Terahertz time-domain imaging for the examination of gilded wooden artifacts.

Terahertz imaging is unlocking unique capabilities for the analysis of cultural heritage artifacts. This paper uses terahertz time-domain imaging for the study of a gilded wooden artifact, providing a means to perform stratigraphic analysis, yielding information about the composition of the artifact, presence of certain materials identifiable through their THz spectral fingerprint, as well as alterations that have been performed over time. Due to the limited information that is available for many historic artifacts, the data that can be obtained through the presented technique can guide proper stewardship of the artifact, informing its long-term preservation.

Preparation and characterization of clay based ceramic porous membranes and their use for the removal of lead ions from synthetic wastewater with an insight into the removal mechanism.

The present study explores the use of local clay from the United Arab Emirates (UAE) to prepare porous ceramic membranes (flat disk shape) for the purpose of removing toxic heavy metals from contaminated water. Four distinct ceramic membranes, crafted from locally sourced clay and incorporated with activated carbon and graphite, underwent careful and thorough preparation. The initial set of membranes was subjected to open-air sintering, resulting in the creation of mACA and mGrA membranes. Concurrently, a second set of meticulously prepared membranes underwent sintering under inert nitrogen conditions, yielding the formation of mACI and mGrI membranes, respectively. Prior to making the membranes, the clay material was characterized by thermogravimetric analysis (TGA), X-ray fluorescence (XRF), Fourier-transform infrared spectroscopy (FTIR), and X-ray diffraction analysis (XRD). The clay presented the lowest weight loss compared to AC and Gr, implying that these two materials could be used as porogen agents. The X-ray fluorescence results indicated that the natural clay contained 65.5 wt% of silicon dioxide (SiO2), aluminium oxide (Al2O3), and iron (III) oxide (Fe2O3) falling within the class C category of clays according to ASTM. The FTIR analysis showed different clay regions allocated to various stretching and deformation vibrations of hydroxide, organic fraction, and (Si, Al, Fe)-O groups. The XRD analysis revealed the presence of kaolinite, illite, smectite and calcite phyllite phases in the clay mineral. The membranes were characterized using FESEM, with those containing AC (used as porogen) exhibiting large pores clearly visible on the surface, and were tested for the removal of lead (Pb2+) ions from synthetic wastewater. The removal efficiencies of the membranes were 33 %, 75.2 %, 100 % and 100 % for mACA, mACI, mGrA and mGrI respectively after 100 min operation. The wettability of the membranes was found to follow the order mACI < mACA < mGrI < mGrA, which corroborated well with water fluxes of 7, 8, 112 and 214 L h-1 m-2 recorded after 60 min duration and 1.0 bar applied pressure. The mechanisms of filtration of Pb2+ ions were adsorption for the AC-based membranes (mACA, mACI) and a combination of adsorption and size exclusion for the Gr-based membranes (mGrA, mGrI).

Mechanisms of Intestinal Serotonin Transporter (SERT) Upregulation by TGF-ß1 Induced Non-Smad Pathways.

TGF-ß1 is an important multifunctional cytokine with numerous protective effects on intestinal mucosa. The influence of TGF-ß1 on serotonin transporter (SERT) activity, the critical mechanism regulating the extracellular availability of serotonin (5-HT), is not known. Current studies were designed to examine acute effects of TGF-ß1 on SERT. Model human intestinal Caco-2 cells grown as monolayer's or as cysts in 3D culture and ex vivo mouse model were utilized. Treatment of Caco-2 cells with TGF-ß1 (10 ng/ml, 60 min) stimulated SERT activity (~2 fold, P<0.005). This stimulation of SERT function was dependent upon activation of TGF-ß1 receptor (TGFRI) as SB-431542, a specific TGF-ßRI inhibitor blocked the SERT stimulation. SERT activation in response to TGF-ß1 was attenuated by inhibition of PI3K and occurred via enhanced recruitment of SERT-GFP to apical surface in a PI3K dependent manner. The exocytosis inhibitor brefeldin A (2.5 µM) attenuated the TGF-ß1-mediated increase in SERT function. TGF-ß1 increased the association of SERT with the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) syntaxin 3 (STX3) and promoted exocytosis of SERT. Caco-2 cells grown as cysts in 3D culture recapitulated the effects of TGF-ß1 showing increased luminal staining of SERT. Ussing chamber studies revealed increase in 3H-5-HT uptake in mouse ileum treated ex vivo with TGF-ß1 (10 ng/ml, 1h). These data demonstrate a novel mechanism rapidly regulating intestinal SERT via PI3K and STX3. Since decreased SERT is implicated in various gastro-intestinal disorders e.g IBD, IBS and diarrhea, understanding mechanisms stimulating SERT function by TGF-ß1 offers a novel therapeutic strategy to treat GI disorders.

Epidermal growth factor upregulates serotonin transporter in human intestinal epithelial cells via transcriptional mechanisms.

Serotonin transporter (SERT) regulates extracellular availability of serotonin and is a potential pharmacological target for gastrointestinal disorders. A decrease in SERT has been implicated in intestinal inflammatory and diarrheal disorders. However, little is known regarding regulation of SERT in the intestine. Epidermal growth factor (EGF) is known to influence intestinal electrolyte and nutrient transport processes and has protective effects on intestinal mucosa. Whether EGF regulates SERT in the human intestine is not known. The present studies examined the regulation of SERT by EGF, utilizing Caco-2 cells grown on Transwell inserts as an in vitro model. Treatment with EGF from the basolateral side (10 ng/ml, 24 h) significantly stimulated SERT activity (∼2-fold, P < 0.01) and mRNA levels compared with control. EGF increased the activities of the two alternate promoter constructs for human SERT gene: SERT promoter 1 (hSERTp1, upstream of exon 1a) and SERT promoter 2 (hSERTp2, upstream of exon 2). Inhibition of EGF receptor (EGFR) tyrosine kinase activity by PD168393 (1 nM) blocked the stimulatory effects of EGF on SERT promoters. Progressive deletions of the SERT promoter indicated that the putative EGF-responsive elements are present in the -672/-472 region of the hSERTp1 and regions spanning -1195/-738 and -152/+123 of hSERTp2. EGF markedly increased the binding of Caco-2 nuclear proteins to the potential AP-1 cis-elements present in EGF-responsive regions of hSERTp1 and p2. Overexpression of c-jun but not c-fos specifically transactivated hSERTp2, with no effects on hSERTp1. Our findings define novel mechanisms of transcriptional regulation of SERT by EGF via EGFR at the promoter level that may contribute to the beneficial effects of EGF in gut disorders.

Enteropathogenic Escherichia coli infection inhibits intestinal serotonin transporter function and expression.

BACKGROUND & AIMS: Serotonin transporter (SERT) plays a critical role in regulating serotonin (5-hydroxytryptamine [5-HT]) availability in the gut. Elevated 5-HT levels are associated with diarrheal conditions such as irritable bowel syndrome and enteric infections. Whether alteration in SERT activity contributes to the pathophysiology of diarrhea induced by the food-borne pathogen enteropathogenic Escherichia coli (EPEC) is not known. The present studies examined the effects of EPEC infection on SERT activity and expression in intestinal epithelial cells and elucidated the underlying mechanisms. METHODS: Caco-2 cells as a model of human intestinal epithelia and EPEC-infected C57BL/6J mouse model of infection were utilized. SERT activity was measured as Na(+) and Cl(-) dependent (3)[H] 5-HT uptake. SERT expression was measured by real-time quantitative reverse-transcription polymerase chain reaction, Western blotting, and immunofluorescence studies. RESULTS: Infection of Caco-2 cells with EPEC for 30-120 minutes decreased apical SERT activity (P < .001) in a type 3 secretion system dependent manner and via involvement of protein tyrosine phosphatases. EPEC infection decreased V(max) of the transporter; whereas cell surface biotinylation studies revealed no alteration in the cellular or plasma membrane content of SERT in Caco-2 cells. EPEC infection of mice (24 hours) reduced SERT immunostaining with a corresponding decrease in SERT messenger RNA levels, 5-HT uptake, and mucosal 5-HT content in the small intestine. CONCLUSIONS: Our results demonstrate inhibition of SERT by EPEC and define the mechanisms underlying these effects. These data may aid in the development of a novel pharmacotherapy to modulate the serotonergic system in treatment of infectious diarrheal diseases.