Green Banking Disclosure Practices in Emerging Economy

Green banking is burning issue in both traditional banking and digital banking. The involvement of green banking ensures the customer loyalty, customer satisfaction and investors retention. The study is conducted to explore the green banking spending by the commercial banks in the emerging economy. A thematic approach has been applied to identify the green banking disclosure by the listed commercial banks. An one to one approach has been applied to identify the green banking disclosures by the selected banks. It is found the green banking spending by the commercial banks in Bangladesh are increasing although some of the banks do not perform any remarkable green banking disclosure. The results of the study portray the holistic green banking disclosure scenario in the context of an emerging economy Bangladesh.  It is expected that the findings of the study will entice the management of the banks to disclose more green banking disclosure related information in both online and offline media. Keywords: Green banking disclosure, Emerging economy, Listed bank. DOI: 10.7176/JESD/14-16-05 Publication date: October 202

Annexin A1–containing extracellular vesicles and polymeric nanoparticles promote epithelial wound repair

Epithelial restitution is an essential process that is required to repair barrier function at mucosal surfaces following injury. Prolonged breaches in epithelial barrier function result in inflammation and further damage; therefore, a better understanding of the epithelial restitution process has potential for improving the development of therapeutics. In this work, we demonstrate that endogenous annexin A1 (ANXA1) is released as a component of extracellular vesicles (EVs) derived from intestinal epithelial cells, and these ANXA1-containing EVs activate wound repair circuits. Compared with healthy controls, patients with active inflammatory bowel disease had elevated levels of secreted ANXA1-containing EVs in sera, indicating that ANXA1-containing EVs are systemically distributed in response to the inflammatory process and could potentially serve as a biomarker of intestinal mucosal inflammation. Local intestinal delivery of an exogenous ANXA1 mimetic peptide (Ac2-26) encapsulated within targeted polymeric nanoparticles (Ac2-26 Col IV NPs) accelerated healing of murine colonic wounds after biopsy-induced injury. Moreover, one-time systemic administration of Ac2-26 Col IV NPs accelerated recovery following experimentally induced colitis. Together, our results suggest that local delivery of proresolving peptides encapsulated within nanoparticles may represent a potential therapeutic strategy for clinical situations characterized by chronic mucosal injury, such as is seen in patients with IBD

Vibrio cholerae Type Three Secretion System Regulators and Effectors: Identification and Role in Pathogenesis

Thesis (Ph.D.)--University of Rochester. School of Medicine & Dentistry. Dept. of Microbiology and Immunology, 2010.AM-19226 is a pathogenic, O39 serogroup Vibrio cholerae strain that lacks the toxin co-regulated pilus (TCP) and cholera toxin (CT), which are virulence factors for colonization and toxin production encoded by epidemic O1 and O139 serogroup V. cholerae strains. Instead, strain AM-19226 carries a 48.5 kb pathogenicity island that encodes a Type III Secretion System (T3SS). A T3SS is a conserved virulence mechanism carried by many gram-negative pathogens, and is a multi protein complex that translocates virulence (effector) proteins from the bacterial cytoplasm into eukaryotic host cells. Annotation of the AM-19226 T3SS island DNA sequence identified more than 50 ORFs (open reading frames): ten encode proteins of the secretion apparatus; two (A33_1664 and A33_1675) are predicted to encode transcriptional regulators that are similar to the ToxR protein (a transmembrane protein that regulates TCP and CT expression in epidemic strains); and more than 35 ORFs encode hypothetical proteins having no known homology. We hypothesized that the T3SS encoded ToxR-like proteins are important for T3SS gene regulation, and predicted that many of the hypothetical ORFs encode unique T3SS effector proteins that mediate the TCP/CT independent pathogenesis of strain AM-19226. Two approaches were used to determine the role of the T3SS encoded transcriptional regulators in pathogenesis. First, strains carrying deletions in ORFs A33_1664 and A33_1675 were shown to be severely attenuated for colonization in vivo using the infant mouse model, suggesting that they encode proteins essential for pathogenesis. Second, lacZ transcriptional reporter fusions were constructed to T3SS gene promoter regions to evaluate the role of A33_1664 and A33_1675 gene products in T3SS gene expression. Growth of reporter strains under different in vitro conditions identified bile and deoxycholate as strongly inducing T3SS structural gene expression. This effect was mediated by the transcriptional regulators encoded by A33_1664 and A33_1675, named vttRA and vttRB respectively. Saccharomyces cerevisiae has been used as a model system to study effector protein activity, since many signaling pathways and cellular mechanisms are conserved among yeast and higher eukaryotes. In different species, effectors are typically encoded by genes located in the T3SS pathogenicity island. Therefore 20 of the V. cholerae ORFs encoding hypothetical proteins were expressed in yeast and observed for growth defects. The results identified a total of 12 ORFs that inhibited yeast growth. A FRET based TEM1-reporter fusion assay determined that 3 of the 12 ORFs encode bona fide effector proteins that were translocated into eukaryotic cells in vitro in a T3SS dependent manner. One protein, encoded by locus A33_1663, was chosen for further study, since BLAST analysis suggested that it is a novel effector protein with conserved sequences found only in T3SS positive V. cholerae and V. parahaemolyticus strains. The role of A33_1663 in pathogenesis was explored using several approaches. A strain deleted for this locus showed a ~five-fold reduction in its colonization ability in vivo. The results of A33_1663-lacZ transcriptional reporter fusion activity showed that A33_1663 expression can be induced by growth in bile, and is co-regulated with the structural genes by VttRA and VttRB. Suppression of the yeast growth defect induced by A33_1663 was used to identify yeast proteins that interact with the A33_1663 product. Growth was assayed in yeast strains deleted for the components of different MAPK signaling pathways. Deletion of the BCK1 and SLT2 genes, components of the protein kinase C-mediated cell wall integrity (CWI) MAPK pathway, did not suppress the yeast growth inhibition by A33_1663. However, deletion of the RLM1 gene, encoding a transcriptional factor in the CWI MAPK pathway, partially suppressed the yeast growth defect induced by A33_1663 expression. The data suggest that Rlm1p may be a target of A33_1663 activity, however, this activity may not require the activation of Rlm1p by its MAPK Slt2p. Tandem affinity purification analysis, using A33_1663 as the bait protein in yeast, did not identify Rlm1p, suggesting an indirect interaction between the two proteins. Collectively, the data presented within describe the identification and initial characterization of essential components of V. cholerae T3SS mediated pathogenesis. Importantly, the studies identified two T3SS encoded transcriptional regulators that control T3SS gene expression and are essential for pathogenesis. In addition, multiple effector proteins were identified using yeast as a model system, and genetic studies suggest that the effector protein encoded by A33_1663 may contribute to pathogenesis by interacting with eukaryotic transcription factors or their downstream targets involved in cell signaling pathways

Using S. cerevisiae as a Model System to Investigate V. cholerae VopX-Host Cell Protein Interactions and Phenotypes

Most pathogenic, non-O1/non-O139 serogroup Vibrio cholerae strains cause diarrheal disease in the absence of cholera toxin. Instead, many use Type 3 Secretion System (T3SS) mediated mechanisms to disrupt host cell homeostasis. We identified a T3SS effector protein, VopX, which is translocated into mammalian cells during in vitro co-culture. In a S. cerevisiae model system, we found that expression of VopX resulted in a severe growth defect that was partially suppressed by a deletion of RLM1, encoding the terminal transcriptional regulator of the Cell Wall Integrity MAP kinase (CWI) regulated pathway. Growth of yeast cells in the presence of sorbitol also suppressed the defect, supporting a role for VopX in destabilizing the cell wall. Expression of VopX activated expression of β-galactosidase from an RLM1-reponsive element reporter fusion, but failed to do so in cells lacking MAP kinases upstream of Rlm1. The results suggest that VopX inhibits cell growth by stimulating the CWI pathway through Rlm1. Rlm1 is an ortholog of mammalian MEF2 transcription factors that are proposed to regulate cell differentiation, proliferation, and apoptosis. The collective findings suggest that VopX contributes to disease by activating MAP kinase cascades that elicit changes in cellular transcriptional programs

Identification of Vibrio cholerae Type III Secretion System Effector Proteins▿ †

AM-19226 is a pathogenic O39 serogroup Vibrio cholerae strain that lacks the typical virulence factors for colonization (toxin-coregulated pilus [TCP]) and toxin production (cholera toxin [CT]) and instead encodes a type III secretion system (T3SS). The mechanism of pathogenesis is unknown, and few effector proteins have been identified. We therefore undertook a survey of the open reading frames (ORFs) within the ∼49.7-kb T3SS genomic island to identify potential effector proteins. We identified 15 ORFs for their ability to inhibit growth when expressed in yeast and then used a β-lactamase (TEM1) fusion reporter system to demonstrate that 11 proteins were bona fide effectors translocated into HeLa cells in vitro in a T3SS-dependent manner. One effector, which we named VopX (A33_1663), is conserved only in V. cholerae and Vibrio parahaemolyticus T3SS-positive strains and has not been previously studied. A vopX deletion reduces the ability of strain AM-19226 to colonize in vivo, and the bile-induced expression of a vopX-lacZ transcriptional fusion in vitro is regulated by the T3SS-encoded transcriptional regulators VttRA and VttRB. An RLM1 yeast deletion strain rescued the growth inhibition induced by VopX expression, suggesting that VopX interacts with components of the cell wall integrity mitogen-activated protein kinase (MAPK) pathway. The collective results show that the V. cholerae T3SS encodes multiple effector proteins, one of which likely has novel activities that contribute to disease via interference with eukaryotic signaling pathways

Bacteroides Fragilis in the gut microbiomes of Alzheimer’s disease activates microglia and triggers pathogenesis in neuronal C/EBPβ transgenic mice

Abstract Gut dysbiosis contributes to Alzheimer’s disease (AD) pathogenesis, and Bacteroides strains are selectively elevated in AD gut microbiota. However, it remains unknown which Bacteroides species and how their metabolites trigger AD pathologies. Here we show that Bacteroides fragilis and their metabolites 12-hydroxy-heptadecatrienoic acid (12-HHTrE) and Prostaglandin E2 (PGE2) activate microglia and induce AD pathogenesis in neuronal C/EBPβ transgenic mice. Recolonization of antibiotics cocktail-pretreated Thy1-C/EBPβ transgenic mice with AD patient fecal samples elicits AD pathologies, associated with C/EBPβ/Asparaginyl endopeptidase (AEP) pathway upregulation, microglia activation, and cognitive disorders compared to mice receiving healthy donors’ fecal microbiota transplantation (FMT). Microbial 16S rRNA sequencing analysis shows higher abundance of proinflammatory Bacteroides fragilis in AD-FMT mice. Active components characterization from the sera and brains of the transplanted mice revealed that both 12-HHTrE and PGE2 activate primary microglia, fitting with poly-unsaturated fatty acid (PUFA) metabolites enrichment identified by metabolomics. Strikingly, recolonization with live but not dead Bacteroides fragilis elicited AD pathologies in Thy1-C/EBPβ transgenic mice, so did 12-HHTrE or PGE2 treatment alone. Collectively, our findings support a causal role for Bacteroides fragilis and the PUFA metabolites in activating microglia and inducing AD pathologies in Thy1- C/EBPβ transgenic mice

Identification of In Vivo-Induced Bacterial Protein Antigens during Human Infection with Salmonella enterica Serovar Typhi

We applied an immunoscreening technique, in vivo-induced antigen technology (IVIAT), to identify immunogenic bacterial proteins expressed during human infection with Salmonella enterica serovar Typhi, the cause of typhoid fever. We were able to assign a functional classification to 25 of 35 proteins identified by IVIAT. Of these 25, the majority represent proteins with known or potential roles in the pathogenesis of S. enterica. These include proteins implicated in fimbrial structure and biogenesis, antimicrobial resistance, heavy metal transport, bacterial adhesion, and extracytoplasmic substrate trafficking as well as secreted hydrolases. The 10 remaining antigens represent proteins with unknown functions. Of the 35 identified antigens, four had no immunoreactivity when probed with control sera from individuals never exposed to serovar Typhi organisms; these four included PagC, TcfB, and two antigens of unknown function encoded by STY0860 and STY3683. PagC is a virulence factor known to be upregulated in vivo in S. enterica serovar Typhimurium infection of mice. TcfB is the major structural subunit of a fimbrial operon found in serovar Typhi with no homolog in serovar Typhimurium organisms. By examining differential immunoreactivities in acute- versus convalescent-phase human serum samples, we found specific anti-PagC and anti-TcfB immunoglobulin G responses in patients with serovar Typhi bacteremia. Serovar Typhi antigens identified by IVIAT warrant further evaluation for their contributions to pathogenesis, and they may have diagnostic, therapeutic, or preventive uses