Mapping the Progress in Surface Plasmon Resonance Analysis of Phytogenic Silver Nanoparticles with Colorimetric Sensing Applications

Nanotechnology is gaining enormous attention as the most dynamic research area in science and technology. It involves the synthesis and applications of nanomaterials in diverse fields including medical, agriculture, textiles, food technology, cosmetics, aerospace, electronics, etc. Silver nanoparticles (AgNPs) have been extensively used in such applications due to their excellent physicochemical, antibacterial, and biological properties. The use of plant extract as a biological reactor is one of the most promising solutions for the synthesis of AgNPs because this process overcomes the drawbacks of physical and chemical methods. This review article summarizes the plant-mediated synthesis process, the probable reaction mechanism, and the colorimetric sensing applications of AgNPs. Plant-mediated synthesis parameters largely affect the surface plasmon resonance (SPR) characteristic due to the changes in the size and shape of AgNPs. These changes in the size and shape of plant-mediated AgNPs are elaborately discussed here by analyzing the surface plasmon resonance characteristics. Furthermore, this article also highlights the promising applications of plant-mediated AgNPs in sensing applications regarding the detection of mercury, hydrogen peroxide, lead, and glucose. Finally, it describes the future perspective of plant-mediated AgNPs for the development of green chemistry.     

Effects of antihypertensive treatment on cardiac IGF-1 during prevention of ventricular hypertrophy in the rat.

There is some evidence that cardiac rather than circulating insulin-like growth factor-1 (IGF-1) levels contribute to the development of renovascular hypertensive left ventricular hypertrophy (LVH), remaining unknown the effects of antihypertensive drugs on IGF-1 levels. We have assessed here the preventive effects of enalapril, losartan, propanolol and alpha-methyldopa on left ventricle (LV) and circulating IGF-1 levels in a rat model of hypertension and LVH (Goldblatt, GB). Our results show that relative LV mass and the LV content of IGF-1 were significantly lower with all antihypertensive drugs in GB rats (p<0.001). Serum concentrations of IGF-1 were lower in GB rats treated with enalapril, alpha-methyldopa and propanolol (p<0.01), but not in those treated with losartan. These results support the hypothesis that local rather than seric IGF-1 contributes to the development of left ventricular hypertrophy induced by pressure overload in the rat.     

Effects of azadirachtin/Neemazal on different stages and adult life table parameters of Trichogramma cacoeciae (Hymenoptera: Trichogrammatidae)

The effects of azadirachtin/Neemazal on adults, emergence, and life table parameters of Trichogramma cacoeciae Marchal were studied. The adults were exposed to fresh residues of the insecticide applied on glass plates. Based on the dose-response study, the LC50 value was 1330 ppm or 13.3 microg (AI)/ml. The effect of Neemazal on three developmental stages of the parasitoid was tested by dipping parasitized Sitotroga cerealella (Olivier) and Cydia pomonella (L.) eggs at the field-recommended concentration 3, 6, and 9 d after parasitization corresponding to larval, prepupal, and pupal stages. The emergence of adult parasitoids was adversely affected in both hosts, but the adverse effect was more in S. cerealella eggs compared with C. pomonella. The adult emergence was reduced by 73.3 and 33.76% in Sitotroga and Cydia eggs compared with controls, respectively. Longevity and progeny production of the emergent adults did not differ significantly from control. Neemazal affected stable population parameters (r(m), T, and DT) significantly. The intrinsic rate of increase for the control and Neemazal-exposed populations was 0.340 and 0.335 female offspring per female per day, respectively. Because some of postemergence life table parameters of adults were significantly reduced by the insecticide treatment, emergence rate of the parasitoid from treated eggs is not an adequate measure of ecological selectivity, and field studies are needed to determine the actual impact of neem on T. cacoeciae.     

Identification of two novel mutations in the SLC25A13 gene and detection of seven mutations in 102 patients with adult-onset type II citrullinemia

Adult-onset type II citrullinemia (CTLN2) is characterized by a liver-specific deficiency of argininosuccinate synthetase (ASS) protein. We have recently identified the gene responsible for CTLN2, viz., SLC25A13, which encodes a calcium-binding mitochondrial carrier protein, designated citrin, and found five mutations of the SLC25A13 gene in CTLN2 patients. In the present study, we have identified two novel mutations, 1800ins1 and R605X, in SLC25A13 mRNA and the SLC25A13 gene. Diagnostic analysis for the seven mutations in 103 CTLN2 patients diagnosed by biochemical and enzymatic studies has revealed that 102 patients had one or two of the seven mutations and 93 patients were homozygotes or compound heterozygotes. These results indicate that CTLN2 is caused by an abnormality in the SLC25A13 gene, and that our criteria for CTLN2 before DNA diagnosis are correct. Five of 22 patients from consanguineous unions have been shown to be compound heterozygotes, suggesting a high frequency of the mutated genes. The frequency of homozygotes is calculated to be more than 1 in 20,000 from carrier detection (6 in 400 individuals tested) in the Japanese population. We have detected no cross-reactive immune materials in the liver of CTLN2 patients with any of the seven mutations by Western blot analysis with anti-human citrin antibody. From these findings, we hypothesize that CTLN2 is caused by a complete deletion of citrin, although the mechanism of ASS deficiency is still unknown.     

Mast cell protease 5 mediates ischemia-reperfusion injury of mouse skeletal muscle

Ischemia with subsequent reperfusion (IR) injury is a significant clinical problem that occurs after physical and surgical trauma, myocardial infarction, and organ transplantation. IR injury of mouse skeletal muscle depends on the presence of both natural IgM and an intact C pathway. Disruption of the skeletal muscle architecture and permeability also requires mast cell (MC) participation, as revealed by the fact that IR injury is markedly reduced in c-kit defective, MC-deficient mouse strains. In this study, we sought to identify the pathobiologic MC products expressed in IR injury using transgenic mouse strains with normal MC development, except for the lack of a particular MC-derived mediator. Histologic analysis of skeletal muscle from BALB/c and C57BL/6 mice revealed a strong positive correlation (R(2) = 0.85) between the extent of IR injury and the level of MC degranulation. Linkage between C activation and MC degranulation was demonstrated in mice lacking C4, in which only limited MC degranulation and muscle injury were apparent. No reduction in injury was observed in transgenic mice lacking leukotriene C(4) synthase, hemopoietic PGD(2) synthase, N-deacetylase/N-sulfotransferase-2 (enzyme involved in heparin biosynthesis), or mouse MC protease (mMCP) 1. In contrast, muscle injury was significantly attenuated in mMCP-5-null mice. The MCs that reside in skeletal muscle contain abundant amounts of mMCP-5 which is the serine protease that is most similar in sequence to human MC chymase. We now report a cytotoxic activity associated with a MC-specific protease and demonstrate that mMCP-5 is critical for irreversible IR injury of skeletal muscle.     

Expression of three mitochondrial solute carriers, citrin, aralar1 and ornithine transporter, in relation to urea cycle in mice

The present report describes the expression profiles of different tissues and developmental changes of mouse aspartate/glutamate carrier (AGC) genes, Slc25a13 and Slc25a12, and an ornithine transporter gene, Ornt1, in relation to urea cycle enzyme genes, carbamoylphosphate synthetase I (CPS) and argininosuccinate synthetase (ASS). Slc25a13 encodes citrin, recently found to be deficient in adult-onset type II citrullinemia and to function as AGC together with its isoform and product of Slc25a12, aralar1. Citrin was broadly distributed, but mainly in the liver, kidney and heart. Aralar1 was expressed in diaphragm, skeletal muscle, heart, brain and kidney, but not in the liver. These distribution profiles are different from the restricted of Ornt1, ASS and CPS. Citrin, ASS, CPS and Ornt1 showed similar patterns of developmental changes in the liver and small intestine, where they play a role in urea and arginine synthesis. Dietary, hormonal and physical manipulations caused varied changes of CPS, ASS and Ornt1 in the liver, but the change of citrin was not so marked as that of the others. Analysis using RT-PCR and restriction enzyme digestion revealed that the ornithine transporter most expressed is Ornt1, although Ornt2 is detectable at a minute level. All these results suggest that citrin as AGC plays a role in urea synthesis as well as many fundamental metabolic pathways in the liver, and shares metabolic functions with aralar1 in other tissues, and that Ornt1 is an important component in urea synthesis in the liver and in arginine synthesis in the small intestine during the neonatal period.     

Effect of autonomic neurotransmitters on excitable gap composition in canine atrial flutter

Atrial arrhythmias are believed to be influenced by autonomic nervous system tone. We evaluated the effects of sympathetic and parasympathetic activation on atrial flutter (AF1) by determining the effects of norepinephrine (NE) and acetylcholine (ACh) on the composition of the excitable gap. A model of reentry around the tricuspid valve was produced in 17 chloralose anesthetized dogs using a Y-shaped lesion in the intercaval area that extended to the right atrial appendage. Excitable gap characteristics were determined during AF1 by scanning diastole with a single premature extrastimulus at progressively shorter coupling intervals to define the reset-response curve. Measurements were made during a constant infusion of NE (15 microg/min) into the right coronary artery and repeated during ACh infusion (2 microg/min) following a 15 min recovery period. The excitable gap (27 +/- 1 ms) was significantly (P < 0.001) increased by NE (34 +/- 1 ms) and ACh (50 +/- 2 ms). The fully excitable portion (7 +/- 1 ms) was also significantly (P < 0.001) increased by NE (17 +/- 1 ms) and ACh (43 +/- 2 ms). We conclude that both neurotransmitters increase the safety margin of full excitability ahead of the wavefront, demonstrating that parasympathetic and sympathetic activation can facilitate the persistence of this refractory atrial arrhythmia.     

The relationship between rooting of poplar shoots and ATPase activity of their crude microsomal vesicles

Poplar shoots raised in vitro were induced to root by a 7 h passage on an auxin (1-naphthaleneacetic acid) medium. The percentage of rooting was reduced from ± 97% to ± 47% when vanadate (200 µM) was included in the auxin medium. Introduction of vanadate in the medium without auxin after the 7 h induction on auxin medium, did not inhibit rooting but affected only the development of the roots produced. The Mg²⁺-dependent ATPase activity of the microsomal vesicles of poplar shoots was increased after 7 h induction on rooting medium and corresponded to an increase in the Vmax of the enzyme. Results from experiments using some inhibitors of the polyamine metabolism suggested that this pathway was not involved in the increase of this activity. The auxin had no effect on the in vitro ATPase activity at any concentration tested except at about 2 mM where it was inhibitory, probably due to a change in the conformation of the enzyme. The transient increase of indole-3-acetic acid during rooting induction could be responsible for the increase in the level of the enzyme. The inhibition of root formation and growth by vanadate indicates strongly that the ATPase activity may be necessary for the induction and expression of rooting.     

Evaluation of mammalian codon usage of fimH in DNA vaccine design

Uropathogenic Escherichia coli (UPEC) bacteria are the principal cause of urinary tract infections (UTI). Because these bacteria propagate intracellularly, the cellular immune response is an important factor in UTIs. Therefore, we designed a genetic construct to induce a cellular immune response. In order to develop a genetic construct that induces strong cellular immunity against this pathogen, we used the fimH synthetic gene according to mammalian codon usage, and the gene expression was compared with wild type codon usage. Initially, we designed two constructs, pVAX/fimH mam and pVAX/fimH wt, which contain mammalian and wild type codon usage, respectively. The Cos-7 cell line was transfected separately with a complex of pVAX/fimH mam-ExGene 500 poly cationic polymer and pVAX/fimH wt-ExGene 500 poly cationic polymer. Expression of the fimH gene in both constructs in COS7 cells was confirmed by RT-PCR, SDS-PAGE, and Western blotting. Both of the pVAX/fimH cassettes expressed inserted fimH genes (mam and wt) in Cos-7 cells. Our results suggest that codon optimization successfully expressed the fimH gene because the fimH gene with mammalian codon usage is compatible with the eukaryotic expression system. Therefore, mammalian codon usage could be appropriate in a pVAX/fimH construct as a DNA vaccine.