Molecular Characterisation of Salmonella enterica Serovar Typhi Isolated from Typhoidial Humans

Aims: Salmonella enterica serovar Typhi is the major causative agent for typhoidial fever around the globe among human population reported till date. Present research work was carried out for detection and molecular characterisation of Salmonella enterica serovar Typhi isolated from humans with Typhoidial fever by biochemical, phenotypical and virulence gene based polymerase chain reaction (PCR) techniques. The isolated strains were also investigated for antibiotic susceptibility patterns as a control measure. Methodology and Results: A total of 16 clinical samples were collected from the same numbers of patients (7 males and 9 females) from Coimbatore, Erode and Salem districts of Tamil Nadu and were processed via broth enrichment methods for isolation and identification of the causative agent S. enterica serovar Typhi. Microbiological and biochemical investigations revealed the presence of S. Typhi from 16 samples. The biotyping of the isolates showed that all the isolates belonged to biotype IV. The PCR analysis confirmed the presence of invA (Invasion gene, 244bp), tyv (Tyveloseepimerase gene, 615 bp), fliC-d (Phage-1 flagellin gene for d-antigen, 750 bp) and viaB (Vi antigen gene, 439bp) in all 16 clinical samples. The antibiotic susceptibility test that was carried out among the isolates against 12 antimicrobial agents, showed 100 % resistance to only ampicillin and 100 % sensitivity to carbenicillin, chloramphenicol, clindamycin, gentamycin, kanamycin and tetracycline.Conclusion, significance and impact of study: This study confirmed the association of virulent strains of S. enterica serovar Typhi from Typhoidial fever among human population and suggested that PCR based diagnostic could be very useful for the rapid detection of S. Typhi isolates. Present study emphasized the use of antibiotic like chloramphenicol or in combination with other antibiotics for the effective control of S. Typhi

First report on distribution of heavy metals and proximate analysis in marine edible puffer fishes collected from Gulf of Mannar Marine Biosphere Reserve, South India

In the present study, the heavy metal concentration in different organs (skin, tissue, liver, kidney, gill, intestine, and ovary) and muscle proximate composition were studied in marine edible puffer fishes Takifugu oblongus, Lagocephalus guentheri, Arothron hispidus, Chelonodon patoca and Arothron immaculatus collected from Mandapam fish landing centre, South east coast of India. Heavy metals (Cd, Cu, Pb & Zn) were analyzed in different organs for the above mentioned species. The heavy metals concentration ranges in fish organs of all the five species were Cu (0.42 â6.31 mg/kg), Cd (0.01â0.79 mg/kg), Pb (5.80â19.87 mg/kg), and Zn (6.75â65.08 mg/kg). Zn was detected higher in all the samples followed by Pb, Cu and Cd. The proximate composition was determined in edible muscle tissues of all the five species. The highest and lowest protein contents were observed in T. oblongus (20.6 ± 0.6%) and C. patoca (17.9 ± 0.3%). In the present study, heavy metal concentrations were found very high in all the internal organs when compared to muscle tissues. Further, this is the first report on distribution of heavy metals and proximate compositions of commercialized important edible puffer fishes from Mandapam coast of Gulf of Mannar, Southeast coast of India. Keywords: Tetraodontiformes, Tetraodontidae, Edible puffer fishes, Heavy metals and proximate analysi

FOXG1 Regulates PRKAR2B Transcriptionally and Posttranscriptionally via miR200 in the Adult Hippocampus

Rett syndrome is a complex neurodevelopmental disorder that is mainly caused by mutations in MECP2. However, mutations in FOXG1 cause a less frequent form of atypical Rett syndrome, called FOXG1 syndrome. FOXG1 is a key transcription factor crucial for forebrain development, where it maintains the balance between progenitor proliferation and neuronal differentiation. Using genome-wide small RNA sequencing and quantitative proteomics, we identified that FOXG1 affects the biogenesis of miR200b/a/429 and interacts with the ATP-dependent RNA helicase, DDX5/p68. Both FOXG1 and DDX5 associate with the microprocessor complex, whereby DDX5 recruits FOXG1 to DROSHA. RNA-Seq analyses of Foxg1cre/+ hippocampi and N2a cells overexpressing miR200 family members identified cAMP-dependent protein kinase type II-beta regulatory subunit (PRKAR2B) as a target of miR200 in neural cells. PRKAR2B inhibits postsynaptic functions by attenuating protein kinase A (PKA) activity; thus, increased PRKAR2B levels may contribute to neuronal dysfunctions in FOXG1 syndrome. Our data suggest that FOXG1 regulates PRKAR2B expression both on transcriptional and posttranscriptional levels.Fil: Weise, Stefan C.. Institute Of Anatomy And Cell Biology; AlemaniaFil: Arumugam, Ganeshkumar. Institute Of Anatomy And Cell Biology; AlemaniaFil: Villarreal, Alejandro. Institute Of Anatomy And Cell Biology; Alemania. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; ArgentinaFil: Videm, Pavankumar. Universität Freiburg Im Breisgau; AlemaniaFil: Heidrich, Stefanie. Institute Of Anatomy And Cell Biology; AlemaniaFil: Nebel, Nils. Institute Of Anatomy And Cell Biology; AlemaniaFil: Dumit, Veronica Ines. Universität Freiburg Im Breisgau; Alemania. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Sananbenesi, Farahnaz. Deutsches Zentrum Für Neurodegenerative Erkrankungen E.v.; AlemaniaFil: Reimann, Viktoria. Albert Ludwigs University Of Freiburg; AlemaniaFil: Craske, Madeline. Active Motif Incorporation; Estados UnidosFil: Schilling, Oliver. Universität Freiburg Im Breisgau; AlemaniaFil: Hess, Wolfgang R.. Universität Freiburg Im Breisgau; AlemaniaFil: Fischer, Andre. Universitätsmedizin Göttingen; Alemania. Deutsches Zentrum Für Neurodegenerative Erkrankungen E.v.; AlemaniaFil: Backofen, Rolf. Universidad de Copenhagen; DinamarcaFil: Vogel, Tanja. Universität Freiburg Im Breisgau; Alemani