Mercury is highly toxic to human health in all of its oxidation states. Thus, developing a low cost, efficient metal ion sensor for the detection of mercury ions at concentration levels down to parts-per-billion (ppb) remains a challenge. In the present work, we have developed a silver nanoparticles (Ag-NPs) impregnated poly(vinyle alcohol) capped 4-nitrophenylanthranilate (PVA-NPA) complex for mercury detection. The fluorescence intensity of the synthesized PVA-NPA is found to be quenched by the impregnated Ag-NPs through dynamic quenching. Moreover, energy transfer (ET) between the acceptor (Ag-NPs) and the donor (PVA-NPA) is observed to follow the nanosurface energy transfer (NSET) mechanism. We have utilized the amalgamation of Ag-NPs with Hg 2+ to develop a low cost prototype, which is highly efficient NSET based ultrasensitive "turn on" fluorescence mercury sensor. This sensor has high selectivity for Hg 2+ ions over a wide range of other competing heavy metal ions, generally present in water of natural sources. The sensor response is found to be linear over the Hg 2+ ions concentration regime from 0 to 1 ppb with a lower detection limit of 100 ppt (0.5 nM). The proposed method demonstrated successfully for monitoring trace Hg 2+ ions in real world samples.

56% in 1990, 59% in 2000, 74% in 2010 and 74% in 2012 whereas in our country it was 52% in 1991, 53% in 2000, 79% in 2010, 80% in 2011and 81% in 2013

Urinary incontinence is one of the most embarrassing disabilities in the elderly people. It may be defined as an involuntary loss of urine in a quantity or frequency sufficient to cause a social or hygienic problem. Its magnitude is both overlooked and underestimated by the medical community. Unfortunately, urinary incontinence lacks the glamour of other 'high tech' medical problems.

SUMMARY There are few reported studies of the lower oesophageal sphincter in preterm infants and none has investigated babies of less than 34 weeks gestation. Using a modified manometric technique suitable for use on very low birth weight infants we have measured sphincter pressures on 68 occasions in 25 infants of postconceptional age between 27 and 41 weeks. In even the most preterm infants the lower oesophageal sphincter could be defined. The mean effective sphincter pressure rose from 3-8 mmHg in infants of less than 29 weeks gestation to 18-1 mmHg in the term infant. This rise in effective sphincter pressure correlated well with increasing postconceptional age (r=0*81). This pattern of maturation in our patients was unaffected by intrauterine growth retardation, postnatal illness, or concurrent xanthine administration.In the preterm infant gastro-oesophageal reflux has been implicated in the pathogenesis of aspiration pneumonia, chronic lung disease, and apnoea.' It is also a significant risk factor for sudden infant death syndrome for which these infants are at high risk.2The lower oesophageal sphincter plays an important role in the prevention of gastro-oesophageal reflux yet little is known about the maturation of this sphincter in the preterm infant. Previous studies used systems now considered unsatisfactory because of damped sensitivity to pressure change as a result of an inadequate pressure frequency response. This could explain the very low sphincter pressures that have been reported in children and infants.34 BoixOchoa studied infants of varying gestation, including preterm infants of 34 weeks and over. All infants were found to have no effective sphincter pressure until six weeks after birth. From this it was inferred that sphincter maturation is completely dependent on postnatal age and independent of gestation.4Accurate systems are now available for use in older infants and children' but the need for a small catheter and low perfusion flow rate precludes their use in preterm infants. Our aim was to devise a manometric system with a high sensitivity and low compliance

The effect of RNA secondary structure on p-independent and p-dependent termination of transcription of T3 DNA by Escherichia cofl RNA polymerase has been studied by incorporating, into nascent transcripts, base analogs that lead to altered base-pairing properties. A guanine -hypoxanthine substitution, with attendant weakening of secondary structure, abolished the p-independent termination at 20% of the genome; in contrast, replacement of cytosine with 5-bromocytosine, which forms stronger pairs with guanine, enhanced termination at this site. p-Independent termination was not altered by replacing uracil with 5-bromouracil. described (11, 12). Transcription of T3 DNA by E. coli RNA Polymerase. Reaction mixtures (0.1 ml) contained 50mM Tris-HCl (pH 7.8), 10 mM MgCl2, 50-200 mM KC1 (as indicated), 4 mM dithiothreitol, the common ribonucleoside triphosphates or their analogs (as indicated) each at 0.4 mM and one labeled with 32p in the a-position, 8.5 nmol of T3 DNA (expressed as deoxynucleotide residues), 2.4 jug of RNA polymerase, and p protein (as indicated); the mixtures were incubated for 20 min at 370C. For measurement of the incorporation of labeled nucleotide into RNA, reactions were stopped by adding 0.5 ml each of 0.1 M Na4P207 and 10% CC13COOH. The precipitated RNA was collected on Millipore filters (7) and assayed for radioactivity in a toluene-based scintillation fluid.p-ATPase Assay. For measurement of hydrolysis of ATP during transcription, reaction mixtures were the same as described above except that [,y-32P]ATP (4 X 104 cpm/nmol) and [3H]UTP (10 X 104 cpm/nmol) were used as the labeled nucleoside triphosphates. After incubation at 370C for 20 min, the amount of [3H]UMP incorporated into an acid-insoluble RNA product was determined by Millipore filtration (7); the release of 32p; by cleavage of ['y-32P]ATP was determined by a modification of the method of Conway and Lipmann (13) as described (14). Control values for free 32P1 present in reaction mixtures containing no p ranged between 0.4 and 0.6 nmol and were subtracted from all values reported here. RESULTS p-Independent Termination during Transcription of T3 DNA. Early in the infection of E. coli by phage T3, E. coli RNA polymerase holoenzyme initiates transcription at one or more promoters located at the left end of the T3 genome (within 1% on the standard genetic map) (15) to copy the early genes (0.3, 0.7 1, 1.1, and 1.3, respectively) and terminates at a site tI located near 20% of the genome (15). Although termination at this site occurs quite efficiently in vivo (16), in vitro the polymerase reads through it to copy a part of the late region (17, 18). 1613The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact.

Hand, foot, and mouth disease (HFMD) also known as vesicular stomatitis with exanthema, first reported in New Zealand in 1957 is caused by Coxsackie virus A16 (CVA16), human enterovirus 71 (HEV71) and occasionally by other HEV-A serotypes, such as Coxsackie virus A6 and Coxsackie virus A10, are also associated with HFMD and herpangina. While all these viruses can cause mild disease in children, EV71 has been associated with neurological disease and mortality in large outbreaks in the Asia Pacific region over the last decade. It is highly contagious and is spread through direct contact with the mucus, saliva, or feces of an infected person. This is characterized by erythrematous papulo vesicular eruptions over hand, feet, perioral area, knee, buttocks and also intra-orally mostly in children, typically occurs in small epidemics usually during the summer and autumn months. HFMD symptoms are usually mild and resolve on their own in 7 to 10 days. Treatment is symptomatic but good hygiene during and after infection is very important in preventing the spread of the disease. Though only small scale outbreaks have been reported from United States, Europe, Australia Japan and Brazil for the first few decade, since 1997 the disease has conspicuously changed its behavior as noted in different Southeast Asian countries. There was sharp rise in incidence, severity, complications and even fatal outcomes that were almost unseen before that period. There are reports of disease activity in different corners of India since 2004, and the largest outbreak of HFMD occurred in eastern part of India in and around Kolkata in 2007and Bhubaneswar, Odisha in 2009. In recent years there are cases of HFMD have been seen in Bangladesh also. Although of milder degree, continuous progress to affect larger parts of the neighboring may indicate vulnerability of Bangladesh from possible future outbreaks.Bangladesh J Child Health 2016; VOL 40 (2) :115-119

No abstract

Polypeptide chain initiation factor IF-2 binds to 30S ribosomal subunits. This binding is enhanced by IF-2, one of the bacterial polypeptide chain initiation factors, is essential for the binding of both GTP and fMet-tRNA in a 30S initiation complex (1). This complex contains a 30S ribosomal subunit, mRNA, fMet-tRNA, and GTP (2,3). The combination of a 50S-subunit with the 30S complex results in the hydrolysis of GTP to GDP and Pi, concomitant with the formation of a functional 70S initiation complex (2,3). It has become clear that IF-2 is responsible for hydrolysis of GTP in the initiation process. In fact, under conditions uncoupled from initiation, IF-2 catalyzes the hydrolysis of GTP to GDP and Pi in the presence of both ribosomal subunits (4, 6). This activity can be coupled to initiation complex formation (6). Hence, IF-2 participates in the formation of a 30S initiation complex, as well as the subsequent transformation of this species into a 70S initiation complex.Recent studies have demonstrated that IF-2 functions stoichiometrically during 30S initiation complex formation, but catalytically during 70S initiation complex formation (2, 7), i.e., in the presence of both 30S and 50S subunits. Hence, it would appear likely that IF-2 binds to a 30S subunit and is released upon addition of a 50S ribosomal subunit. The released factor would then be able to catalyze another round of initiation. Examination of crude cell extracts reveals that IF-2 activity is localized on 30S subunits (8), and that no IF-2 (nor other initiation factors) are found on 70S ribosomes.In this communication, we provide a direct demonstration that IF-2 binds to 30S subunits. Upon formation of a 70S initiation complex, IF-2 is released from the ribosomes. In contrast to IF-1 and IF-3, release of IF-2 requires the hydrolysis of GTP. MATERIALS AND METHODSInitiation factors were purified (9) from Escherichia coli MRE-600. IF-1 and IF-3 were homogeneous, while IF-2 was about 90% pure by the criteria of native and Na dodecyl S04 disc-gel electrophoresis. Salt-washed ribosomes were prepared from E. coli Q13. Such ribosomes exist primarily as dissociated subunits. The preparation of f [3H]Met-tRNA, as well as the source of all reagents, has been described (9).Assay of fMet-tRNA and IF-2 Binding to Ribosomes. Reaction mixtures (0.125 ml) contained 50 mM Tris HCl (pH 7.8), 80 mM NH4CI, 10 mM magnesium acetate, and 4 mM 2-mercaptoethanol. In addition, the complete system con- (w/v) sucrose gradient containing reaction buffer, and centrifuged for 75 min at 55,000 rpm at 40 in a Spinco SW65 rotor. 0.2-ml fractions were collected and radioactivity was determined by counting aliquots in Bray's counting solution. The location of ribosomes was determined by monitoring the absorbancy at 260 nm. Gradient fractions were assayed for IF-2 activity by addition of 50-,ul aliquots to the complete reaction mixture described above, from which IF-2 had been omitted.