Nutritional assessment and bioactive potential of Sargassum polycystum C. Agardh (Brown Seaweed)

492-498The phytochemical screening, nutritional composition and bioactive potential of Sargassum polycystum (Brown Seaweed) were investigated. The bioactive compounds of Sargassum polycystum showed significant activity against four human pathogens, namely, Bacillus subtilis, Escherichia coli, Staphylococcus aureus, and Klebsiella pneumoniae. The biochemical composition of Sargassum polycystum exhibited high nutritional potential of protein (14.2%), carbohydrate (25.0%), lipid (7.6%), fiber (21.3%), and ash (29.0%) than that in terrestrial plants and animal products. The Sargassum polycystum could be providing more opportunities for discovering new drugs which may be used as a source of healthy food for human regular diet

Taxonomy and Distribution of Scleria foliosa (Cyperaceae) in Kerala, India

Scleria foliosa (Cyperaceae) an interesting sedge species is reported here as a new record for Kerala. Detailed description with photographs and relevant notes on distribution are provided for easy identification

Inclusion in neuroscience through high impact courses

Recognizing that STEM disciplines, including neuroscience, have a long way to go to attract and retain diverse talent, educators can take action by being more intentional about their departmental curricula, course design, and pedagogical strategies. A deep body of research suggests that one way we can promote inclusion is through the use of high impact practices (HIPs). These active learning teaching practices promote deep learning and student engagement and have been shown to have a positive differential impact on historically underserved student populations. Here we describe the characteristics of two different types of HIP courses, makerspace classes, and course-based undergraduate research experiences (CUREs). In addition, we provide ideas for how these courses can be structured to help all students engage and learn. With experience overseeing a large campus-wide program introducing these course types to the curriculum, we also provide insights about faculty experiences and assessment. We propose that including these types of courses in a curriculum can engage a more diverse group of students to choose neuroscience as a major and as a career

Changes in expression of VE-cadherin and MMPs in endothelial cells: Implications for angiogenesis

The mechanism of cell-cell contact dependent regulation of pericellular proteolysis in angiogenesis was examined by studying the expression of MMPs using isolated HUVECs in culture. Zymography, Immunoblot and RT-PCR analysis showed that the production and secretion of matrixmetalloproteinase-2 and matrixmetalloproteinase-9 by HUVECs in culture were high when they remain as individual cells and significantly decreased during later stages of culture when cells developed cell-cell contact and tubular network-like structure. As MMPs decreased there was significant upregulation of VE-cadherin in cells undergoing angiogenic transition. Investigations to understand the signaling pathways downstream of VE-cadherin showed a relatively high level of β-catenin in the nucleus of endothelial cells in culture during initial stages and decrease in its levels in the nucleus, associated with an increase in the cytosol during later stages of culture. The distribution of β-catenin was found to be regulated by Tyr/Ser phosphorylation status of this protein. Cell-cell contact dependent downregulation of MMPs during angiogenesis was also observed in experiments using proangiogenic substances which caused a rapid rate of downregulation of MMP-2 and MMP-9 and absence of downregulation of MMPs when treated with anti-angiogenic agents

(2E)-1-(6-Chloro-2-methyl-4-phenyl­quinolin-3-yl)-3-phenyl­prop-2-en-1-one

In the title compound, C25H18ClNO, the conformation about the C=C double bond is E. Significant twists are evident in the mol­ecule, with the benzene ring forming a dihedral angle of 53.92 (11)° with the quinolinyl residue. Further, the chalcone residue is approximately perpendicular to the quinolinyl residue [Cq—Cq—Cc—Oc torsion angle = −104.5 (3)°, where q = quinolinyl and c = chalcone]. In the crystal, the presence of C—H⋯O and C—H⋯π inter­actions leads to supra­molecular layers lying parallel to (02)

A Molecular Signature of Proteinuria in Glomerulonephritis

Proteinuria is the most important predictor of outcome in glomerulonephritis and experimental data suggest that the tubular cell response to proteinuria is an important determinant of progressive fibrosis in the kidney. However, it is unclear whether proteinuria is a marker of disease severity or has a direct effect on tubular cells in the kidneys of patients with glomerulonephritis. Accordingly we studied an in vitro model of proteinuria, and identified 231 “albumin-regulated genes” differentially expressed by primary human kidney tubular epithelial cells exposed to albumin. We translated these findings to human disease by studying mRNA levels of these genes in the tubulo-interstitial compartment of kidney biopsies from patients with IgA nephropathy using microarrays. Biopsies from patients with IgAN (n = 25) could be distinguished from those of control subjects (n = 6) based solely upon the expression of these 231 “albumin-regulated genes.” The expression of an 11-transcript subset related to the degree of proteinuria, and this 11-mRNA subset was also sufficient to distinguish biopsies of subjects with IgAN from control biopsies. We tested if these findings could be extrapolated to other proteinuric diseases beyond IgAN and found that all forms of primary glomerulonephritis (n = 33) can be distinguished from controls (n = 21) based solely on the expression levels of these 11 genes derived from our in vitro proteinuria model. Pathway analysis suggests common regulatory elements shared by these 11 transcripts. In conclusion, we have identified an albumin-regulated 11-gene signature shared between all forms of primary glomerulonephritis. Our findings support the hypothesis that albuminuria may directly promote injury in the tubulo-interstitial compartment of the kidney in patients with glomerulonephritis

Perturbation of adhesion molecule-mediated chondrocyte-matrix interactions by 4-hydroxynonenal binding: implication in osteoarthritis pathogenesis

ABSTRACT: INTRODUCTION: Objectives were to investigate whether interactions between human osteoarthritic chondrocytes and 4-hydroxynonenal (HNE)-modified type II collagen (Col II) affect cell phenotype and functions and to determine the protective role of carnosine (CAR) treatment in preventing these effects. METHODS: Human Col II was treated with HNE at different molar ratios (MR) (1:20 to 1:200; Col II:HNE). Articular chondrocytes were seeded in HNE/Col II adduct-coated plates and incubated for 48 hours. Cell morphology was studied by phase-contrast and confocal microscopy. Adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and alpha1beta1 integrin at protein and mRNA levels were quantified by Western blotting, flow cytometry and real-time reverse transcription-polymerase chain reaction. Cell death, caspases activity, prostaglandin E2 (PGE2), metalloproteinase-13 (MMP-13), mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-kappaB) were assessed by commercial kits. Col II, cyclooxygenase-2 (COX-2), MAPK, NF-kappaB-p65 levels were analyzed by Western blotting. The formation of alpha1beta1 integrin-focal adhesion kinase (FAK) complex was revealed by immunoprecipitation. RESULTS: Col II modification by HNE at MR approximately 1:20, strongly induced ICAM-1, alpha1beta1 integrin and MMP-13 expression as well as extracellular signal-regulated kinases 1 and 2 (ERK1/2) and NF-kappaB-p65 phosphorylation without impacting cell adhesion and viability or Col II expression. However, Col II modification with HNE at MR approximately 1:200, altered chondrocyte adhesion by evoking cell death and caspase-3 activity. It inhibited alpha1beta1 integrin and Col II expression as well as ERK1/2 and NF-kappaB-p65 phosphorylation, but, in contrast, markedly elicited PGE2 release, COX-2 expression and p38 MAPK phosphorylation. Immunoprecipitation assay revealed the involvement of FAK in cell-matrix interactions through the formation of alpha1beta1 integrin-FAK complex. Moreover, the modification of Col II by HNE at a 1:20 or approximately 1:200 MR affects parameters of the cell shape. All these effects were prevented by CAR, an HNE-trapping drug. CONCLUSIONS: Our novel findings indicate that HNE-binding to Col II results in multiple abnormalities of chondrocyte phenotype and function, suggesting its contribution in osteoarthritis development. CAR was shown to be an efficient HNE-snaring agent capable of counteracting these outcomes