This is further complicated by the fact that, due to concerns of intussusception, infants older than 32 weeks of age should not receive further doses of rotavirus vaccines as advised by WHO [3]. Therefore, infants will likely experience longer periods of time between doses or will only be eligible to receive 1 or 2 doses of vaccine and will be at risk for rotavirus for longer periods of time than was encountered by participants in this trial. This aspect is likely to challenge the performance of PRV and is best explored in observational studies after vaccine introduction which are likely to provide critical information regarding the potential check details public

health impact of this vaccine. Effectiveness trials in other countries have demonstrated decreased selleck chemical performance than that observed in well controlled efficacy trials and this “real world” application of rotavirus vaccines is likely

to be a critical piece of information as decision makers in Africa move forward [30] and [31]. Our data demonstrate that rotavirus continues to be a public health problem in the second year of life and the performance of 1 or 2 doses of vaccine in that setting is also likely to yield important results. The major limitation of this post hoc analysis is that the study was not powered for these supplemental analyses, including by country or by year of life. Nevertheless, the potential benefits of introducing rotavirus vaccines in Africa are substantial and far-reaching. In the continent where the highest rates of rotavirus mortality per capita are found, the introduction of these vaccines into Urease the routine childhood immunization schedule would have a profound public health impact. African countries have responded to their need for these vaccines and almost 20 countries in the region have applied for GAVI support to subsidize vaccine procurement. Now, we should look towards studying the effectiveness of this vaccine when it is introduced into routine EPI immunization schedules, and

assess how to improve its performance in the field. This research study was funded by PATH’s Rotavirus Vaccine Programme under a grant from the GAVI Alliance, and was co-sponsored by Merck. The study was designed by scientists from Merck & Co., Inc., with substantial input from PATH staff and site investigators. PATH staff independently monitored study execution at sites and participated in pharmacovigilance and data analyses. We also acknowledge the sincere effort of all our study staffs and the support of the community members throughout the study area without which this study would never have been materialized. Conflict of Interest Statement: SOS received Merck funding as a member of the Advisory Board for Pediatric Vaccines and Vaccine New Products; MC was an employee of Merck when the clinical trial was conducted and owned equity in the company.

À ce jour, pour approximativement 20 % des formes familiales d’HTAP, ABT-888 solubility dmso aucun gène n’a été identifié. Elle fait partie du groupe

1 des HTP et a été une des premières formes d’HTAP avec une cause reconnue après l’épidémie de cas d’HTAP post-prise d’anorexigènes des années 1960 [15]. Le tableau I reprend les principaux médicaments et toxiques susceptibles d’induire une HTAP et le niveau de risque pour chaque produit : certain, probable, possible ou peu probable, en fonction des données disponibles à ce jour. Les patients atteints d’HTAP induite par la prise de fenfluramine et dexfenfluramine ont les mêmes caractéristiques cliniques, fonctionnelles, hémodynamiques et génétiques que l’HTAP idiopathique, suggérant http://www.selleckchem.com/products/cobimetinib-gdc-0973-rg7420.html que l’exposition à ces anorexigènes serait un facteur déclenchant de l’HTAP n’influençant pas l’évolution clinique de la maladie [15] and [16]. L’hypothèse principale suggère qu’il existe une interaction entre l’aminorex et les dérivés de la fenfluramine et la voie de la sérotonine, un puissant agent vasoconstricteur et mitogène pour les cellules musculaires lisses [17]. Le benfluorex (Mediator, Laboratoires Servier, France) a été utilisé en Europe depuis 1976 comme un médicament hypoglycémiant et hypolipémiant. Il fait partie de la même classe des dérivés de fenfluramine et il a comme métabolite

final, la norfenfluramine, similaire à l’isoméride. En 2012, Savale et al. ont publié une série de 85 cas d’HTP associés à un antécédent d’exposition au benfluorex, dont 70 cas correspondant à des HTAP pré-capillaires

avec des caractéristiques cliniques, fonctionnelles et hémodynamiques proches de l’HTAP idiopathique [18]. Un quart de ces patients a également été exposé aux dérivés de fenfluramine avant le benfluorex et un tiers avait un autre facteur de risque d’HTP [18]. Un quart des patients avait des valvulopathies mitrales et/ou aortiques [18]. L’originalité du rapport consiste justement en cette haute fréquence des atteintes « doubles » valvulaires mitro-aortiques et vasculaires pulmonaires, par rapport au valvulopathies isolées décrites dans les années Cediranib (AZD2171) 1990 avec les dérivés de la fenfluramine [18]. Les inhibiteurs de tyrosine kinase (ITK) comme l’imatinib, le dasatinib ou le nilotinib ont transformé le pronostic de la leucémie myéloïde chronique mais, en raison de leur mécanisme complexe d’action, sont associés à de nombreux effets indésirables. L’imatinib agit également sur la voie du platelet derived growth factor (PDGF), reconnue comme étant impliquée dans l’HTAP. Le produit été testé comme traitement de l’HTAP, mais les études ont été interrompues en raison des effets indésirables : hématomes sous-duraux et toxicité cardiaque directe [19]. Cependant, le dasatinib, un autre ITK inhibiteur du PDGF, a été associé au développement de plusieurs cas d’HTAP.

Ltd., India for their support as Contract Research Organization. MSD provided the funds for this support by GVK Biosciences Pvt. Ltd., India. The authors thank Michelle Goveia and Megan O’Brien for their guidance and critical review of this manuscript. “
“Rotavirus is the leading cause of diarrhea related hospitalization among infants and young children worldwide. Annually in India, rotavirus diarrhea causes nearly 100,000 deaths and over half a million hospitalizations in children less than 5 years [1] and [2]. Severe dehydration, leading to acute shock with electrolyte imbalance is believed to be the major cause of death in rotavirus gastroenteritis (RVGE) [3], [4] and [5].

A low serum bicarbonate or venous pH has been reported to be the best predictor of dehydration correlating strongly with worsening clinical dehydration, greater diarrhea IOX1 datasheet severity and younger age [6]. The amount of bicarbonate lost in stool depends on the volume of diarrhea and the bicarbonate concentration of the stool which tends to increase with more severe diarrhea [7]. Studies have reported that in acute episodes of RVGE as compared to non-rotavirus diarrhea, there is a higher incidence of complications from severe dehydration and acid-base and electrolyte imbalances [8] and [9]. Vaccination is considered one of the most

effective public health strategies to prevent rotavirus infection and reduce disease burden [10]. Data on the age-specific burden of RVGE and frequency of complications would better identify vulnerable age check details groups to target for rotavirus vaccination and guide research on rotavirus vaccines. The purpose of this study was to assess the age distribution of children with RVGE admitted to an urban pediatric unit and to evaluate the incidence of complications from severe dehydration, acid–base and electrolyte abnormalities in RVGE at admission. The study was conducted at St. Stephens’ Hospital Delhi (SSH), India: a 595 bedded multi-specialty isothipendyl tertiary care hospital with approximately 3000 deliveries taking place annually. The pediatric department has 40 beds, an intensive care unit with 6 beds and a neonatal intensive care unit. Patients

are admitted from the city and nearby villages, and referred from general practitioners, clinics and various hospitals in Delhi. Most patients are of middle and lower income groups. During a 3-year period from December 2005 through November 2008, children less than 59 months of age hospitalized in the ward or pediatric intensive care unit with acute gastroenteritis (AGE) (>3 loose or watery stools in a 24 h period) were included in the study after written informed consent was obtained. The history, severity of dehydration and treatment were recorded in patients’ hospital records. Electrolytes and blood gas analysis were done as clinically indicated by the admitting physician. Treatment for dehydration, electrolyte and fluid imbalance was based on WHO and department protocols [11].

11 Seaweed sample was collected by hand picking at a depth of 1–2 m in Gulf of Mannar, Southeast Coast of India. The samples were surface sterilized with natural seawater followed by double distilled water in the laboratory. The seaweed samples were identified as S. tenerrimum. Seaweed material as a whole was shade dried for 15 days to prevent photolysis and powdered with a mixer grinder. The solid liquid extraction (Soxhlet extraction) was performed with dried seaweed powder of 25 g in 200 ml of methanol (purity grade 99%). The extraction was done for

about 12 h at 35 °C until the colour of the seaweed turns from dark brown to pale brown. Selleck Lonafarnib Later, the soxhleted material was removed and concentrated under reduced pressure to as low as 1 ml using a rotary evaporator (Buchi, Switzerland) and refrigerated at −4 °C. FT-IR analysis was performed with a mixture containing powdered potassium bromide (KBr) and lyophilized methanolic seaweed extract. The molecular functional vibrations of chemical groups present in the sample was recorded with Perkin-Elmer FT-IR spectrum – 1 spectrophotometer operated at a resolution of 2 cm−1 ranging from 4000 to 400 cm−1. The Gas Chromatography–Mass Spectrometry (GC–MS) analysis was performed with a GC–MS (Shimadzu QP-2010 Plus – Tokyo, Japan)

of thermal Desportion System TD 20. The system was equipped with HP-5MS capillary column of 30 m × 0.25 mm and 0.25 μm of film thickness. The ionization energy used in the present PAK6 study was about 70 eV. Helium gas (99.999% purity) was mTOR inhibitor used as a carrier gas at a constant flow rate of 1.21 ml/min. One μl of samples was injected in the split mode with 10:0 ratios.

The GC injector and MS transfer line temperatures were set at 230 and 280 °C respectively. The ion source temperature was constantly maintained at 300 °C. Oven temperature programme was initially set at 100 °C with a hold time of 2 min. Further, it was ramped to 200 °C (at 5 °C/min) with the hold time of 5 min and to 235 °C (at 10 °C/min) with the hold time of 10 min. The resulting peaks were analyzed in inbuilt mass spectrum library such as NIST05.LIB and WILEY8.LIB. Antibacterial activity of methanolic extracts was evaluated by disk diffusion technique. Pathogenic bacterial strains such as Escherichia coli (MTCC 1687), Klebsiella pneumoniae (MTCC 530), Pseudomonas aeruginosa (MTCC 1688), Salmonella typhii (MTCC 531), Staphylococcus aureus (MTCC 96) and Vibrio cholerae (MTCC 3906) were procured from Microbial Type Culture Collection (MTCC), Indian Institute of Microbial Technology, Chandigarh, India. The pathogens were inoculated in Luria Bertani (LB) broth and kept overnight at 37 °C for exponential growth of cultures. Later, the bacterial cultures (106 CFU ml−1) were swabbed on freshly prepared LB plates and sterile disks of 6 mm (HIMEDIA) were placed on the plate.

The substantially lower attack rates in seropositives are an important consideration that should not be ignored in these discussions. Therapeutic efficacy of the vaccines was not specifically evaluated in the end of study publications, in large measure because there was no evidence for it in interim analyses. Although the clinical trials were primarily designed to evaluate immunoprophylaxis, the fact that women who had prevalent cervicovaginal infection or low grade disease were not excluded at entry provided a cohort to evaluate therapeutic efficacy. In the CVT, time to clearance

of prevalent infection was evaluated. There was no difference in the rate of clearance of vaccine or non-vaccine Fulvestrant BEZ235 types in Cervarix® vaccinees and control [37]. For example, 48.9% and 49.8% of HPV16/18 infections were cleared after 12 months in vaccine recipients and controls, respectively. The therapeutic activity of Gardasil® was evaluated in FUTURE II [15]. No significant difference in the rate of progression of HPV16/18 infection to CIN2+ was observed in VLP vaccinees versus controls,

11.1% and 11.9%, respectively. Thus the VLP vaccines do not appear to alter the course of established cervicovaginal HPV infection or disease. Both vaccines exhibited excellent safety profiles in the clinical trials. Mild to moderate injection-site symptoms, headache and fatigue were the most common adverse events in Cervarix® and Gardasil® vaccinees and controls. Injection-site pain ranged from 83.0–93.4%

in vaccine groups and from 75.5–87.25% in control groups [14], [15], [38] and [39]. Headache and fatigue was reported in 50-60% of participants in both groups. These solicited symptoms were transient and resolved spontaneously and did not increase with number of doses. Symptoms were not notably different in women with evidence of prevalent or past infection [32] and [35]. In a randomized control trial directly comparing the two vaccines, injection-site pain was somewhat higher with Cervarix® than with Gardasil®; 92.9% (95% CI: 90.4–95.0) and 71.6% (95% Non-specific serine/threonine protein kinase CI: 67.5–75.4) respectively [40]. Grade 3 severity was reported in 17.4% (95% CI: 14.2–20.9) and 3.4% (95% CI: 2.0–5.4) in Cervarix® and Gardasil® groups respectively. However, compliance rates with the three-dose schedule were similarly high (>84%). The inclusion of the immune stimulating component MPL in the Cervarix® adjuvant might account for somewhat higher reactogenicity of the vaccine [38]. For both Cervarix® and Gardasil®, vaccine and control groups experienced similar rates of serious adverse events (SAEs) (Table 8). The numbers of SAEs judged to be possibly related to vaccine injection was low for both vaccines and similar to the numbers in the control groups (Table 8). Pregnancy outcomes have received special attention, given the target ages of catch up vaccination programs.

The excellent safety of the vaccine-adjuvant combinations demonstrated in this trial will facilitate follow-on studies to optimize dmLT-vaccine formulations. MEV also induced systemic IgA and IgG responses to LTB in serum in almost all vaccinated volunteers, with the highest response rate (97%) in the group receiving vaccine plus 10 μg dmLT. Indeed, the combination of MEV with 10 μg dmLT gave rise to comparable anti-LTB responses, both in IgA and IgG, as induced by a fourfold higher dose of LCTBA in a previous study [11]. Interestingly, the anti-LTB responses determined

by ELISA were closely mirrored by increases in LT neutralizing titers, supporting that anti-LTB responses reflect functional LT immunity. dmLT may also be capable of enhancing systemic anti-toxin immune responses, as suggested by

Gefitinib datasheet the finding (see Supplementary material) that MEV plus 10 μg dmLT induced significantly higher LT neutralizing learn more as well as anti-LT IgA and IgG antibody responses in serum than the first-generation ETEC vaccine containing a comparable dose of CTB. As in previous studies of oral, inactivated as well as live ETEC vaccines in Swedish and American volunteers [5] and [24], IgA antibody responses against all of the different CFs in serum were infrequent and low. Serum IgA antibody responses induced by MEV against O78 LPS were, however, frequent. Fecal and ALS IgA responses against O78 LPS were also observed in a majority of vaccinees. Although O78 LPS is only expressed by about 10% of clinical ETEC isolates [25], these responses may add to the protective coverage of the vaccine since we have previously shown that anti-O antibodies may provide protection against ETEC expressing the homologous serogroup [5]. A combination of LT and CF antigens seems to be required for

broad protective coverage. It has been estimated that a vaccine containing LT antigen and the most prevalent CF antigens, as those in MEV and in an oral, live ETEC candidate vaccine, ACE527, recently evaluated in humans [26], may have the Isotretinoin potential to protect against at least 80% of all ETEC strains causing disease in humans [1] and [5]. In contrast, a vaccine based on LT antigen alone will not offer protection against ST-only ETEC strains and is likely to provide shorter duration of protective immunity [27]. Based on the excellent safety profile and capacity of MEV to induce highly significant mucosal immune responses against the most prevalent ETEC virulence factors, studies are planned to evaluate the safety and immunogenicity of the vaccine alone and in combination with different dosages of dmLT in descending-age groups in Phase I/II trials in Bangladesh and for protective efficacy in visitors to ETEC-endemic areas. AMS and AL were the principal investigators. AMS, AL, JH, LB, RW, JC, NC and BG participated in the design of the studies and interpretation of results.

The data presented here includes all AEs, even if a volunteer subsequently dropped out of the study. Where an AE stopped and restarted within 30 days of vaccination it has only been reported once in these results, but durations have been summed. AE durations have been rounded up to the nearest day. Volunteers underwent

P. falciparum sporozoite challenge at Imperial College, London two weeks after the final vaccination. They each received bites from five mosquitoes subsequently confirmed to have more than 100 sporozoites per paired salivary gland. Anopheles stephensi mosquitoes were infected with the chloroquine-sensitive 3D7 strain PI3K inhibitor drugs of the parasite at the Walter Reed Army Institute of Research (WRAIR), Maryland, US and reared in the laboratory as previously described [18]. Volunteers began attending clinic for malaria screening from the evening of day 6 after infection. At each visit they were questioned about possible symptoms, had their temperature, pulse and blood pressure measured and gave blood Ibrutinib in vivo for both thick film microscopy and PCR for malaria parasites. This process was repeated twice daily from day 7 to day 14 and then once daily from days 15 to 21, or until diagnosis. Two experienced

microscopists examined a minimum of 200 high power fields (100× objective) for parasite ring forms on each sample. A diagnosis of malaria was made as soon as one or more viable parasites were seen on a volunteer’s slide. Oral anti-malarial treatment was commenced on diagnosis as an outpatient with oral Riamet® (Novartis, 20 mg artemether with 120 mg lumefantrine) given at diagnosis and then approximately 8, 24, 36 and 48 h later. Artemether combination therapy was chosen in line with World Health Organisation recommendations on the treatment of uncomplicated

malaria. Volunteers returned for repeat blood film examinations daily after treatment commenced until two consecutive negative films had been seen. Quantitative real-time however PCR was performed at challenge baseline and at all post-challenge visits until treatment commenced using a method described previously [19]. Clinicians, volunteers and staff performing other assays were blinded to the PCR results during the study. Data was adjusted using a standard curve derived from counted cultured parasites in whole blood to give the number of parasites per mL of blood. The PCR data was also used to estimate overall growth rates of blood stage parasites during the challenge for each volunteer and to back-calculate a starting number of merozoites emerging into the blood (around day 6–7) and hence an estimate of the number of infected hepatocytes responsible for initial seeding of blood-stage parasite forms. The methods employed are based on an iterative adjustment model to derive a best fit curve to the measured data, as described [20]. Ex vivo IFNγ-ELISPOTs were carried out broadly as described [21].

S.A). Amplification of the complete VP7 gene (1062 bp) was carried out using the primers Beg9 and End9 [26] as described previously [24]. The partial VP4 gene (VP8* region: 10 to 729 bp) was amplified with primers con2 and www.selleckchem.com/Akt.html con3 [27] using One-step RT-PCR kit (Qiagen, Germany). The PCR conditions involved an initial reverse transcription step of 30 min at 45 °C, followed by PCR activation at 95 °C for 15 min, 40 cycles of amplification (1 min at 94 °C,

1 min at 50 °C and 2.5 min at 70 °C) with a final extension of 7 min at 70 °C. The VP7 and VP8* amplicons were sequenced as reported previously [24]. Sequencing of the complete VP4 genes was carried out as described earlier [28] for six G1P[8] strains (NIV-0613158, NIV-06361, NIV-061060, NIV-0715880, NIV-07523, NIV-083375) representing each of the two P[8] lineages (P[8]-3 and P[8]-4) identified in Pune on the basis of VP8* sequences. The VP7 sequences were submitted to GenBank under the accession numbers DQ886943-46, DQ886953-56, DQ886958, DQ886959, DQ886962, DQ886964-68, DQ886972, DQ875602, FJ948829-55, JN192054-55, JN192060-61, JN192063-64, JN192068-69, CHIR-99021 order JN192071-75, JN192079,

JN192082-83, JN192086, JN192089, JN192093-96, JN192098-99, JN192100-01, JN192112-13, JN192115-16, JN192119-26 and JN192128-31. The VP4 sequences were submitted under the accession numbers HQ881499 to HQ881575, EU984107 and HM467806-08. The VP7 and VP4 sequences of the G1P[8] reference strains [8] and [9] representing each of the 11 G1 and 4 P[8] subgenotypic lineages and the sequences of the Rotarix and RotaTeq vaccine strains were retrieved from GenBank. The sequences available in GenBank for G1P[8] strains from other cities [Kolkata (n = 8), Delhi (n = 3) and Manipur (n = 4)] included in the study were classified into lineages during comparative analysis. Multiple sequence alignments were conducted using the ClustalW implementation in MEGA 5.05 [29]. Phylogenetic trees were constructed using the neighbour joining algorithm and Kimura 2-parameter model in MEGA 5.05. The statistical significance

of the genetic relationships was estimated by bootstrap resampling analysis (1000 replications). Nucleotide and amino acid distances were calculated using Kimura 2-parameter model and isothipendyl P-distance model, respectively. Phylogenetic analysis of the VP7 (Fig. 1(A)) and VP4 genes (Fig. 1(B)) showed clustering of the G1P[8] strains from Pune into G1-Lineage 1 or 2 and P[8]-Lineage 3 or 4 (Fig. 2). All the strains from the years 1992 (8/8, 100%) and 1993 (11/11, 100%) were placed into G1-Lineage 1, P[8]-Lineage 3. In the year 2006, the G1P[8] strains from Pune were distributed into G1-Lineage 1, P[8]-Lineage 3 (20/21, 95.2%) and G1-Lineage 2, P[8]-Lineage 3 (1/21, 4.8%). In 2007, while the G1-Lineage 1, P[8]-Lineage 3 strains continued to predominate (23/29, 79.3%), the prevalence of G1-Lineage 2, P[8]-Lineage 3 strains increased (5/29, 17.

Efforts to develop a DENV vaccine have mainly focused on attenuated

or inactivated virus-based vaccine formulations. Despite the success of similar vaccine approaches in controlling other Flaviviruses, such as the yellow fever virus and the Japanese encephalitis virus, and several clinical trials conducted using most promising formulations, an effective dengue vaccine is still not available for human use [4], [5] and [6]. Inefficient induction of protective immunity to the four viral types (DENV1, 2, 3 and 4), and safety concerns involving induction of antibody dependent enhancement (ADE), a mechanism believed to be involved in DHF and DSS occurrence, and deleterious cross-reactive reactions are the most relevant obstacles for the development of an effective dengue vaccine based on live virus particles [7]. DENV subunit vaccine formulation, based either on DNA or purified recombinant proteins represent Tyrosine Kinase Inhibitor Library in vivo safer alternatives to attenuated or recombinant viruses [3]. The most studied subunit vaccine approaches for dengue virus are based on either the complete envelope glycoprotein or fragments of this protein [1], [8],

[9], [10] and [11]. Immunization of mice with the DENV non-structural protein 1 (NS1), either as purified protein or encoded by DNA vaccines, have also shown promising results [12], [13], [14], [15] and [16]. The DENV NS1 is a highly immunogenic 46–50 kDa glycoprotein TGF-beta inhibitor expressed by infected cells both as a secreted oligomeric form and as a membrane-associated protein [17] and [18]. Although the precise functions of NS1 in the infection cycle remains unclear, it is accepted that this Thymidine kinase protein has an important role in the viral pathogenesis interfering with the complement activation cascade [19]. Mice immunized with NS1-based vaccines, particularly those encoded by DNA vaccines, develop protective immunity that involves both antibody and

T cell responses [14], [15] and [16]. In contrast, the protective immunity generated in mice immunized with purified NS1 protein alone seems to be based mainly on the generation of antigen-specific serum antibodies [12], [13], [20] and [21]. However, further studies have raised concern regarding the safety of NS1 as a vaccine antigen. Anti-NS1 antibodies detected in infected subjects or elicited in vaccinated mice may cross-react with proteins exposed on the surface of platelets, endothelial cells and proteins involved in the blood coagulation cascade, which may lead to vascular damages, thrombocytopenia and hemorrhage [22], [23], [24], [25], [26] and [27]. Adjuvants are key components of most vaccine formulations, particularly those based on purified proteins. Besides reducing the amount of antigen and number of doses required to achieve a specific immune response, adjuvants are modulators of the adaptive immunity but may lead to deleterious inflammatory reactions [28]. During decades aluminum hydroxide (alum) has been the only adjuvant alternative for human use.

A small acceptor favored magenta contour is observed near the donor disfavored region suggesting an acceptor favored groups at this region is recommended. An acceptor disfavored red contour is observed near the NH of benzimidazole and an acceptor favored contour is observed near the meta position of phenyl ring attached to the benzimidazole ring. Overall information obtained from the 3D QSAR study is depicted in Fig. 7 that shows structural

requirements to be incorporated for increasing the activity. Substituting methyl click here group on the phenyl ring of benzimidazole ring with bulky groups like phenyl, t-butyl, p-methylphenyl substituents and electronegative groups such as bromine have shown relatively increased activity. Structure and predicted activity of designed molecules are given in Table 3. 3D QSARs are widely employed to design new molecules that have an improved biological property. CoMFA and CoMSIA methodologies were used to build models for heparanase inhibitors. Statistical results obtained

clearly indicate the stability of the model. 3D QSAR model generated Gemcitabine has a good predicative ability and can be used to design new molecules with better activity. Based on the detailed contour map analysis, improvement in activity has been achieved by substituting bulky and electronegative groups at the benzimidazole group. This contributes majorly towards enhancing the electrostatic character and retaining hydrophobicity. Designed molecules showed better activity than the reference molecule which indicates that these molecules can act as potential inhibitors. All authors have none to declare. We gratefully acknowledge new support for this research from Council of Scientific and Industrial Research (Project No. 01/(2436)/10/EMR-II), Department of Science and Technology, New Delhi, India, University Grants Commission, New Delhi, India and Department of Chemistry, Nizam College, Hyderabad, India. We also acknowledge Tripos Inc. for SYBYL X-1.2 molecular modeling software. “
“Aging is a time progressive deterioration of adaptation among adult organisms with increasing

age due to degeneration of internal physiological process.1 It is an age-dependent intrinsic physiological function degeneration which leads to an increase rate of age-specific mortality and a decline in the rate of age-specific reproduction.2 Determination of aging related genes and proteins has thus become the fundamental necessity in the aspect of investigating aging. Till this date, structure and function of different aging related genes and proteins have been characterized in many organisms. However, it has been found that the number of structurally characterized proteins is very small compared with the number of proteins sequenced. Reliable structural prediction of uncharacterized aging related proteins may be beneficial to characterize their functions.