The test organisms were Rhizopus oryzae (MTCC 262), Chrysosporium tropicum (MTCC) and Aspergillus niger Selleck Compound Library (MTCC 281). Cultures of test organisms were maintained on potato dextrose agar slants and were subcultured in petri dishes prior to testing. The readymade potato dextrose agar medium (39 g) was suspended in distilled water (1000 ml) and heated to boiling until it dissolved completely. The medium and the petri dishes were autoclaved at a pressure of 15 ib/inch for 20 min.

Stock solutions were prepared by dissolving compound in DMSO and different concentrations were prepared (30 μg/ml). Agar cup bioassay was employed for testing antifungal activity of plant extract following the standard procedure. 14 The Crizotinib clinical trial medium was poured into petri dishes under aseptic conditions in a laminar flow chamber. When the medium in the plates solidified, 0.5 ml of 24 h old culture of test organism was inoculated. After inoculation, cups were scooped out with 6 mm sterile cork borer and the lids of the dishes were replaced. To each cup different concentration of test solutions (30, 100 μg) were added. Controls were maintained with DMSO using sample Clotrimazole. The treated and the control samples were kept at RT for 24–96 h

and inhibition zones were measured and diameter was calculated. Clotrimazole is taken as standard reference agent. (6a) 5-(phenyl)-4-methyl-3yl-(Imidazolidin-1ylmethyl, 2-ylidene nitro imine) isoxazole IR: νmax: 3310, 1580, 1590, 1410, 1297 cm−1, 1H NMR: δ 5.3 (s, 2H, –CH2–N–), 2.3 (s, 3H, isoxazole–CH3), 2.1 (brs, 1H, –NH), 2.8–3.1 (m, 4H, CH2), 7.4–7.55 (m, 3H, Ar.H), 7.7–7.8 (m, 2H, Ar.H), EI mass (m/z) 301 (M+), 247, 216. (6b) 5-(4-chlorophenyl)4- methyl-3yl-(Imidazolidin-1ylmethyl, 2-ylidene nitro imine) isoxazole IR: νmax: 3310, 2998, 1580 cm−1, 1H NMR: δ 5.5 (s, 2H, –CH2–N), 2.3 (s, 3H, isoxazole–CH3), 2.1 (brs, 1H, -NH), 2.9–3.2 (m, 4H), 7.4 (d, 2H, Ar.H, J = 8.0 Hz),7.65 (d, 2H, Ar.H = 8.2 Hz), EI mass (m/z) 335 (M+), 262, 247, 111. (6c) 5-(4-bromophenyl)-4-methyl-3yl-(Imidazolidin-1yl methyl, 2-ylidene nitro imine) isoxazole second IR: νmax: 3310, 1580, 1415, 1297 cm−1, 1H NMR: δ

4.6 (s, 2H, –CH2N–), 2.4 (s, 3H, isoxazole–CH3), 2.2 (brs, 1H, –NH), 2.7–3.1 (m, 4H), 7.5 (dd, J = 7.9 and 2.5 Hz, 2H, Ar.H), 7.8 (dd, J = 8.1 and 2.4 Hz 2H, Ar.H), EI mass (m/z) 379 (M+), 262, 225. (6d) 5-(4-flourophenyl)-4-methyl-3yl-(Imidazolidin-1ylmethyl, 2-ylidenenitroImine)isoxazole. IR: νmax: 3411, 1586, 1417, 1296 cm−1, 1H NMR: δ 5.5 (s, 2H, –CH2–N–), 2.3 (s, 3H, isoxazole–CH3), 2.10 (brs, 1H, –NH), 2.55–2.8 (m, 4H), 7.15 (m, 2H, Ar.H), J = 8.5 Hz, 7.75 (m, 2H, Ar.H), EI mass (m/z) 319 (M+), 270, 245. (6e) 5-(4-methyl phenyl)-4-methyl-3yl-(Imidazolidin-1ylmethyl, 2-ylidene nitro imine) isoxazole IR: νmax: 3406, 1555, 1410 cm−1, NMR: δ 2.4 (s, 3H, –ArCH3), 5.4 (s, 2H, –CH2–N), 2.2 (s, 3H, isoxazole–CH3), 2.1 (brs, 1H, –NH), 2.6–3.1 (m, 4H), 7.3 (d, 2H, Ar.H, J = 7.5 Hz), 7.7 (d, 2H, Ar.H = 7.

This study therefore seeks to assess C. orchioides for its toxic effects by seeing body weight and organ weight changes and hematological and serum biochemical parameters and changes in histopathology. The root parts of C. orchioides were collected, shade-dried and then finely powdered (collected from the Bharathidasan University, Tamil Nadu). 500 g of powder was extracted with methanol using a Soxhlet apparatus. The solvent was then evaporated under reduced pressure at 40 °C and dried in vacuum dessicator. Adult albino

see more rats of the Wistar strain of either sex (170–190 g) were used in the present study and were obtained from Madras Veterinary College, TANUVAS, Chennai, India. The animals were housed

in clean polypropylene cages under conditions of controlled temperature (25 ± 2 °C) with a 12/12-h day–night cycle, they had free access to food and water ad libitum. Animal experimentation Ixazomib was carried out as per the rules and protocols approved by the Institutional Animal Ethical Committee (IAEC). The phytochemical tests were carried out on the methanolic extract of root parts of C. orchioides to determine the bioactive compounds using standard procedures. 5 The acute oral toxicity study was performed as per the Organisation for Economic and Cooperation and Development (OECD) 423 guidelines. Nine female rats were divided in to three groups (3 per group) i.e., control and two test groups. Control group received

0.5% carboxy methyl cellulose as vehicle at a dose of 10 ml/kg bwt while the test groups received an oral dose of 2000 mg/kg bwt of MECO (10 ml/kg bwt in 0.5% CMC). All the experimental animals were observed for their mortality and clinical signs of toxicity at 30 min, Phosphatidylinositol diacylglycerol-lyase 1, 2 and 4 h and thereafter once a day for 14 days following vehicle, MECO administration. Body weights were recorded once a week. On 15th day the overnight fasted rats (water allowed) were euthanized using CO2 euthanasia chamber and subjected to gross pathological examination of all the major internal organs such as brain, heart, lung, liver, kidney, spleen, adrenals and sex organs. LD50 cut-off value of MECO was determined in accordance with Globally Harmonized System of Classification and labeling of chemicals.6 In the present study, MECO was administered at three dose levels i.e., at 200, 400 and 800 mg/kg/day. Both sexes of Wistar Albino rats (170–190 g) were divided in to 4 groups with 10 animals (5 males + 5 females) in each. Group I served as control and received 0.5% CMC as vehicle orally at a dose of 10 ml/kg bwt. Remaining 3 groups received MECO at 200 (Group II), 400 (Group III) and 800 (Group IV) mg/kg/day, p.o, respectively (10 ml/kg bwt. in 0.5% CMC), for a period of 28 days. In order to determine the reversibility or recovery from toxic effects, additional satellite groups were preset (Group V & VI).

Thus we confirmed the role of quantitative PTEN protein expression as a key determinant and putative biomarker of therapeutic resistance. One of the major barriers to more successful translation of I-BET-762 solubility dmso the results of modelling studies into clinical practice and anti-cancer drug development is a high level of individual variability of the cellular networks involved in seemingly identical cancers, not only due to genomic abnormalities (Kan et al., 2010), but also complex post-transcriptional and post-translational variability

in protein signalling networks (Faratian et al., 2009a). This causes a significant variation in individual responses to targeted anti-cancer treatments and therefore questions the practical utility of conclusions that can be drawn from network models with fixed parameters. Indeed, the majority of existing cancer-related modelling studies have been performed selleck products in a canonical way, where network model construction is followed by its parameterisation

via fitting the model to experimental data, and further analysis of one or several best solutions (Birtwistle et al., 2007, Chen et al., 2009, Faratian et al., 2009b and Schoeberl et al., 2009). The experimental data, used for model calibration, usually represent a set of time-course profiles of changes in protein phosphorylation, observed in response to perturbation of signalling with various receptor ligands. Given that such data are normally registered

for a particular cancer cell line, the quantitative predictions (e.g. on promising drug targets) drawn from the model analysis, though applicable to the reference cell type, may not be readily transferable TCL to other subtypes of cancer, due to possible biological variation of the network parameters in different cell lines, as well as potential noise in parameter estimates caused by the noise in experimental data. This may explain the slow incorporation of systems biology approaches as credible clinical tools. Another key but related impediment is the non-identifiability of model parameters, a problem common to many large-scale network models (Chen et al., 2009, Hengl et al., 2007, Rodriguez-Fernandez et al., 2006 and Yue et al., 2006). In complex biochemical models many parameters remain uncertain even when additional data are generated and different fitting algorithms are implemented (Brown and Sethna, 2003 and Chen et al., 2009). The majority of modelling studies employ various types of sensitivity analysis (SA) to assess how variation in input parameters can affect the model output. The most generally used method is local sensitivity analysis (LSA), based on evaluation of the impact of single parametric perturbations on the model output in close proximity to a reference solution, defined by nominal parameter values.

In summary, PIV5 is safe, stable, efficacious, cost–effective to produce, and overcomes pre-existing anti-vector immunity. In this work, we have shown that PIV5-based RSV vaccine candidates have the potential to be effective RSV vaccines, providing an additional option for RSV vaccine development. We appreciate the helpful discussion and technical assistance from all members of Biao He’s laboratory. This work was partially supported by grants from the National Institute of Allergy and Infectious Diseases (R01AI070847) to B.H. and (R01AI081977) to M.N.T. “
“The novel H1N1 influenza virus was detected in the United

States in April 2009. Worldwide, a pandemic was declared, and a national public health emergency was announced in the United States. In the US, plans were made for High Content Screening a national vaccination campaign to be rolled out in Fall 2009, when the pandemic H1N1 vaccine would be available. The campaign was implemented as a public–private partnership, with federal purchase of the vaccine. The Centers for Disease Control

and Prevention (CDC) allocated vaccine pro rata to states by total population as the vaccine became available. States determined how vaccine would be allocated in their jurisdiction and either retained Selleckchem EPZ-6438 control of vaccine allocation to individual providers at the central level or delegated fully or partially to local jurisdictions. States or local jurisdictions invited providers to participate in the program and vaccine was shipped to designated providers through a centralized distribution process supervised by the CDC that built on an existing contract for

Digestive enzyme management and distribution of vaccines in the Vaccine for Children (VFC) program. Fig. 1 shows a basic scheme of the supply chain for H1N1 vaccine from manufacturer to provider. State decisions about where to direct vaccine were guided by recommendations of the CDC’s Advisory Committee on Immunization Practices (ACIP) [6], which recommended that the vaccine be initially directed to: pregnant women, persons who live with or provide care for infants aged <6 months, health-care and emergency medical services personnel who have direct contact with patients or infectious material, all people 6 months to 24 years of age, and persons aged 25 through 64 years with certain health conditions (“high-risk”). The recommendations also provided further specification of priority groups in the event of vaccine shortage and stated that decisions to broaden availability of vaccine should be made at the local level. Overall, more than 120 million doses of vaccine were distributed to over 70 thousand locations by April 2010 [4], [8] and [9] and 80.8 million people reported having been vaccinated [10]. The vaccine supply was insufficient to meet demand initially, and became more plentiful after Thanksgiving, a time when demand for influenza vaccination traditionally slows.

anthracis by murine macrophages [20] and human NK cells [21] involve IFN-γ; although IFN-γ production by NK cells may be down-regulated somewhat by anthrax lethal toxin [21]. In mice, IFN-γ-inducible chemokines CXCL9, -10 and -11, contributed directly to in vitro anti-microbial effects against B. anthracis Sterne strain spores [22], and IFN-γ was produced by NK cells in response to B. anthracis spores [23]. Human peak TNA response occurs at different time points for different individuals [1], but typically between 28 and

35 days after CB-839 concentration the first dose in the series. The timeframe of peak circulation of T cells is not known. It is clear that sampling only at one time point (7 days after the second dose) provides an indication of the potential of two doses of AV7909 to induce T cell responses, but does not fully capture the differential kinetics of in vivo T cell activation, migration to lymphoid organs and recirculation in peripheral blood. Hence, because sampling the blood compartment only detects T cells in transit, these data are biased by sampling one time point. However, studies of T cell responses with Melan-A peptide vaccine adjuvanted with 0.5 mg of CpG demonstrated circulating levels of Melan-A specific T cells peaked at 7 days (4/7 subjects) and 10 days (3/7 subjects) after second immunization, and decline Bcl 2 inhibitor to near baseline by day 14 [24], suggesting that our PBMC samples were obtained within an

appropriate window for sampling. Nonetheless, the use of a CYTH4 single post-immunization sampling point may explain some inter-group variability in this small study population. Of note is the observation that of subjects that had positive ELISpot responses, half responded to both rPA and PAp, revealing an overlap in processed epitopes and predicted peptides (PAp). This overlap in responses of rPA compared to the pool of PAp suggests predicted peptides to be a suitable strategy for ELISpot testing in unknown HLA populations with

limited PBMC samples. In summary (1) immunization with two doses (14 days apart) of an anthrax vaccine candidate consisting of AVA plus CPG 7909 was sufficient to induce IFN-γ-positive T cell recall responses in ex vivo-stimulated PBMC collected 21 days following the first immunization; (2) in this pilot study, a dose (0.25 mg) of CPG 7909, lower than used in other vaccines in development, was adequate to increase innate and adaptive immune responses beyond that elicited by AVA (BioThrax) alone; (3) rPA and predicted peptides of PA may be adequate as recall antigens in assessing anthrax vaccine-induced T cell recall responses of frozen PBMC; finally, (4) the innate responses to CpG, such as decreased ALC and increased CRP, explain a contribution of roughly 60% to the later peak anti-PA antibody titer ( Fig. 3B); the remaining variability is attributed to Subject differences in response to PA antigen, perhaps HLA-related. This work was supported by BARDA/NIAID contract number HHSN272200800051C.

Astragalus polysaccharides are known to possess effective pharmacological effect to increase γ-globin mRNA expression and raise the level of HbF in K562 cells. Astragalus is known to be a useful candidate for the development of new medicine of gene therapy for beta-thalassemia. 26 Curcuma comosa is a Thai herbal medicine and is known for its anti-inflammatory activity. It is reported that the n-hexane extract of the aerial parts of Curcuma comosa increases HbF production in K562 cell line. 27 Resveratrol (trans-3,4′,5-trihydroxystilbene) is a stilbenoid containing two aromatic rings joined together by methylene group. Resveratrol is a natural

phytoalexin synthesized by about 72 plants species.28 It inhibits EPZ-6438 price the progression of fungal infections in plants.29Botrytis cinerea infection leads to the excessive production of resveratrol in the outer layer of grapes and in the epidermis of leaves. It was originally isolated by M.

Takaoka in 1939 from the roots of Veratrum grandiflorum. 28 Over the past decades, interest in the possible health benefits related to intake of resveratrol had risen rapidly. 29 Resveratrol is present in different fruits especially berries, red grapes and peanuts. Pomegranates, click here soybeans and peanuts are the richest source of resveratrol.28 and 30 It is helpful in prevention of inflammations, cancers and neurodegenerative diseases. It also acts as an antioxidant and helps in scavenging free radicals generated in body.31 When cultured erythroid cells (obtained from both normal and beta-thalassemic patients) were treated with resveratrol (in a concentration of 100 μM), the amount of HbF was found to be increased from 0.55 ± 0.6% to 3.81 ± 0.54% in beta-thalassemic erythroid cells. The efficacy

of resveratrol for the production of HbF in vivo as well as its dependency on genetic features of beta-thalassemia patients with different mutations should be checked. 32 Although resveratrol has wide range of therapeutic significances, it possesses Dichloromethane dehalogenase some drawbacks like unstable structure, poor bioavailability, and low solubility in water, rapid excretion and no change in resting metabolic rate. To overcome these limitations, resveratrol’s nanodelivery systems have been developed. Two types of nanocarriers of resveratrol have been constructed. Lipid carriers carrying resveratrol have been found to be more stable as compared to solid lipid containing resveratrol. There is a need of further studies to confer its parameters and bioavailability in human body.33 Take home message The life of human beings is dependent on nature. Natural compounds have always played an important role in our life. The compounds with following concepts ‘less cytotoxic, cheap, no side effects’ can be consumed daily for the treatment of beta-thalassemia.

The samples were considered positive if the OD values were ≥X2 above the day 0 sera. To assess the likely disruptive effect of the A− G-H loop deletion, the predicted amino

acid sequences of the VP1 polypeptides Rucaparib of either A+ or A− were substituted for that of O1/BFS 1860/UK/67 (accession 1FOD; [18]) using the structural prediction software ESyPred3D [19]. The subsequent structures were plotted using RasMol 2.7.3.1 [20]. Sequence comparison of the capsid coding regions of A+ and A− confirmed the absence of the VP1 G-H loop in A− (13 deletions located at residues 142–154) and only 2 other amino acid substitutions, both in VP1; residues 141 (A to V) and 155 (A to K). A comparison of the A+ and A− VP1 polypeptides Selleckchem ABT199 using ESyPred3D, and based on the co-ordinates of O1/BFS 1860/UK/67 [18], demonstrated that the residual G-H loop amino acids of the A− virus were sufficient to form a smaller loop leaving the core tertiary structure of the protein unchanged (Fig. 1). To confirm the loss of

the antigenic site in the shortened VP1 G-H loop of A−, the characteristics of A+ and A− were examined by a panel of MAbs generated against A22/IRQ/24/64 (Fig. 2) whose epitopes are located on the VP1 G-H loop coding region and were similar to that of A+, differing at only six amino acid residues. These positions, namely 133, 136, 139, 140, 142 and 160, were not predicted as antigenically significant by Bolwell et al. [16]. All six of the anti VP1 G-H loop MAbs reacted well with A+ and homologous A22/IRQ/24/64 but did not react with A− or trypsin very treated A+ (Fig. 2). Sera collected on days 0, 7, 14 and 21 were tested by virus neutralisation test (VNT) to assess the virus neutralising antibody response to vaccination. Fig. 3 shows that vaccines prepared from A− or A+ produced a similar response and induced

detectable levels of anti-FMDV neutralising antibody as early as 7 days post vaccination with an identical response at day 21. In order to determine whether a vaccine prepared from A− is likely to protect cattle from challenge against the homologous and A+ viruses, serum antibody titres were used to calculate the degree of predicted protection by cross referencing serum neutralising titres obtained in this study against protection titres defined by Brehm et al. [21]. Brehm et al. [21] demonstrated that serum neutralising titres of 0.5, 1.0, 1.5, 2.0 and 2.5 can provide protection in 44%, 79%, 85%, 94% and 100%, respectively, of animals vaccinated with a high potency serotype A vaccine and then challenged with different serotype A viruses of variable antigenic relatedness to the vaccine strain [21]. Taking into account that this is a new approach for predicting protection which encompassed different sera and viruses and did not include control sera from the original Brehm study, relationship values (r1) were also determined from the serum neutralising antibody titres.

45%) in non-site-specific assay. In plasmid nicking assay, the extracts (except hexane and chloroform extracts) were found to be effective in preventing the degradation of supercoiled plasmid DNA from hydroxyl radical into linear and open circular forms. The results showed that the extracts

(methanol, ethyl acetate and water extract) have potent hydroxyl radical scavenging activity. These activities could be due to the presence of terpenoids and phenolic compounds in extracts as determined using IR and 1H NMR during the phytochemical studies of the extracts of roots of the plant. 27 Antioxidants are molecules which can safely interact with free radicals and terminate the chain reaction before vital molecules get damaged. The free radical damage can be prevented by several enzymes and the principal antioxidants Temozolomide chemical structure such as vitamin E, beta-carotene, and vitamin C, present in the defense system of our body. Several studies have shown that plant phenolics also have antioxidant properties.28, 29 and 30 Natural polyphenols can have simple structures for example phenolic acid, phenylpropanoids, flavonoids or they can have structure like polymers e.g., lignins, melanins, tannins.31 Free radical scavenging property, metal chelating property, effects on cell signaling pathways and on gene expression contributes to the potential of phenolics as antioxidant therapeutic agents.32 S. oleosa has been

found as potent antioxidant due to Calpain the presence of phenolic compounds. 33 Thind et al evaluated the antiradical properties and determined the total phenolic selleck compound content in methanolic extract/fractions from bark of S. oleosa by several in vitro systems – 2,2′-diphenyl-1-picrylhydazyl (DPPH), deoxyribose degradation (non-site-specific and site- specific), reducing power, chelating power, plasmid nicking assays and by Folin-Ciocalteu’s

method, 34 respectively. Results revealed that residue fraction which was obtained by drying the supernatent of the precipitate had greater free radical scavenging activity than the precipitate and aqueous extract as the content of phenolic compounds present in the extracts follows the order; residue fraction (942 mg/g gallic acid equivalents) > aqueous extract (896 mg/g gallic acid equivalents) > precipitate (604 mg/g gallic acid equivalent) and the potential of antioxidant activity of the extract also follows the same order as determined by the assays thus reconfirming the fact that antioxidant activity depends on the phenolic contents in the extract. 33 Studies have been carried out on the antimicrobial activity of S. oleosa showing great potential of the plant as an upcoming antimicrobial agent. Archana Moon 35 deliberated the same, in which clinical isolates from methanolic extracts of the plant were examined against defiant drug strains of Escherichia coli, Staphylococus aureus, Klebsiella.

Unlike LAC, the selected school districts in SCC are small and preferred not to be identified by name. Thus, in the analysis they are labeled as District A, B, C, and D. The SCC protocol was reviewed and approved by the Ann and Robert H. Lurie

Children’s Hospital of Chicago Research Center Institutional Review Board. All LAUSD schools in LAC and all schools in the four selected school districts in SCC were included in the comparison described for the school years (SY) 2010–11 to 2011–2012. To compare the changes in nutrient levels after implementation of the nutrition interventions in both counties, we used the October 2010 school breakfast and lunch menus for elementary OSI-744 mw and secondary schools in LAUSD and compared them to the October 2011 menus. For SCC, we used the May–June 2011 (three consecutive weeks) school breakfast and lunch menus for elementary schools and compared them to the March–May 2012 (three consecutive weeks) menus. These comparison time points were chosen based on the timeline of intervention implementation in each county, accounting for lag time between the two locales, but preserving the pre- and post-intervention interval at approximately 12 months apart. The post intervention results were then examined to see if they aligned with the IOM (for LAUSD) and Alliance for a Healthier Afatinib Generation (for SCC) school

meal recommendations. Both counties had data for the following nutrients: food energy (kcal), protein (grams “g”), fiber (g), total fat (g), saturated fat (g), sugar (g), and sodium (milligrams “mg”). Means, 95% CIs, and percent change of nutrient

levels pre- and post-intervention were compared for all LAUSD schools and all schools in the four districts in SCC. T-tests were performed to determine if nutrient changes were significant; where appropriate, log transformations were employed. Participation frequency (i.e., the number of students participating in school breakfast and lunch), average change in kilocalories per meal for breakfast and lunch, and the number of serving days per year were calculated and used to estimate net calories (kcal) offered annually for full-time (5 days per week) meal program participants (per student per year). Nutrition Oxalosuccinic acid interventions implemented by LAUSD, which were based on IOM recommendations for healthy school meals (IOM, 2009), resulted in significant reductions in mean caloric and mean sugar content of breakfast and lunch school meals (Table 3). Similarly, for most meal categories, mean sodium content dropped. The most dramatic reductions were observed in the breakfast category for mean sugar, mean total fat, and mean sodium content. Although protein increased in the lunch meal category for elementary schools, the nutrient decreased in all other meal categories. Dietary fiber also decreased in all meal categories.

2), indicating the formation of silver nanoparticles with the reduction of silver ions. Silver nanoparticle synthesized, initially observed by color change from pale white to brown was further conformed by UV–visible spectroscopy. The color change occurs due to the excitation of surface plasmon resonance in the silver metal nanoparticle. Silver nanoparticles from endophytic fungi, Pencillium sp showed maximum absorbance Quizartinib nmr at 425 nm after 24 h of incubation

( Fig. 3), implying that the bioreduction of AgNO3 has taken place following incubation of the cell free culture filtrate along with AgNO3. Surface plasmon peaks were also located at 410 nm as reported by Shivaraj et al 15 using 5-FU in vitro Aspergillus flavus. Whereas, Afreen et al 16 reported peak at 422 nm with Rhizopus stolonifer. Maliszewska et al 17 reported the absorption spectrum of spherical silver nanoparticles produced by Pencillium sp presents a maximum peak between 420 nm and 450 nm. TEM measurements were carried out to determine the morphology and size details of the synthesized silver nanoparticles. Size and shape of the nanoparticles were recorded from drop coated films of silver nanoparticles synthesized extracellularly by endophytic fungi, Pencillium sp. ( Fig. 4). TEM micrographs revealed nanosized and well dispersed silver nanoparticles formed predominantly spherical in shape with the size of 25 nm. FTIR spectroscopic

analysis is carried out to determine the possible interaction between silver and bioactive molecules which are responsible for the synthesis and stabilization of silver nanoparticles.

FTIR spectrum revealed that the silver nanoparticles synthesized from endophytic fungi, Pencillium sp. revealed two bands at 1644 and 1538 cm−1 that corresponds to the binding vibrations of amide I and amide II bands of proteins respectively 18( Fig. 5). While their corresponding stretching vibration were seen at 2923 and 3290 cm−1 and during it is also known that protein nanoparticles interactions can occur either through free amino groups or cysteine residues in protein and via electrostatic attraction of negatively charged carboxylate groups in enzymes. 19 The three bands observed at 1393, 1233, and 1074 cm−1 can be assigned to C–N stretching vibrations of aromatic and aliphatic amines respectively. 18 These observations indicate the presence and binding of proteins with silver nanoparticles which plays an important role in stabilization and also as reducing agents by which well dispersed nanoparticles can be obtained. Antimicrobial activity of biosynthesized silver nanoparticles were studied against pathogenic bacteria (clinical isolates) using agar well diffusion assay method and zone of inhibition were depicted in Fig. 6 and Table 1. Wells were loaded with different concentrations-20 μl, 40 μl, 60 μl and 80 μl of silver nanoparticles respectively.