Compression and strength behaviour of viscose/polypropylene nonwoven fabrics

Compression and strength properties of viscose/polypropylene nonwoven fabrics has been studied. Compressionbehavior of the nonwoven samples (sample compressibility, sample thickness loss & sample compressive resilience) havebeen analyzed considering the magnitude of applied pressure, fabric weight, fabric thickness, and the porosity of thesamples. Based on the calculated porosity of the samples, pore compression behavior (pore compressibility, porosity loss &pore compressive resilience) are determined. Equations for the determination of pore compressibility, porosity loss, and porecompressive resilience, are established. Tensile strength and elongation as well as bursting strength and ball traverseelongation are also determined. The results show that the sample compression behavior as well as pore compressionbehavior depend on the magnitude of applied pressure. At the high level of applied pressure, a sample with highercompressibility has the lower sample compressive resilience. Differences in pore compressibility and porosity loss betweeninvestigated samples have also been registered, except in pore compressive resilience. Sample with the higher fabric weight,higher thickness, and lower porosity shows the lower sample compressibility, pore compressibility, sample thickness loss,porosity loss, and tensile elongation, but the higher tensile strength, bursting strength, and ball traverse elongation

Quality of clothing fabrics in terms of their comfort properties

Quality of various clothing woven fabrics with respect to their comfort properties, such as electro-physical properties, air permeability, and compression properties has been studied. Fabrics are produced from cotton and cotton/polyester fibre blends in plain, twill, satin and basket weave. Results show that cotton fabrics have lower values of the volume resistivity, air permeability and compressive resilience but higher values of effective relative dielectric permeability and compressibility as compared to fabrics that have been produced from cotton/PES fibre blends. Regression analysis shows a strong linear correlative relationship between the air permeability and the porosity of the woven fabrics with very high coefficient of linear correlation (0.9807). It is also observed that comfort properties are determined by the structure of woven fabrics (raw material composition, type of weave) as well as by the fabrics surface condition. Findings of the studies have been used for estimating the quality of woven fabrics in terms of their comfort properties by the application of ranking method. It is concluded that the group of cotton fabrics exhibits better quality of comfort as compared to the group of cotton/PES blend fabrics.

TGFβR signalling determines CD103⁺CD11b⁺ dendritic cell development in the intestine

CD103+CD11b+ dendritic cells (DCs) are unique to the intestine, but the factors governing their differentiation are unclear. Here we show that transforming growth factor receptor 1 (TGFβR1) has an indispensable, cell intrinsic role in the development of these cells. Deletion of Tgfbr1 results in markedly fewer intestinal CD103+CD11b+ DCs and a reciprocal increase in the CD103−CD11b+ dendritic cell subset. Transcriptional profiling identifies markers that define the CD103+CD11b+ DC lineage, including CD101, TREM1 and Siglec-F, and shows that the absence of CD103+CD11b+ DCs in CD11c-Cre.Tgfbr1fl/fl mice reflects defective differentiation from CD103−CD11b+ intermediaries, rather than an isolated loss of CD103 expression. The defect in CD103+CD11b+ DCs is accompanied by reduced generation of antigen-specific, inducible FoxP3+ regulatory T cells in vitro and in vivo, and by reduced numbers of endogenous Th17 cells in the intestinal mucosa. Thus, TGFβR1-mediated signalling may explain the tissue-specific development of these unique DCs

Potential of a multiparametric optical sensor for determining in situ the maturity components of red and white vitis vinifera wine grapes

A non-destructive fluorescence-based technique for evaluating Vitis vinifera L. grape maturity using a portable sensor (Multiplex ®) is presented. It provides indices of anthocyanins and chlorophyll in Cabernet Sauvignon, Merlot and Sangiovese red grapes and of flavonols and chlorophyll in Vermentino white grapes. The good exponential relationship between the anthocyanin index and the actual anthocyanin content determined by wet chemistry was used to estimate grape anthocyanins from in field sensor data during ripening. Marked differences were found in the kinetics and the amount of anthocyanins between cultivars and between seasons. A sensor-driven mapping of the anthocyanin content in the grapes, expressed as g/kg fresh weight, was performed on a 7-ha vineyard planted with Sangiovese. In the Vermentino, the flavonol index was favorably correlated to the actual content of berry skin flavonols determined by means of HPLC analysis of skin extracts. It was used to make a non-destructive estimate of the evolution in the flavonol concentration in grape berry samplings. The chlorophyll index was inversely correlated in linear manner to the total soluble solids (°Brix): it could, therefore, be used as a new index of technological maturity. The fluorescence sensor (Multiplex) possesses a high potential for representing an important innovative tool for controlling grape maturity in precision viticulture

To respond or not to respond - a personal perspective of intestinal tolerance

For many years, the intestine was one of the poor relations of the immunology world, being a realm inhabited mostly by specialists and those interested in unusual phenomena. However, this has changed dramatically in recent years with the realization of how important the microbiota is in shaping immune function throughout the body, and almost every major immunology institution now includes the intestine as an area of interest. One of the most important aspects of the intestinal immune system is how it discriminates carefully between harmless and harmful antigens, in particular, its ability to generate active tolerance to materials such as commensal bacteria and food proteins. This phenomenon has been recognized for more than 100 years, and it is essential for preventing inflammatory disease in the intestine, but its basis remains enigmatic. Here, I discuss the progress that has been made in understanding oral tolerance during my 40 years in the field and highlight the topics that will be the focus of future research

Increased S-nitrosylation and proteasomal degradation of caspase-3 during infection contribute to the persistence of adherent invasive escherichia coli (AIEC) in immune cells

Adherent invasive Escherichia coli (AIEC) have been implicated as a causative agent of Crohn's disease (CD) due to their isolation from the intestines of CD sufferers and their ability to persist in macrophages inducing granulomas. The rapid intracellular multiplication of AIEC sets it apart from other enteric pathogens such as Salmonella Typhimurium which after limited replication induce programmed cell death (PCD). Understanding the response of infected cells to the increased AIEC bacterial load and associated metabolic stress may offer insights into AIEC pathogenesis and its association with CD. Here we show that AIEC persistence within macrophages and dendritic cells is facilitated by increased proteasomal degradation of caspase-3. In addition S-nitrosylation of pro- and active forms of caspase-3, which can inhibit the enzymes activity, is increased in AIEC infected macrophages. This S-nitrosylated caspase-3 was seen to accumulate upon inhibition of the proteasome indicating an additional role for S-nitrosylation in inducing caspase-3 degradation in a manner independent of ubiquitination. In addition to the autophagic genetic defects that are linked to CD, this delay in apoptosis mediated in AIEC infected cells through increased degradation of caspase-3, may be an essential factor in its prolonged persistence in CD patients

NLRP12 attenuates colon inflammation by maintaining colonic microbial diversity and promoting protective commensal bacterial growth

Inflammatory bowel diseases involve the dynamic interplay of host genetics, microbiome and inflammatory response. Here, we report that NLRP12, a negative regulator of innate immunity, is reduced in human ulcerative colitis by comparing monozygotic twins and other patient cohorts. In parallel, Nlrp12-deficiency in mice caused increased colonic basal inflammation, leading to a less-diverse microbiome, loss of protective gut commensal strains (Lachnospiraceae) and increased colitogenic strains (Erysipelotrichaceae). Dysbiosis and colitis susceptibility associated with Nlrp12-deficency were reversed equally by treatment with antibodies targeting inflammatory cytokines or by administration of beneficial commensal Lachnospiraceae isolates. Fecal transplants from specific pathogen free reared mice into germ-free Nlrp12-deficient mice showed that NLRP12 and the microbiome each contribute to immune signaling that culminates in colon inflammation. These findings reveal a feed-forward loop where NLRP12 promotes specific commensals that can reverse gut inflammation, while cytokine blockade during NLRP12-deficiency can reverse dysbiosis

A systems-level analysis highlights microglial activation as a modifying factor in common epilepsies

Aims: The causes of distinct patterns of reduced cortical thickness in the common human epilepsies, detectable on neuroimaging and with important clinical consequences, are unknown. We investigated the underlying mechanisms of cortical thinning using a systems-level analysis. Methods: Imaging-based cortical structural maps from a large-scale epilepsy neuroimaging study were overlaid with highly spatially resolved human brain gene expression data from the Allen Human Brain Atlas. Cell-type deconvolution, differential expression analysis and cell-type enrichment analyses were used to identify differences in cell-type distribution. These differences were followed up in post-mortem brain tissue from humans with epilepsy using Iba1 immunolabelling. Furthermore, to investigate a causal effect in cortical thinning, cell-type-specific depletion was used in a murine model of acquired epilepsy. Results: We identified elevated fractions of microglia and endothelial cells in regions of reduced cortical thickness. Differentially expressed genes showed enrichment for microglial markers and, in particular, activated microglial states. Analysis of post-mortem brain tissue from humans with epilepsy confirmed excess activated microglia. In the murine model, transient depletion of activated microglia during the early phase of the disease development prevented cortical thinning and neuronal cell loss in the temporal cortex. Although the development of chronic seizures was unaffected, the epileptic mice with early depletion of activated microglia did not develop deficits in a non-spatial memory test seen in epileptic mice not depleted of microglia. Conclusions: These convergent data strongly implicate activated microglia in cortical thinning, representing a new dimension for concern and disease modification in the epilepsies, potentially distinct from seizure control

A systems-level analysis highlights microglial activation as a modifying factor in common epilepsies

Aims: The causes of distinct patterns of reduced cortical thickness in the common human epilepsies, detectable on neuroimaging and with important clinical consequences, are unknown. We investigated the underlying mechanisms of cortical thinning using a systems-level analysis. // Methods: Imaging-based cortical structural maps from a large-scale epilepsy neuroimaging study were overlaid with highly spatially resolved human brain gene expression data from the Allen Human Brain Atlas. Cell-type deconvolution, differential expression analysis and cell-type enrichment analyses were used to identify differences in cell-type distribution. These differences were followed up in post-mortem brain tissue from humans with epilepsy using Iba1 immunolabelling. Furthermore, to investigate a causal effect in cortical thinning, cell-type specific depletion was used in a murine model of acquired epilepsy. // Results: We identified elevated fractions of microglia and endothelial cells in regions of reduced cortical thickness. Differentially expressed genes showed enrichment for microglial markers, and in particular, activated microglial states. Analysis of post-mortem brain tissue from humans with epilepsy confirmed excess activated microglia. In the murine model, transient depletion of activated microglia during the early phase of the disease development prevented cortical thinning and neuronal cell loss in the temporal cortex. Although the development of chronic seizures was unaffected, the epileptic mice with early depletion of activated microglia did not develop deficits in a non-spatial memory test seen in epileptic mice not depleted of microglia. // Conclusions: These convergent data strongly implicate activated microglia in cortical thinning, representing a new dimension for concern and disease modification in the epilepsies, potentially distinct from seizure control