Dynamic input match correction in R.F. low noise amplifiers

An R.F. circuit that recognizes its faults, and then corrects its performance in real-time has been the holy-grail of RFIC design. This work presents, for the first time, a complete architecture and successful implementation of such a circuit. It is the first step towards the grand vision of fault-free, package independent, integrated R.F. Front End circuitry. The performance of R.F. front-end circuitry can degrade significantly due to process faults and parasitic package inductances at its input. These inductances have wide tolerances and are difficult to co-design for. A novel methodology, which overcomes current obstacles plaguing such an objective, is proposed wherein the affected performance metric of the circuit is quantified, and the appropriate design parameter is modified in real-time, thus enabling self-correction. This proof of concept is demonstrated by designing a cascode LNA and the complete self-correction circuit in IBM 0.25 µm CMOS RF process. The self-correction circuitry ascertains the input match frequency of the circuit by measuring its performance and determines the frequency interval by which it needs to be shifted to restore it to the desired value. It then feeds back a digital word to the LNA which adaptively corrects its input-match. It offers the additional flexibility of using different packages for the front-end since it renders the circuitry independent of package parasitics, by re-calibrating the input match on-the-fly. The circuitry presented in this work offers the advantages of low power, robustness, absence of DSP cores or processors, reduction in design cycle times, guaranteed optimal performance under varying conditions and fast correction times (less than 30 µs)

Fault-tolerant design of RF front-end circuits

The continuing trends of scaling in the CMOS industry have, inevitably, been accompanied by an ever-increasing array of process faults and fabrication complexities. The relentless march towards miniaturization and massive integration, in addition to increasing operating frequencies has resulted in increasing concerns about the reliability of integrated RF front-ends. Coupled with rising cost per chip, the fault-tolerant paradigm has become pertinent in the RFIC domain. Two main reasons have contributed to the fact that fault-tolerant solutions for circuits that operate in the GHz domain have not been realized so far. First, GHz signals are extremely sensitive to higher-order effects such as stray pick-ups, interference, package & on-chip parasitics, etc. Secondly, the use of passives, especially inductors, in the feedback path poses huge area overheads, in addition to a slew of instability problems due to wide variations and soft faults. Hence traditional fault-tolerance methods used in digital and low frequency analog circuits cannot be applied in the RF domain. This work presents a unique methodology to achieve fault-tolerance in RF circuits through dynamic sensing and on-chip self-correction, along with the development of robust algorithms. This technique is minimally intrusive and is transparent during \u27normal\u27 use of the circuit. It is characterized by low area and power overheads, does not need any off-chip computing or DSP cores, and is characterized by self-correction times in the range of a few hundreds of microseconds. It compares very well with existing commercial RF test solutions that use DSP cores and require hundreds of milliseconds. The methodology is demonstrated on a LNA, since it is critical for the performance of the entire front-end. It is validated with simulation and fabrication results of the system designed in IBM 0.25 µm CMOS 6RF process

In Vitro Antifungal Activity of Epigallocatechin 3-O-Gallate against Clinical Isolates of Dermatophytes

Previously, we reported that epigallocatechin 3-O-gallate (EGCg) has growth-inhibitory effect on clinical isolates of Candida species. In this study, we investigated the antifungal activity of EGCg and antifungal agents against thirty-five of dermatophytes clinically isolated by the international guidelines (M38-A2). All isolates exhibited good susceptibility to EGCg (MIC50, 2-4 µg/mL, MIC90, 4-8 µg/mL, and geometric mean (GM) MICs, 3.36-4 µg/mL) than those of fluconazole (MIC50, 2-16 µg/mL, MIC90, 4-32 µg/mL, and GM MICs, 3.45-25.8 µg/mL) and flucytosin (MIC50, MIC90, and GM MICs, >64 µg/mL), although they were less susceptible to other antifungal agents, such as amphotericin B, itraconazole, and miconazole. These activities of EGCg were approximately 4-fold higher than those of fluconazole, and were 4 to 16-fold higher than flucytosin. This result indicates that EGCg can inhibit pathogenic dermatophyte species. Therefore, we suggest that EGCg may be effectively used solely as a possible agent or combined with other antifungal agents for antifungal therapy in dermatophytosis

Large scale meta-analysis characterizes genetic architecture for common psoriasis associated variants

Psoriasis is a complex disease of skin with a prevalence of about 2%. We conducted the largest meta-analysis of genome-wide association studies (GWAS) for psoriasis to date, including data from eight different Caucasian cohorts, with a combined effective sample size amp;gt;39,000 individuals. We identified 16 additional psoriasis susceptibility loci achieving genome-wide significance, increasing the number of identified loci to 63 for European-origin individuals. Functional analysis highlighted the roles of interferon signalling and the NFkB cascade, and we showed that the psoriasis signals are enriched in regulatory elements from different T cells (CD8(+) T-cells and CD4(+) T-cells including T(H)0, T(H)1 and T(H)17). The identified loci explain similar to 28% of the genetic heritability and generate a discriminatory genetic risk score (AUC = 0.76 in our sample) that is significantly correlated with age at onset (p = 2 x 10(-89)). This study provides a comprehensive layout for the genetic architecture of common variants for psoriasis.Funding Agencies|National Institutes of Health [R01AR042742, R01AR050511, R01AR054966, R01AR063611, R01AR065183]; Foundation for the National Institutes of Health; Dermatology Foundation; National Psoriasis Foundation; Arthritis National Research Foundation; Ann Arbor Veterans Affairs Hospital; Dawn and Dudley Holmes Foundation; Babcock Memorial Trust; Medical Research Council [MR/L011808/1]; German Ministry of Education and Research (BMBF); Doris Duke Foundation [2013106]; National Institute of Health [K08AR060802, R01AR06907]; Taubman Medical Research Institute; Department of Health via the NIHR comprehensive Biomedical Research Center; Kings College London; KCH NHS Foundation Trust; Barbara and Neal Henschel Charitable Foundation; Heinz Nixdorf Foundation; Estonian Ministry of Education and Research [IUT20-46]; Centre of Translational Genomics of University of Tartu (SP1GVARENG); European Regional Development Fund (Centre of Translational Medicine, University of Tartu); German Federal Ministry of Education and Research (BMBF); National Human Genome Research Institute of the National Institutes of Health [R44HG006981]; International Psoriasis Council</p

Large scale meta-analysis characterizes genetic architecture for common psoriasis associated variants

Psoriasis is a complex disease of skin with a prevalence of about 2%. We conducted the largest meta-analysis of genome-wide association studies (GWAS) for psoriasis to date, including data from eight different Caucasian cohorts, with a combined effective sample size >39,000 individuals. We identified 16 additional psoriasis susceptibility loci achieving genome-wide significance, increasing the number of identified loci to 63 for European-origin individuals. Functional analysis highlighted the roles of interferon signalling and the NFκB cascade, and we showed that the psoriasis signals are enriched in regulatory elements from different T cells (CD8+ T-cells and CD4+ T-cells including TH0, TH1 and TH17). The identified loci explain ∼28% of the genetic heritability and generate a discriminatory genetic risk score (AUC=0.76 in our sample) that is significantly correlated with age at onset (p=2 × 10−89). This study provides a comprehensive layout for the genetic architecture of common variants for psoriasis

Integrated Nutrient Management Enhances Yield, Improves Soil Quality, and Conserves Energy under the Lowland Rice–Rice Cropping System

Identifying sustainable crop production systems that improve yield from existing farmland while improving resource use efficiency is critical to meet the growing demands of the increasing human population and diminishing natural resources. Considering the increasing cost associated with inorganic fertilizer, integrated nutrient management using both organic and inorganic sources is important. Therefore, optimizing nutrient management practices that increase yield, improve soil quality, build up soil organic carbon storage, and maintain energy balance can help achieve sustainability in farming systems. In this regard, different nutrient management practices under the rice–rice (Oryza sativa L.) cropping system were evaluated using five different criterions, namely, (i) crop yield response, (ii) soil quality, (iii) soil carbon stock, (iv) energy efficiency, and (v) profitability under lowland situations in the Goa state situated in the western coast of India. We tested six nutrient management treatments, namely, inorganic fertilizers, organic (farmyard manure), rice straw, and their combinations over three years from 2016 to 2019. The results revealed that integrated nutrient management improved soil carbon stock, microbial biomass carbon, and soil fertility more than the other treatments. The integrated use of farmyard manure and chemical fertilizer showed significantly higher crop yield (9.86 v/s 9.41 Mg ha−1), microbial biomass carbon (354 v/s 233.7 mg kg−1 soil), soil carbon stock (36.65 v/s 25.5 Mg C ha−1), energy efficiency (23.8 v/s 22.3), and net return (1776 v/s 1508 USD) than those associated with chemical fertilizer alone. We conclude that the application of chemical fertilizers/organic sources alone may not be sustainable for the rice–rice cropping system in the Goa state of India; the focus should be on integrated nutrient management systems

Genome-wide Association Analysis of Psoriatic Arthritis and Cutaneous Psoriasis Reveals Differences in Their Genetic Architecture

Psoriasis vulgaris (PsV) is a common inflammatory and hyperproliferative skin disease. Up to 30% of people with PsV eventually develop psoriatic arthritis (PsA), an inflammatory musculoskeletal condition. To discern differences in genetic risk factors for PsA and cutaneous-only psoriasis (PsC), we carried out a genome-wide association study (GWAS) of 1,430 PsA case subjects and 1,417 unaffected control subjects. Meta-analysis of this study with three other GWASs and two targeted genotyping studies, encompassing a total of 9,293 PsV case subjects, 3,061 PsA case subjects, 3,110 PsC case subjects, and 13,670 unaffected control subjects of European descent, detected 10 regions associated with PsA and 11 with PsC at genome-wide (GW) significance. Several of these association signals (IFNLR1, IFIH1, NFKBIA for PsA; TNFRSF9, LCE3C/B, TRAF3IP2, IL23A, NFKBIA for PsC) have not previously achieved GW significance. After replication, we also identified a PsV-associated SNP near CDKAL1 (rs4712528, odds ratio [OR] = 1.16, p = 8.4 x 10(-11)). Among identified psoriasis risk variants, three were more strongly associated with PsC than PsA (rs12189871 near HLA-C, p = 5.0 x 10(-19); rs4908742 near TNFRSF9, p = 0.00020; rs10888503 near LCE3A, p = 0.0014), and two were more strongly associated with PsA than PsC (rs12044149 near IL23R, p = 0.00018; rs9321623 near TNFAIP3, p = 0.00022). The PsA-specific variants were independent of previously identified psoriasis variants near IL23R and TNFAIP3. We also found multiple independent susceptibility variants in the IL12B, NOS2, and IFIH1 regions. These results provide insights into the pathogenetic similarities and differences between PsC and PsA