Wired and Wireless Reliable Real-Time Communication in Industrial Systems

In modern factory automation systems, data communication plays a vital role. Different nodes like control systems, sensors and actuators can communicate over a wireless or wired industrial network. The data traffic generated is often scheduled for periodic transmission, where each single message or packet must arrive in time. For this real-time communication, methods have been developed to support communication services with a guaranteed throughput and delay bound for such periodic traffic, but merely under the assumption of error-free communication. However, the possibility for errors in the transmission still exists due to, e.g. noise or interference. A node receiving sensor values from a sensor in the system might then be forced to rely upon an older sensor value from the latest period, possibly leading to inaccuracies in control loops which can compromise the functioning of the system. In safety-critical systems, redundant networks or communication channels are frequently added to cope with errors, leading to more expensive systems. In this chapter, we will describe an alternative approach where erroneous data packets are retransmitted in a way that does not jeopardise any earlier stated real-time guarantees for ordinary transmissions. Using our framework, the reliability of real-time communication can be increased in a more cost-efficient way. We describe in this chapter an overview of our framework for reliable real-time communication, while details of our approach can be found in our earlier publications. In the light of the emerging use of wireless communication, the framework proves to be especially useful due to the high bit error rate inherent to the wireless medium. However, the framework is naturally also attractive for wired communication systems

A Microstructural and Kinetic Investigation of the KCl-Induced Corrosion of an FeCrAl Alloy at 600 A degrees C

The corrosion behaviour of a FeCrAl alloy was investigated at 600 A degrees C in O-2 + H2O with solid KCl applied. A kinetics and microstructural investigation showed that KCl accelerates corrosion and that potassium chromate formation depletes the protective scale in Cr, thus triggering the formation of a fast-growing iron-rich scale. Iron oxide was found to grow both inward and outward, on either side of the initial oxide. A chromia layer is formed with time underneath the iron oxide. It was found that although the alloy does not form a continuous pure alumina scale at the investigated temperature, aluminium is, however, always enriched at the oxide/alloy interface

Stronger induction of callose deposition in barley by Russian wheat aphid than bird cherry-oat aphid is not associated with differences in callose synthase or ≤-1,3-glucanase expression

The effects of infestation by the bird cherry-oat aphid (BCA), (Rhopalosiphum padi L) and the Russian wheat aphid (RWA) (Diuraphis noxia Mordvilko) on callose deposition and gene expression related to callose accumulation were investigated in barley (Hordeum vulgare L. cv. Clipper). The BCA, which gives no visible symptoms, induced very limited callose deposition, even after 14 days of infestation. In contrast, RWA, which causes chlorosis, white and yellow streaking and leaf rolling, induced callose accumulation already after 24h in longitudinal leaf veins. The deposition was pronounced after 72 h, progressing during 7 and 14 days of infestation. In RWA-infested source leaves, callose was also induced in longitudinal veins basipetal to the aphid-infested tissue, whereas in sink leaves, more callose deposition was found above the feeding sites. Nine putative callose synthase genes were identified in a data base search, of which eight were expressed in the leaves, but with similar level of expression in control and aphid-infested tissue. Four out of 12 examined β-1,3-glucanases were expressed in the leaves, and three of them were up-regulated in aphid-infested tissue. They were all more strongly induced by RWA than BCA. The results suggest that callose accumulation may be partly responsible for the symptoms resulting from RWA feeding and that a callose-inducing signal may be transported in the phloem. Furthermore it is concluded that the absence of callose deposition in BCA-infested leaves is not due to a stronger induction of callose-degrading β-1,3-glucanases in this tissue, as compared to RWA-infested leaves

Altered Metabolic Signature in Pre-Diabetic NOD Mice

Altered metabolism proceeding seroconversion in children progressing to Type 1 diabetes has previously been demonstrated. We tested the hypothesis that non-obese diabetic (NOD) mice show a similarly altered metabolic profile compared to C57BL/6 mice. Blood samples from NOD and C57BL/6 female mice was collected at 0, 1, 2, 3, 4, 5, 6, 7, 9, 11, 13 and 15 weeks and the metabolite content was analyzed using GC-MS. Based on the data of 89 identified metabolites OPLS-DA analysis was employed to determine the most discriminative metabolites. In silico analysis of potential involved metabolic enzymes was performed using the dbSNP data base. Already at 0 weeks NOD mice displayed a unique metabolic signature compared to C57BL/6. A shift in the metabolism was observed for both strains the first weeks of life, a pattern that stabilized after 5 weeks of age. Multivariate analysis revealed the most discriminative metabolites, which included inosine and glutamic acid. In silico analysis of the genes in the involved metabolic pathways revealed several SNPs in either regulatory or coding regions, some in previously defined insulin dependent diabetes (Idd) regions. Our result shows that NOD mice display an altered metabolic profile that is partly resembling the previously observation made in children progressing to Type 1 diabetes. The level of glutamic acid was one of the most discriminative metabolites in addition to several metabolites in the TCA cycle and nucleic acid components. The in silico analysis indicated that the genes responsible for this reside within previously defined Idd regions

Pregnancy, Microchimerism, and the Maternal Grandmother

A WOMAN OF REPRODUCTIVE AGE OFTEN HARBORS A SMALL NUMBER OF FOREIGN CELLS, REFERRED TO AS MICROCHIMERISM: a preexisting population of cells acquired during fetal life from her own mother, and newly acquired populations from her pregnancies. An intriguing question is whether the population of cells from her own mother can influence either maternal health during pregnancy and/or the next generation (grandchildren).Microchimerism from a woman's (i.e. proband's) own mother (mother-of-the-proband, MP) was studied in peripheral blood samples from women followed longitudinally during pregnancy who were confirmed to have uncomplicated obstetric outcomes. Women with preeclampsia were studied at the time of diagnosis and comparison made to women with healthy pregnancies matched for parity and gestational age. Participants and family members were HLA-genotyped for DRB1, DQA1, and DQB1 loci. An HLA polymorphism unique to the woman's mother was identified, and a panel of HLA-specific quantitative PCR assays was employed to identify and quantify microchimerism. Microchimerism from the MP was identified during normal, uncomplicated pregnancy, with a peak concentration in the third trimester. The likelihood of detection increased with advancing gestational age. For each advancing trimester, there was a 12.7-fold increase in the probability of detecting microchimerism relative to the prior trimester, 95% confidence intervals 3.2, 50.3, p<0.001. None of the women with preeclampsia, compared with 30% of matched healthy women, had microchimerism (p = 0.03).These results show that microchimerism from a woman's own mother is detectable in normal pregnancy and diminished in preeclampsia, supporting the previously unexplored hypothesis that MP microchimerism may be a marker reflecting healthy maternal adaptation to pregnancy

Harnessing nature-based solutions for smallholder plant health in a changing climate

The impacts of climate change on resource-poor farmers are especially severe and include increased challenges with food security and food safety. This report explores how linking the frameworks of nature-based solutions, integrated pest management (IPM), and One Health can facilitate the design of climate-resilient plant health systems, with particular benefits for reduced pesticide use and exposure. Climate-smart approaches to IPM are proposed as a means to reduce emerging risks from pest insects, nematodes, weeds, and diseases under climate change. We elaborate the main climate change threats – and adaptation options – for five key nature-based solutions central to IPM: host plant resistance and tolerance, habitat manipulation, biological control, semiochemical control, and the use of biopesticides. We conclude by laying out a road map for ‘climate-smart IPM’, which outlines the types of support required for practical implementation, such as climate-informed advisory services, information and communication technology, and policy. While emphasis throughout is placed on smallholder production systems – particularly for sub-Saharan Africa – the principles of climate-smart IPM can be considered relevant to crop production generally

Recurrent gross mutations of the PTEN tumor suppressor gene in breast cancers with deficient DSB repair

Basal-like breast cancer (BBC) is a subtype of breast cancer with poor prognosis. Inherited mutations of BRCA1, a cancer susceptibility gene involved in double-strand DNA break (DSB) repair, lead to breast cancers that are nearly always of the BBC subtype; however, the precise molecular lesions and oncogenic consequences of BRCA1 dysfunction are poorly understood. Here we show that heterozygous inactivation of the tumor suppressor gene Pten leads to the formation of basal-like mammary tumors in mice, and that loss of PTEN expression is significantly associated with the BBC subtype in human sporadic and BRCA1-associated hereditary breast cancers. In addition, we identify frequent gross PTEN mutations, involving intragenic chromosome breaks, inversions, deletions and micro copy number aberrations, specifically in BRCA1-deficient tumors. These data provide an example of a specific and recurrent oncogenic consequence of BRCA1-dependent dysfunction in DNA repair and provide insight into the pathogenesis of BBC with therapeutic implications. These findings also argue that obtaining an accurate census of genes mutated in cancer will require a systematic examination for gross gene rearrangements, particularly in tumors with deficient DSB repair

CD44 isoforms are heterogeneously expressed in breast cancer and correlate with tumor subtypes and cancer stem cell markers

<p>Abstract</p> <p>Background</p> <p>The CD44 cell adhesion molecule is aberrantly expressed in many breast tumors and has been implicated in the metastatic process as well as in the putative cancer stem cell (CSC) compartment. We aimed to investigate potential associations between alternatively spliced isoforms of CD44 and CSCs as well as to various breast cancer biomarkers and molecular subtypes.</p> <p>Methods</p> <p>We used q-RT-PCR and exon-exon spanning assays to analyze the expression of four alternatively spliced CD44 isoforms as well as the total expression of CD44 in 187 breast tumors and 13 cell lines. ALDH1 protein expression was determined by IHC on TMA.</p> <p>Results</p> <p>Breast cancer cell lines showed a heterogeneous expression pattern of the CD44 isoforms, which shifted considerably when cells were grown as mammospheres. Tumors characterized as positive for the CD44⁺/CD24<it>^-</it>phenotype by immunohistochemistry were associated to all isoforms except the CD44 standard (CD44S) isoform, which lacks all variant exons. Conversely, tumors with strong expression of the CSC marker ALDH1 had elevated expression of CD44S. A high expression of the CD44v2-v10 isoform, which retain all variant exons, was correlated to positive steroid receptor status, low proliferation and luminal A subtype. The CD44v3-v10 isoform showed similar correlations, while high expression of CD44v8-v10 was correlated to positive EGFR, negative/low HER2 status and basal-like subtype. High expression of CD44S was associated with strong HER2 staining and also a subgroup of basal-like tumors. Unsupervised hierarchical cluster analysis of CD44 isoform expression data divided tumors into four main clusters, which showed significant correlations to molecular subtypes and differences in 10-year overall survival.</p> <p>Conclusions</p> <p>We demonstrate that individual CD44 isoforms can be associated to different breast cancer subtypes and clinical markers such as HER2, ER and PgR, which suggests involvement of CD44 splice variants in specific oncogenic signaling pathways. Efforts to link CD44 to CSCs and tumor progression should consider the expression of various CD44 isoforms.</p