pinecone/core-2020-05-10-deduplication huggingface dataset:
Fault detection and diagnosis in a food pasteurization process with Hidden Markov Models

Hidden Markov Models (HMM) are used to detect abnormal operation of dynamic processes and diagnose sensor and actuator faults. The method is illustrated by monitoring the operation of a pasteurization plant and diagnosing causes of abnormal operation. Process data collected under the influence of faults of different magnitude and duration in sensors and actuators are used to illustrate the use of HMM in the detection and diagnosis of process faults. Case studies with experimental data from a high-temperature-short-time pasteurization system showed that HMM can diagnose the faults with certain characteristics such as fault duration and magnitude.USDA (NRI Grant 97-35503-4887
Mechanistic Investigations of Oxidation of Some Dipeptides by Sodium N-chloro-p-toluenesulfonamide in Alkaline Medium:A Kinetic Study

The kinetics of oxidation of five dipeptides (DPP) viz., glycylglycine (Gly-Gly), L-alanyl-L-alanine (Ala-Ala), L-valyl-L-valine (Val-Val), L-leucyl-L-leucine (Leu-Leu) and phenylglycyl-phenylglycine (Phg-Phg) by sodium N-chloro-p-toluenesulfonamide or chloramine-T (CAT) in NaOH medium was studied at 308 K. The reactions follow identical kinetics for all the dipeptides, being first-order dependence each on [CAT]o, [DPP]o and fractional-order on [OH−]. Addition of p-toluenesulfonamide or halide ions (Cl− or Br−) has no significant effect on the rate of reaction. The reaction rate was found to increase with increase in ionic strength of the medium. The solvent isotope effect was studied using D2O. The activation parameters for the reaction were computed from Arrhenius plots. Equilibrium and decomposition constants were evaluated. The oxidation products of the dipeptides were identified as their corresponding aldehydes. An isokinetic relationship was observed with β=352 K, indicating that enthalpy factors control the reaction rate. CH3C6H4SO2NCl− of the oxidant has been postulated as the reactive oxidizing species. Under comparable experimental conditions, the rate of oxidation of the dipeptides increases in the order:Phg-Phg>Ala-Ala>Val-Val>Leu-Leu>Gly-Gly. The kinetics of oxidation of the dipeptides have also been compared with those of their corresponding monomer amino acids. The observed results have been explained by a plausible mechanism and the related rate law has been deduced
Photo Catalytic Degradation of Azo Dyes over Mn2+ Doped TiO2 Catalyst under UV/Solar Light: An Insight to the Route of Electron Transfer in the Mixed Phase of Anatase and Rutile

Mn2+ ion was doped into the TiO2 matrix and its photocatalytic activity was evaluated for the degradation of a mono azo dye methyl orange (MO) and a di-azo dye brilliant yellow (BY) under UV/solar light. X-ray diffraction results revealed the phase transformation from anatase to rutile due to the inclusion of Mn2+ ion into the TiO2 matrix. All the doped catalysts showed a red shift in the band gap to the visible region. The degradation reaction of the dyes was found to be dependent on its structure. It was found that mono azo dye degrades faster than di azo dye under UV/solar light. The rate constant under identical conditions calculated for the degradation of MO is 2.4 times (under UV light) and 4.5 times (under solar light) higher compared to BY. Among the photocatalysts studied, Mn2+(0.06 at.%)-TiO2 showed higher activity under both UV and solar light illumination. The synergestic effect in the bicrystalline framework of anatase and rutile effectively suppresses the charge carrier recombination and enhances the photocatalytic activity. The degradation reaction was followed by UV-visible spectroscopy and the photoproducts formed were analyzed by GC-MS techniques
Deposition of SnO2 on the Anatase TiO2 {105} Facets with High Photocatalytic Performance

Anatase TiO2 as a promising photocatalyst has been widely employed in the decontamination treatment of polluted water, air purification and water splitting. Coupling TiO2 with other semiconductor materials could further enhance the photocatalytic activity. Here, we successfully synthesized the SnO2/TiO2 catalyst by depositing SnO2 particles on the anatase TiO2 {105} facets through a gas phase oxidation process. The SnO2/TiO2 catalyst shows higher photocatalytic activity for decomposition of MB than that of the pure TiO2 catalyst. The enhanced photocatalytic activity can be attributed to the efficient charge separation since TiO2 and SnO2 catalyst have staggered energy level.Full Tex
Graphene-Based Sulfur Composites for Energy Storage and  Conversion in Li-S Batteries

There are growing research interests in developing high-performance energy storage systems to meet the demands for large-scale and sustainable energy storage. The lithium-sulfur (Li-S) batteries have drawn numerous attentions due to their exceptionally high energy density compared with other batteries. However, achieving the high capacities with long-term cycle stability and retaining an essentially high sulfur loading remains a tremendous challenge for the designs of Li-S batteries. Graphene is regarded as a very suitable and promising addition to the compositions for Li-S batteries due to its unique two dimensional (2D) structure, high conductivity and superior mechanical flexibility. Besides, the functional groups of graphene surface can be tuned flexibly to immobilize the S/Li2Sx on the graphene surface during the cycling process. In this review, the development of graphene-sulfur composites and their applications in Li-S batteries are discussed. The attempts are also devoted to the synthesis approaches of various graphene-based sulfur composites, the graphene-sulfur interaction and the impacts on the electrochemical performances as well as the major issues of Li-S batteries.Full Tex
The Prognosis of MYC Translocation Positive Diffuse Large B-Cell Lymphoma Depends on The Second Hit

A proportion of MYC translocation positive diffuse large B-cell lymphomas (DLBCL) harbour a BCL2 and/or BCL6 translocation, known as double-hit DLBCL, and are clinically aggressive. It is unknown whether there are other genetic abnormalities that cooperate with MYC translocation and form double-hit DLBCL, and whether there is a difference in clinical outcome between the double-hit DLBCL and those with an isolated MYC translocation. We investigated TP53 gene mutations along with BCL2 and BCL6 translocations in a total of 234 cases of DLBCL, including 81 with MYC translocation. TP53 mutations were investigated by PCR and sequencing, while BCL2 and BCL6 translocation was studied by interphase fluorescence in situ hybridization. The majority of MYC translocation positive DLBCLs (60/81=74%) had at least one additional genetic hit. In MYC translocation positive DLBCL treated by R-CHOP (n=67), TP53 mutation and BCL2, but not BCL6 translocation had an adverse effect on patient overall survival. In comparison with DLBCL with an isolated MYC translocation, cases with MYC/TP53 double-hits had the worst overall survival, followed by those with MYC/BCL2 double-hits. In MYC translocation negative DLBCL treated by R-CHOP (n=101), TP53 mutation, BCL2 and BCL6 translocation had no impact on patient survival. The prognosis of MYC translocation positive DLBCL critically depends on the second hit, with TP53 mutations and BCL2 translocation contributing to an adverse prognosis. It is pivotal to investigate both TP53 mutations and BCL2 translocations in MYC translocation positive DLBCL, and to distinguish double-hit DLBCLs from those with an isolated MYC translocation. This article is protected by copyright. All rights reserved.The authors would like to thank Dr. Ian McFarlane, the Microarray CoreLab, David Withers, IMS Metabolic Research Laboratories, National Institute of Health Research, Cambridge Comprehensive Biomedical Research Centre for their help in DNA sequencing. We also thank Dr. Ramesh Bulusu, Dr. Kanchan Regge, Dr. Muttuswamy Sivakumaran, Dr. Sateesh Nagumantry, Dr. Andrew Hodson, Dr. Mamtha Karanth, Dr. Sandra Young-Min, Dr. Jane Keidan, and Dr. Martin Lewis for providing clinical data. The research in MQD lab was supported by grants from Leukaemia & Lymphoma Research, U.K. Kay Kendall Leukaemia Fund (KKLF), The Pathological Society of UK & Ireland, and the Addenbrooke’s Charitable Trust (ACT). NG was supported by a KKLF and an ACT fellowship. Research in JG's lab was funded by Tenovus Tayside; JB was supported by a research grant from the Paul Abrahams Fund.This is the final version of the article. It was first published by Wiley at http://doi.org/10.1002/cjp2.1
Stanniocalcin 2 expression is associated with a favourable outcome in male breast cancer.

Breast cancer can arise in either gender; however, it is rare in men, accounting for <1% of diagnosed cases. In a previous transcriptomic screen of male and female breast cancer we observed that Stanniocalcin 2 (STC2) was overexpressed in the former. The aim of this study was to confirm the expression of STC2 in male breast cancer, and to investigate whether this had an impact on patient prognosis. Following an earlier transcriptomic screen, STC2 gene expression was confirmed by RT-qPCR in matched male and female BC samples as well as in tumour-associated fibroblasts derived from each gender. Subsequently, STC2 protein expression was examined immunohistochemically in tissue microarrays containing 477 male breast cancer cases. Cumulative survival probabilities were calculated using the Kaplan-Meier method and multivariate survival analysis was performed using the Cox hazard model. Gender-specific STC2 gene expression showed a 5.6-fold upregulation of STC2 transcripts in male breast cancer, also supported by data deposited in Oncomine(TM) . STC2 protein expression was a positive prognostic factor for disease-free survival (Log rank; total p=0.035, HR=0.49; tumour cells p=0.017, HR=0.44; stroma p=0.030, HR=0.48), but had no significant impact on overall survival (Log rank; total p=0.23, HR=0.71; tumour cells p=0.069, HR=0.59; stroma p=0.650, HR=0.87). Importantly, multivariate analysis adjusted for patient age at diagnosis, node staging, tumour size, ER and PR status revealed that total STC2 expression as well as expression in tumour cells was an independent prognostic factor for disease-free survival (Cox regression; p=0.018, HR=0.983; p=0.015, HR=0.984 respectively). In conclusion STC2 expression is abundant in male breast cancer where it is an independent prognostic factor for disease-free survival. This article is protected by copyright. All rights reserved
High expression of podoplanin in squamous cell carcinoma of the tongue occurs predominantly in patients ≤40 years but does not correlate with tumour spread

More than 30% of patients with squamous cell carcinoma (SCC) of the mobile tongue have clinically undetectable lymph node metastasis. Tumour cells can spread as single cells or collectively. A protein known to play a role in both processes is podoplanin, which is expressed in endothelial cells not only in lymph vessels but also in some aggressive tumours with high invasive and metastatic potential. Here we studied samples from 129 patients with primary SCC of the tongue for expression of podoplanin using immunohistochemistry. mRNA levels were analysed in another 27 cases of tongue SCC with adjacent clinically tumour-free tongue tissue and 14 tongue samples from healthy donors. Higher levels of podoplanin were seen in tumours compared to both normal tongue and clinically normal tongue in the tumour vicinity. No association was found between levels of podoplanin, presence of lymph node metastases or other clinical factors. Patients aged 40 or less were more likely to express high levels of podoplanin protein compared to older patients (p = 0.027). We conclude that levels of podoplanin in primary tongue SCCs are not associated with lymph node metastases. However, tongue SCCs arising in young patients (≤40 years of age) are more likely to express high levels of podoplanin than tongue SCCs that arise in the more elderly. The data suggest that podoplanin has a distinctive role in young patients, who are known to have a poor prognosis: these patients may, therefore, benefit from podoplanin inhibitory therapies
The pathological and biochemical identification of possible seed-lesions of transmitted transthyretin amyloidosis after domino liver transplantation.

The most serious issue in domino liver transplantation (DLT) using liver grafts from patients with transthyretin (TTR)‐related familial amyloid polyneuropathy (FAP) is the development of iatrogenic transmitted amyloidosis (de novo amyloidosis) in DLT‐recipients. However, little is known regarding the mechanisms of the initial stage of amyloid formation in these recipients. We detected initial lesions (possible seed‐lesions) of this iatrogenic amyloidosis in two recipients following liver grafting from FAP patients. Patient 1 underwent DLT at age 65 from an FAP patient with a Val30Met TTR variant and patient 2 received DLT from an FAP patient with a Val30Leu TTR variant at age 32. Patient 2 was started on diflunisal administration from 4 years after DLT. While neither patient had symptoms of FAP, small amyloid deposits were detected on the gastroduodenal mucosae 14 months and 12 years after DLT in patient 1 and patient 2, respectively. The amyloid was analyzed using a laser microdissection system and tandem mass spectrometry. Biochemical analysis indicated that the amyloid was composed mostly of variant TTR produced from the transplanted liver in both patients. In patient 1, wild‐type TTR amyloid was detectable in the duodenal mucosa obtained 2 years after DLT. This is the first study to successfully capture the pathological and biochemical features of initial‐stage amyloid lesions in DLT recipients. The findings clearly indicate that amyloid deposition can start by deposition of variant TTR followed by deposition of wild‐type TTR, and blocking of amyloid seed formation from variant TTR may be a key to prevent or delay the development of DLT‐associated amyloidosis
Inflammatory response in serrated precursor lesions of the colon classified according to WHO entities, clinical parameters and phenotype-genotype correlation.

Studies on traditional serrated adenoma (TSA) and sessile serrated adenoma with dysplasia (SSA-D) are rare due to the low frequency of these lesions, which are well defined by the latest WHO classification. However, introducing new morphological criteria such as intra-epithelial lymphocytes (IELs) might facilitate colorectal polyp diagnoses. Additionally, the phenotype-genotype correlation needs to be updated as the terminology has repeatedly changed. This study analysed 516 polyps, consisting of 118 classical adenomas (CAD), 116 hyperplastic polyps (HPP), 179 SSAs, 41 SSA-Ds, and 62 TSAs. The lesions were analysed in relation to the patients' clinical parameters including gender, age, localisation, and size. The inflammatory background of the polyps was quantified and BRAF and KRAS mutations as well as MLH1 and CDKN2A promoter methylation were assessed. In multivariate analyses, an increase in IELs was an independent and robust new criterion for the diagnosis of SSA-D (p < 0.001). Superficial erosions and acute neutrophil granulocytes led to reactive changes potentially resembling dysplasia. KRAS and BRAF mutations were associated with CAD/TSA and HPP/SSA, respectively. However, almost half of TSAs had a BRAF mutation and were KRAS wild type. CDKN2A seems to precede MLH1 hyper-methylation within the serrated carcinogenesis model. The genotyping of WHO-based entities - and especially SSA - has sharpened in comparison to previously published data. TSAs can be sub-grouped according to their mutation status. Of note, the higher number of IELs in SSA-D reflects their close relationship to colorectal cancers with micro-satellite instability. Therefore, IELs might represent a new diagnostic tool for SSA-D
Rapid and reliable diagnosis of Wilson disease using X-ray fluorescence

International audienceWilson's disease (WD) is a rare autosomal recessive disease due to mutations of the gene encoding the copper-transporter ATP7B. The diagnosis is hampered by the variability of symptoms induced by copper accumulation , the inconstancy of the pathognomonic signs and the absence of a reliable diagnostic test. We investigated the diagnostic potential of X-ray fluorescence (XRF) that allows quantitative analysis of multiple elements. Studies were performed on animal models using Wistar rats (n = 10) and Long Evans Cinnamon (LEC) rats (n = 11), and on human samples including normal livers (n = 10), alcohol cirrhosis (n = 8), haemo-chromatosis (n = 10), cholestasis (n = 6) and WD (n = 22). XRF experiments were first performed using synchrotron radiation to address the elemental composition at the cellular level. High-resolution mapping of tissue sections allowed measurement of the intensity and the distribution of copper, iron and zinc while preserving the morphology. Investigations were further conducted using a laboratory X-ray source for irradiating whole pieces of tissue. The sensitivity of XRF was highlighted by the discrimination of LEC rats from wild type even under a regimen using copper deficient food. XRF on whole formalin-fixed paraffin embedded needle biopsies allowed profiling of the elements in a few minutes. The intensity of copper related to iron and zinc significantly discriminated WD from other genetic or chronic liver diseases with 97.6% specificity and 100% sensitivity. This study established a definite diagnosis of Wilson's disease based on XRF. This rapid and versatile method can be easily implemented in a clinical setting
Construction and analysis of tissue microarrays in the era of digital pathology: a pilot study targeting CDX1 and CDX2 in a colon cancer cohort of 612 patients.

CDX1 and CDX2 are possibly predictive biomarkers in colorectal cancer. We combined digitally-guided (next generation) TMA construction (ngTMA) and the utility of digital image analysis (DIA) to assess accuracy, tumour heterogeneity and the selective impact of different combined intensity-percentage levels on prognosis.CDX1 and CDX2 immunohistochemistry was performed on ngTMAs covering normal tissue, tumour centre and invasive front. The percentages of all epithelial cells per staining intensity per core were analysed digitally. Beyond classical prognosis analysis following REMARK guidelines, we investigated pre-analytical conditions, three different types of heterogeneity (mosaic-like, targeted and haphazard) and influences on cohort segregation and patient selection. The ngTMA-DIA approach produced robust biomarker data with infrequent core loss and excellent on-target punching. The detailed assessment of tumour heterogeneity could - except for a certain diffuse mosaic-like heterogeneity - exclude differences between the invasive front and tumour centre, as well as detect haphazard clonal heterogeneous elements. Moreover, lower CDX1 and CDX2 counts correlated with mucinous histology, higher TNM stage, higher tumour grade and worse survival (p < 0.01, all). Different protein expression intensity levels shared comparable prognostic power and a great overlap in patient selection. The combination of ngTMA with DIA enhances accuracy and controls for biomarker analysis. Beyond the confirmation of CDX1 and CDX2 as prognostically relevant markers in CRC, this study highlights the greater robustness of CDX2 in comparison to CDX1. For the assessment of CDX2 protein loss, cut-points as percentage data of complete protein loss can be deduced as a recommendation
Fluorescence in situ Hybridization in Surgical Pathology: Principles and Applications

Identification of recurrent tumour-specific chromosomal translocations and novel fusion oncogenes has important diagnostic, therapeutic and prognostic implications. Over the past decade, fluorescence in situ hybridization (FISH) analysis of tumour samples has been one of the most rapidly growing areas in genomic medicine and surgical pathology practice. Unlike traditional cytogenetics, FISH affords a rapid analysis of formalin-fixed, paraffin-embedded cells within a routine pathology practice workflow. As more diagnostic and treatment decisions are based on results of FISH, demand for the technology will become more widespread. Common FISH-detected alterations are chromosome deletions, gains, translocations, amplifications and polysomy. These chromosome alterations may have diagnostic and therapeutic implications for many tumour types. Integrating genomic testing into cancer treatment decisions poses many technical challenges, but rapid progress is being made to overcome these challenges in precision medicine. FISH assessment of chromosomal changes relevant to differential diagnosis and cancer treatment decisions has become an important tool for the surgical pathologist. The aim of this review is to provide a theoretical and practical survey of FISH detected translocations with a focus on strategies for clinical application in surgical pathology practice
Endothelial protein C receptor is overexpressed in colorectal cancer as a result of amplification and hypomethylation of chromosome 20q.

Endothelial Protein C Receptor (EPCR) is a Major Histocompatibility Complex homologue, with established roles downregulating coagulation and in endothelial protection. Expressed predominantly on endothelium, EPCR affects inflammatory, apoptotic and cell proliferation pathways by binding to activated protein C (APC). However, EPCR can also be expressed on cancer cells, although the underlying reasons are unclear. Moreover, although EPCR has been linked with chemosensitivity in lung cancer, its clinical significance in many tumours is unknown. Here, we explored its significance in colorectal cancer (CRC). Bioinformatic methods revealed EPCR overexpression in many epithelial cancers, which was confirmed on CRC epithelial tumour cells by immunohistochemistry. EPCR upregulation resulted from gene amplification and DNA hypomethylation, and occurred in concert with a cohort of neighbouring genes on chromosome 20q, a region previously implicated in chemoresistance. As in endothelial cells, EPCR reproducibly mediated ERK pathway activation in a model CRC cell line following APC treatment. However, EPCR knockdown studies failed to highlight compelling EPCR-intrinsic impact on CRC cell phenotype, with limited effects on chemosensitivity and no effect on invasion observed, while EPCR appeared to decrease CRC cell migration. Consistent with these observations, differential EPCR expression did not influence response to chemotherapy in a human CRC cohort. Our results provide a compelling explanation for how EPCR is upregulated in diverse epithelial malignancies. They indicate that the clinical significance of EPCR varies across different tumour types. Furthermore, they raise the possibility that the prognostic significance of EPCR in certain tumours relates significantly to co-upregulation of neighbouring genes on chromosome 20q. Therefore, efforts to exploit EPCR as a prognostic marker should be focussed on specific tumours, and in such scenarios EPCR-co-dysregulated genes may represent potential axes for therapeutic intervention.The work was supported by a Cancer Research UK clinical PhD studentship to NL, and Wellcome Trust Investigator award funding to BEW, supporting CRW (Grant code: 099266/Z/12/Z). We gratefully acknowledge the contribution to this study made by the University of Birmingham's Human Biomaterials Resource Centre which has been supported through Birmingham Science City - Experimental Medicine Network of Excellence project. We thank Chris Paraskeva (University of Bristol) for kindly providing the AA/C1 and AA/C1/10C cell lines.Peer-reviewedPublisher Versio