I and type II seesaw mechanisms. The latest data on neutrino oscillation can be fitted provided that the flavor symmetry is broken via two different directions S_3 \rightarrow Z_2 and S_3 \rightarrow Z_3 (or equivalently in the sequel S_3 \rightarrow Z_2 \rightarrow Identity), in which the second direction is due to a scalar triplet and another antisextet as small perturbation. In addition, breaking of either lepton parity in the model with neutral fermions or lepton number in the model with right-handed neutrinos must be happened due to the \mathcal{L}-violating scalar potential. The TeV seesaw scale can be naturally recognized in the former model. The degenerate masses of fermion pairs (\mu, \tau), (c, t) and (s, b) are respectively separated due to the S_3 \rightarrow Z_3 breaking.Comment: 26 page

Long-term outcomes of primary cardiac malignant tumors: Difference between African American and Caucasian population

BACKGROUND: The survival outcome for primary cardiac malignant tumors (PMCTs) based on race has yet to be fully elucidated in previously published literature. This study aimed to address the general long-term outcome and survival rate differences in PMCTs among African Americans and Caucasian populations. METHODS: The 18 cancer registries database from the Surveillance, Epidemiology, and End Results (SEER) Program from 1975 to 2016 were utilized. Ninety-four African American (AA) and 647 Caucasian (CAU) patients from the SEER registry were available for survival analysis. The log-rank test was used to compare the difference in mortality between two populations and presented by the Kaplan-Meier curves. A multivariate Cox proportional hazards regression was used to determine the independent predictors of all-cause mortality. RESULTS: The overall 30-day, 1-year, and 5-year survival rates were 74%, 44.3%, and 16.6%, respectively, with a median survival of 10 months. There was no significant difference in survival rate between the two races (p-value = 0.55). The 1-year survival rate improved significantly during the study timeline in the AA population (13.3% during 1975-1998, 40.9% during 1999-2004, 50% during 2005-2010, and 59.7% during 2011-2016, p-value = 0.0064). Age of diagnosis, type of tumor, disease stage, and chemotherapy administration are the main factors that predict survival outcomes of PMCT patients. Interactive nomogram was developed based on significant predictors. CONCLUSIONS: PMCTs have remained one of the most lethal diseases with poor survival outcome. Survival rate improved during the timeline in AA patients, but in general, racial differences in survival outcome were not observed

Oxygen Tension and the VHL-Hif1α Pathway Determine Onset of Neuronal Polarization and Cerebellar Germinal Zone Exit.

Postnatal brain circuit assembly is driven by temporally regulated intrinsic and cell-extrinsic cues that organize neurogenesis, migration, and axo-dendritic specification in post-mitotic neurons. While cell polarity is an intrinsic organizer of morphogenic events, environmental cues in the germinal zone (GZ) instructing neuron polarization and their coupling during postnatal development are unclear. We report that oxygen tension, which rises at birth, and the von Hippel-Lindau (VHL)-hypoxia-inducible factor 1α (Hif1α) pathway regulate polarization and maturation of post-mitotic cerebellar granule neurons (CGNs). At early postnatal stages with low GZ vascularization, Hif1α restrains CGN-progenitor cell-cycle exit. Unexpectedly, cell-intrinsic VHL-Hif1α pathway activation also delays the timing of CGN differentiation, germinal zone exit, and migration initiation through transcriptional repression of the partitioning-defective (Pard) complex. As vascularization proceeds, these inhibitory mechanisms are downregulated, implicating increasing oxygen tension as a critical switch for neuronal polarization and cerebellar GZ exit