1B). A molecular concepts visualization of the gene sets that are indicative for the proliferation rate is shown in Supplementary Fig. 2. The downregulation of the cell cycle related gene sets indicates a major inhibiting effect of DON on the proliferation. These gene sets

include genes that are specifically upregulated during a particular cell cycle phase (Whitfield et al., 2002 and Bar-Joseph et al., 2008). Interestingly, genes upregulated during the G1–S phase of the cell cycle were upregulated after 3-h treatment with 5 μg/kg and particularly 10 μg/kg DON (Fig. 2A). This indicates that 10 mg/kg DON rapidly stimulates entry of cells into the G1–S phase of the cell cycle but inhibits cell division shortly thereafter. A heat map of the expression of the genes of the merged proliferation-related gene sets is given in Fig. 2B. Dabrafenib ic50 This figure (upper part of heat map at the left) shows that many of the cell cycle genes were temporarily Cyclopamine datasheet upregulated during the first 3 h. As shown in Fig. 3A, genes that are upregulated in T lymphocytes during the T cell activation response are also upregulated by DON. These gene sets include NFkB, CD40, Fos, and Jun (Supplementary Fig. 3), which are well-known for being induced by T cell activation (Gwack et al., 2007). In agreement with this, NFkB target genes and CD40 upregulated genes are also induced by DON (Fig. 3A). These T cell activation-related genes

were upregulated within 3 h. These genes remain highly upregulated after 24 h for the highest dose of DON but return within 24 h close to control levels for the lowest and middle dose

of DON (Fig. 3B). DON upregulated of many inflammatory response-related gene sets including chemokine activity, chemotaxis, inflammatory response, and acute phase response (Supplementary Fig. 4A). These gene sets contained many cytokine-related genes (Supplementary Fig. 4B). The upregulation of gene sets such as dendritic cells, monocytes, and polymorphonuclear leucocytes (Supplementary Fig. 5A and C) indicates an infiltration of blood cells Mannose-binding protein-associated serine protease with phagocytotic ability. One other cluster of gene sets upregulated by DON was related to cell adhesion and cytoskeleton (Supplementary Fig. 6A). The expression pattern over time of inflammatory response, blood cell infiltration, and cell adhesion–cytoskeleton genes was remarkable similar to that of the T cell activation-induced genes (Supplementary Figs. 4B, 5B, D and 6B). Genes highly expressed in either the very earliest precursor T lymphocytes stage (DN2) or the late precursor stages (CD4+ or CD8+) were upregulated by DON treatment, while genes highly expressed in early precursor cells of the double-positive stage (CD4+ and CD8+) were downregulated by DON (Supplementary Fig. 7A, B, and D). Genes highly expressed in early precursor stages DN3 and DN4 are upregulated at 3 h and downregulated at 6 and 24 h (Supplementary Fig. 7A and B).

Gelatinous fibrinous deposits are removed with a curved ring forceps clips. The visceral pleural peel can be debrided using ring-forceps and a dissector as in an open decortication. Once a pleural

space has been created the removal of fibrinous material is performed starting from the apex of the lung and proceeding Selleck PI3K Inhibitor Library to the diaphragm or vice versa. The sucker and ring clamp are used together to remove the fibrinous material from the pleural cavity. Intermittent ventilation of the lung is used to assess the completeness of the decortication as the dissection proceeds. If adequate progress is not being made or there is inadequate expansion of the lung to fill the chest, then conversion to open decortication should be performed. Particular

care should be taken with hemostasis both on the parietal and visceral pleura. Once adequate debridement has been accomplished, Target Selective Inhibitor Library irrigation is performed and the lung expansion is visualized to ensure the pleural cavity is filled by the lung. Chest tubes can be placed anteriorly and posteriorly for air and fluid drainage. The chest tubes are maintained on suction to make sure there is complete lung expansion and adequate drainage of the pleural space In all 11 children a video-assisted thoracoscopic surgery (VATS) with debridement, and placement of pleural tubes under visual control was performed. In every case the lung expansion was partial after VATS, despite of active suction and drainage (Fig. 2 and Fig. 5). Starting from the 2nd post-operative day, all children received fibrinolytics once daily Dolichyl-phosphate-mannose-protein mannosyltransferase for 2–4 days via chest tubes. The fibrynolytic agents used for treatment were urokinase (UK) in 2 cases and streptokinase (SK) in the rest. Urokinase

was used for procedures performed after 2007 year. The tube was clamped for 1 h and then left open and connected to a water seal device and placed to 15 cm H2O suction. The fibrinolytic agent was diluted in 10–50 ml of normal saline, with the volume arbitrarily selected on the basis of patient age and size and estimated volume of the pleural space to be treated. Treatment doses of streptokinase ranged from 12,000 IU to 250,000 IU, and treatment doses of urokinase were 50.000 IU (children weighing about 60 kg – to produce a concentration of 1.000 IU/ml). The activated partial thromboplastin time, prothrombin time, and hemogram were determined routinely before instillation of the fibrinolytic agent. The vital signs were closely observed. Fever and chest pain observed in two cases after use of streptokinase, was not noted after urokinase. The discomfort was easily managed by the administration of acetaminophen. Daily anteroposterior chest radiographs were obtained with the patient in an upright or semiupright position. Fibrinolytic treatments were continued until chest radiographs showed improvement (Fig. 4 and Fig. 5). In 3 patients, lack of lung expansion made the second VATS debridement necessary.

These binary measures were then summed to create the overall allostatic load score (ranging from 0 to 9) (Seeman et al., selleck kinase inhibitor 2004 and Bird et al., 2010). SEP was based on head of household occupational social class (Registrar General’s 1980 Social Class (RGSC) OPCS, 1980) and operationalized as the accumulated SEP over two time periods spanning 20 years. SEP was measured at baseline in 1987 and again at wave 5, with current or most recent social class data used. The six-category variable at each wave was dichotomized into manual (VI,

V and III-M) and non-manual SEP (III-NM, II, I), thereby giving a possible score of 0, 1 or 2 (waves defined as being in a non-manual social class, i.e. higher SEP). The RGSC measure has been described as being “…(theoretically) a measure of prestige or social standing, (thus) it could be argued that the relation of this classification to health should be interpreted as due to the advantages bestowed by elevated social standing and increased prestige. In practice it

is often interpreted as an indicator of both social standing and material reward and resources” (Galobardes et al., 2006b). Data on car ownership, home ownership and income were based on self-report. Car ownership and home ownership, amongst other measures find more of household assets, have been hypothesized to be more direct indicators of material circumstances within the SEP construct (Davey-Smith and Egger, 1992). Both measures reflect income, but also access to resources and power (Carr-Hill et al., 1992). There may also be direct causal mechanisms between car/home ownership and health through for example, safer transport, changes in exposure to pollutants (positive and negative) or damp or overcrowded housing. It must also be noted that these measures have overlaps with behavioral, as well as MYO10 psychological and psychosocial, factors, for example, owning a car resulting in decreased physical activity (behavioral), but increased pride/self-esteem (psychosocial) (Macintyre et al., 1998). Income is linked to health through

multiple pathways including behavioral and psychological/psychosocial, (Benzeval et al., 2014) although the material pathway may be considered the primary driver through access to resources. Car ownership was based on a simple yes/no question. Respondents were classed as home renters if they rented their home either from social housing stock or from a private landlord (‘1’) or were classed as homeowners (‘0’). Income was based on monthly net household income, equivalised for household size and used as a continuous measure of British Pounds (£) per week. The top and bottom 1% of values on the income distribution were excluded (trimmed) to limit the effect of outliers, a common method when measuring income inequality (Cowell and Victoria-Feser, 1996).

Habituation to the fear conditioning

chambers (TSE Systems Inc., USA) was carried out for Crizotinib ic50 15 mins for 4 days before training. The training phase consisted of a 2 min pause, and 6 repeats of 30 s tone with a 0.8 mA shock presented in the last 2 s of the 30 s tone. During the test phase 24 h later, the tone was sounded for 30 s without the shock. The time spent in freezing was recorded for 5 min following the tone. Freezing was detected by an array of infrared light beam sensors mounted 14 mm apart to monitor the position and movement of the animal inside the chamber (TSE Systems Inc., USA). All recordings were done via the TSE Systems software. This programme uses an averaging procedure to define the centre of gravity of the rat. An instance of freezing was defined as the animal not moving for more than a threshold duration of 5 s. Percentage freezing was calculated as the cumulative duration of freezing as a percentage of total time. RT-PCR gel and western blot images were analysed with ImageJ. The density

of each band was measured and normalised to its corresponding actin band (RT-PCR: ABT-199 in vitro n=4 each for sham and NI-lesioned; western blot: n=3 for naïve, n=3 for saline, n=3 for true sham, n=6 for sham-lesioned and n=7 for NI-lesioned). The densitometry data was statistically analysed with unpaired t tests (GraphPad Prism, USA) comparing sham-lesioned and NI-lesioned groups for each protein. For the real-time PCR (n=4 each for sham and NI-lesioned), the amplified transcripts were quantified using the comparative CT method ( Livak and Schmittgen, 2001), with the formula for relative fold change=2–ΔΔCT. The means were analysed with unpaired t tests (GraphPad Prism, USA). Freezing behaviour (threshold set at 3 s) of the sham-lesioned (10) and NI-lesioned (n=8)

rats was recorded in 30 s epochs for a total of 5 min. Total percentage freezing time was calculated and analysed with an unpaired t test (GraphPad Prism, USA). The data were expressed as mean±SEM. This work was funded by the Biomedical Research Council (07/1/21/19/512 and 10/1/21/19/645) and the National Medical Research buy ZD1839 Council (IRG10Nov104), Singapore. The authors wish to thank Ms. Lim Zhining for executing pilot studies; Ms. Hong Jia Mei and Dr. Tan Chee Kuan, Francis, for expert technical advice and support; and Mr. Ho Woon Fei for excellent technical and administrative assistance. “
“Important mechanisms for the control of sodium and water intake are present in the lateral parabrachial nucleus (LPBN), a pontine structure located dorsolaterally to the superior cerebellar peduncle (Andrade et al., 2006, Callera et al., 2005, De Luca et al., 2003, De Oliveira et al., 2007, Menani et al., 2002 and Menani and Johnson, 1995).

Wild species of cotton represent a significant genetic repository for potential exploitation by cotton breeders, who have long recognized the beneficial effects of exotic genes [4]. The introduction of alien genetic variation into upland cotton from the chromosomes of wild species is a valuable and proven technique for cotton improvement. The most successful examples of the use of wild species during the history of cotton breeding history include Gossypium harknessii as a source of cytoplasmic male sterility [5] and Gossypium thurberi as a source of fiber quality [6] and [7].

More recently, other important traits, such as nematode resistance and the low- and high-gossypol plant traits, were successfully introduced from diploid species into upland cotton using various

strategies [8] and [9]. Despite these successes, most SB431542 order of the genetic variation in wild Gossypium species remains to be exploited. G. anomalum (2n = 2x = 26, B1) is a wild species belonging to the B1 genome group. G. anomalum grows in Southwest Africa and along the southern fringes of the Sahara, almost from the Atlantic to the Red Sea [1]. As a member of subsection Anomala Todaro, G. anomalum possesses several desirable characters such as extremely fine fibers, good strength, low fiber weight, resistance to insect pests, immunity Roxadustat to the diseases black arm and bacterial blight and tolerance to water deficit, as this species is endemic to relatively dry areas [10]. Some efforts have been made to introduce desirable characters from G. anomalum to cultivated cotton [11] and [12]. G. anomalum represents an inestimable source of genes that can potentially be transferred to the cultivated cotton gene pool. However, the genomic differences between tetraploid cultivated cotton (A1A1D1D1) and the diploid G. anomalum (B1B1) represent serious interspecific reproductive barriers, which limit gene transfer between the species. In a previous study, we obtained triploid hybrids with the genome composition A1D1Bl by crossing

G. hirsutum (A1A1D1D1) with G. anomalum (B1B1) [11]. Hybrid seedling plants were then treated with 0.15% colchicine and a putative fertile hexaploid (A1A1D1D1B1B1) was obtained. This putative hexaploid produced flowers and set bolls normally. The objectives of this study were: (1) to confirm Oxymatrine the hexaploid nature of the plants using morphological, cytological and molecular methods; (2) to compare EST-SSR transferability from other species to G. anomalum; and (3) to obtain a set of informative G. anomalum-specific SSR markers to monitor G. anomalum-specific chromosome segments. Seedling plants of triploid hybrids from the cross between G. hirsutum (A1A1D1D1) var. 86-1 and G. anomalum (B1B1) were treated with 0.15% colchicine [11]. A putative fertile hexaploid (A1A1D1D1B1B1) was selfed and the resulting hexaploid seeds were stored in a − 20 °C freezer. In 2009, all experimental materials, including the putative hexaploid, G.

Os cálculos

biliares podem provocar uma inflamação crónica por aumento da pressão intravesicular, o que reduz o fluxo arterial, a drenagem venosa e linfática, favorecendo a necrose da parede e a consequente fistulização5. Episódios anteriores de colecistite aguda são também importantes para a formação de fístulas, uma vez que resultam numa inflamação extensa e aderência entre a vesícula e o duodeno, facilitando a erosão da parede learn more vesicular pelo cálculo2. Embora o nosso doente não apresentasse episódios prévios de colecistite aguda sintomática, a existência de uma vesícula atrófica com múltiplas aderências duodenais parece relacionar-se com processos inflamatórios vesiculares repetidos que, juntamente com os cálculos e o processo inflamatório transmural da DC duodenal, podem ter contribuído para a formação da fístula. Estão descritos na literatura casos raros sobre o envolvimento da vesícula pela DC, com identificação de granulomas epitelioides, infiltração linfoplasmocitária e agregados linfoides15 and 16. No caso do nosso doente, apesar do atingimento duodenal e da formação da fístula bilioentérica, não parece haver envolvimento

da vesícula pela DC, uma vez que o exame histológico identificou apenas lesões de colecistite aguda. Além disso, os achados da laparotomia eram consistentes com uma fístula colecistoentérica vulgar, não se identificando Nintedanib solubility dmso indícios de DC. As manifestações clínicas resultantes da presença de cálculos a nível intestinal são variáveis, dependendo do seu tamanho, segmento intestinal envolvido e existência de estenoses7. A maioria dos autores sugere que, na ausência de patologia intestinal que origine estenose, são necessários cálculos com tamanho superior a 2,5 cm para ocorrer obstrução5. No caso do nosso doente, as alterações inflamatórias da mucosa duodenal contribuíram para a impactação these de um cálculo de menores dimensões e, consequentemente, para os sintomas obstrutivos da SB. A raridade da SB, associada a manifestações clínicas

inespecíficas, contribui para que esta síndrome permaneça um importante desafio diagnóstico. A dor abdominal, as náuseas e os vómitos pós-prandiais de início súbito são os sintomas mais frequentes. Os exames imagiológicos e endoscópicos são importantes para o diagnóstico de SB. Os achados radiológicos típicos, aerobilia, obstrução intestinal alta e cálculo biliar ectópico17 foram também identificados no nosso doente. A EDA permite a observação do cálculo e da fístula bilioentérica, embora, neste caso, apenas tenha sido possível a identificação da fístula pelo estudo imagiológico. Na maioria dos casos de SB descritos na literatura, o tratamento é cirúrgico, consistindo na remoção do cálculo e da vesícula biliar e no encerramento da fístula colecistoentérica7. Apesar disso, decidiu-se instituir inicialmente um tratamento médico, com resolução sintomática.

However, the pre-treatment with other anti-inflammatory drugs (H1 receptor antagonist

and non-selective COX inhibitor) had less effect on this response. Unlike the persistent protective effect of aprotinin and icatibant, the latter drugs were efficient in attenuating the edematogenic response only in the first 30 min. These results evidences that one of the main pathways involved in SpV-induced edema is the kallikrein-kinin system (KKS), and suggests that histamine receptors and production of arachidonic acid metabolites are involved in an initial phase of edema generation. The KKS participation also has been demonstrated in edema response induced by Bothrops lanceolatus ( Faria et al., 2001) and Trimeresurus mucrosquamatus ( Wang and Teng, 1988) snake venoms, Lonomia obliqua caterpillar bristles ( Bohrer et al.,

learn more 2007), Vespula vulgaris wasp ( Griesbacher et al., 1998) and the toadfish T. nattereri ( Lopes-Ferreira click here et al., 2004). Investigations upon the molecular mechanisms underlying the inflammatory activity of fish venoms revealed different classes of toxins involved. Inflammation resulting from local administration of T. nattereri venom was related to a new class of kininogenases of 35–40 kDa, named Natterins ( Magalhães et al., 2006). In addition, further inflammatory reaction was associated with a Th1 response induced by a 15 kDa lectin-like protein present in this venom, Nattectin ( Saraiva et al., 2011). Junqueira et al. (2007) suggested that the inflammatory activity provoked by catfish C. spixii venom was also related with 14 kDa proteins. However in stonefish Synanceja horrida venom, which is considered one of the most dangerous fish in the world, the local inflammation was attributed to the action of a multifunctional toxin named Stonustoxin.

Besides its edematogenic activity, this toxin was also lethal, hemolytic and active in vascular preparations ( Low et al., 1993; Poh et al., 1991). A fraction exhibiting similar pharmacological properties was detected in Synanceja trachynis venom ( Kreger, 1991), and further was called Trachynilysin ( Colasante et al., 1996). Both stonefish toxins are ∼150 kDa proteins possessing subunits of 70–85 kDa, and probably its effects result from a non-specific cell membrane disturbing action ( Kreger, Adenosine triphosphate 1991; Chen et al., 1997). Since kallikrein-like enzymes have been extensively described in a large number of animal venoms, and their activity is intrinsically related with venom inflammatory potential, we decided to investigate the presence of such proteases in S. plumieri venom. Despite SpV hydrolyzed specific substrates for kinin-releasing enzymes (containing the signature Pro-Phe-Arg), screening the fractions eluted from gel filtration chromatography ( Fig. 5) revealed that this activity was mainly detected in F1 and mismatched with the edema inducing fractions (F2 and F3).

5). Attempts to extract the fluorescent peptides deposited in the eggs were only partially successful. Invariably, most of the fluorescence was maintained in the pellets after Galunisertib clinical trial homogenization and centrifugation (data not shown). Inspections of the pellets showed that the fluorescence was associated with the egg shell. In order to separate the fragments of the vicilins putatively produced in the fat body and transported to the eggs, we decided to homogenate the genitalia of adults and the freshly laid eggs. The presence of a vicilin derived peptide in the genitalia of C. maculatus adults and in the eggs was confirmed by separation

of a band from SDS–PAGE with Rf similar to the band recognized by the anti-vicilin polyclonal antibody followed by determination of partial sequence by using mass spectrometry ( Fig. 6). The recognition of vicilin fragments with similar electrophoretical migration suggests that the same form of

the vicilin fragments was maintained following partial proteolysis in the fat body and subsequent incorporation in the genitalia of both sexes and in the eggs. The absorption of intact proteins across the midgut epithelium of insects has received limited attention until recently, but a growing number of papers have confirmed that this phenomenon is much more common than previously documented (review by Jeffers and Roe, 2008). Despite of the potential use of absorbable proteins as a promising method for delivering insecticides into the haemocoel of target insects (Casartelli

et al., selleck chemicals 2005, Jeffers and Roe, 2008 and Fiandra et al., 2009), the studies about absorption of proteins in insects is in its infancy and one of the less understood aspects of this process is its adaptive value. We have demonstrated that C. maculatus larvae absorb intact vicilin molecules through their midgut epithelium and that vicilin is partially degraded in the fat body ( Uchôa et al., 2006). More recently, we demonstrated that vicilin-derived peptides can be found in the fat body of both females and males and aminophylline in the eggs ( Souza et al., 2010). As vicilin-derived peptides have been associated to fungicidal and fungistatic activities, we proposed that the deposition of vicilin peptides may function as a component of the humoral defensive arsenal of the eggs. However, as the males do not lay eggs, why do they emerge from the seed host with vicilin in their fat bodies? Our hypothesis was that males may transfer the vicilin peptides to the females during copulation. This type of transfer of chemical substances from males to females during copulation is known as seminal nuptial gift ( Vahed, 1998, Gilliot, 2003 and Gwynne, 2008). C. maculatus females, like females of many insect species, mate with more than one male (polyandry). Two broader hypothesis aim to explain why females take multiple mates: material and genetic benefits ( Arnqvist and Nilsson, 2000, Jennions and Petrie, 2000 and Tseng et al., 2007).

Some of anti-parasitic agents have also shown the capacity to promote different PCD phenotypes in distinct morphological forms of Leishmania sp. ( Monte Neto et al., 2011; Schurigt et al., 2010) and T. cruzi ( Menna-Barreto et al., 2009; Sandes et al., 2010), as was observed with the use of naphthoimidazoles against T. cruzi epimastigotes and trypomastigotes ( Menna-Barreto et al., 2009). Our current results with the melittin peptide, together with the published crude A. mellifera venom data, agree with the

concept that the same compound can generate different selleck chemicals cell death phenotypes. The lytic effect of melittin on red blood cell membranes has made it an unlikely therapeutic for human use (Blondelle and Houghten, 1991). The ability of melittin to bind to cell membranes is dependent on the phospholipid composition of the membrane, which may confer some selectivity to the effect of the AMP (Raghuraman

and Chattopadhyay, 2007). For this reason, the ability of melittin to affect eukaryotic cell membranes was evaluated prior to determining the effects of the peptide on T. cruzi intracellular forms. Our results confirm that melittin as a single peptide can be used to treat infected host cells in vitro at low concentrations (up to 1 μg/ml). However, previous Screening Library studies have shown that low concentrations of melittin, or its use as a hybrid with other AMPs, present low toxicity to mammalian cells ( Alberola et al., 2004; Chicharro et al., 2001; Díaz-Achirica et al., 1998; Jacobs et al., Mephenoxalone 2003; Luque-Ortega et al., 2001, 2003; Seeber, 2000; Wade et al., 1990; Boman et al., 1989). Because melittin was

effective against the amastigote forms, we believe that a hybrid melittin compound may be employed in future in vitro and in vivo Chagas disease chemotherapies. Chagas disease is an important but neglected disease whose eradication is hampered by inefficient treatment regimens, growing oral transmission within endemic countries and global spread via the emigration of infected people. The ideal drug for the treatment of chagasic patients must be capable of killing the T. cruzi parasite without triggering host defenses. AMPs are a component of the innate immune response of organisms in virtually every kingdom and phylum found worldwide. More importantly, they represent a great source of compounds for drug development because they carry a low likelihood of resistance development and display a rapid mode of action. Our findings demonstrate that all T. cruzi developmental forms were susceptible to the melittin peptide and that distinct PCD phenotypes were detected in different forms of treated parasites.

Greenberger Thomas Gremmel Weihua Guan Prajwal Gurung Kirk Hamilton Joshua Hare David Harris Daniel Hayes Chuan He Steffen Heeg Britney Helling Norah Henry Eli Hershkovitz Helen Heslop Jeffrey Hodgin Mimi Hu R. Stephanie Huang H.David Humes Warrick Inder Allan Jaffe Manu Jain Edward N. Janoff Craig Jefferies Sonata Jodele Duncan Johnstone

Michelle Kahlenberg Ravi Kalhan Nigel S. Key Farrah Kheradmand Seong-Kyu Kim Michael King Petra Kleinbongard Hon Wai Koon Sean Koppe Krishnan Koyamangalath Lucia Kucerova Yoshiki Kusama Richard Lafayette Luigi Laghi James Lane Irene Lang Benjamin Laskin Rodrigo Leal Andrew Leask Emilia Lecuona Joshua Leonard Kevin Leslie Edward Lesnefsky Maciej Lesniak Paul Transferase inhibitor Lewis Yi Li ES Lianidou Weei-Chin Lin Shing-Jong Lin De Lin Marc Lippman Wei Liu Sumei Liu Gang Liu Fei Liu Dakai Liu Emil Lou Alessandro Lugli Malcom PI3K assay Macleod Meena Madhur Lars Maegdefessel Patrudu Makena Deepak Malhotra Sunil Mallanna Massimo Mangino A.J. Marian Cary Mariash Philipp Mario Caroline Marshall George Martin James Martins Philip Mason Biji Mathew Sandra McAllister Kim McBride Susanna McColley Akira

Meguro Farrell Mendelsohn Steven Mentzer Jordan Metcalf Martha Mims

SALVATORE MINISOLA Abhisek Mitra Nicholas Mitsiades Markus Mohaupt Aaron Mohs Zahra Montazeri Daniel Musher Roland Nau Georges Nemer Paul Ney Dennis E. Niewoehner Timothy B Niewold Shuji Ogino Jill Ohar Gil Omenn Giuseppe Orlando Carl Orringer Tadeusz Osadnik John O’Toole Gavin Oudit Ratnasari Padang Vasantha Padmanabhan Udai Pandey Francisco Pan-Montojo Ralph J. Panos Choul Yong Park Linda Partridge Subramaniam Pennathur Maikel Peppelenbosch Maria Pereira Francisco Campos Pérez Eileen Pernot Phillip K. Peterson Richard Phipps Massimo Pietropaolo Irina Pinchuk Carteolol HCl Graham Poage Catherine Poh Michael Polymenis Bogdan Popescu Kailash Prasad Josef Prchal Vasu Punj Edward Purdue Hershel Raff Nalini Rajamannan Narayan Ramakrishna Nithya Ramnath Toralf Reimer Jun Ren Robert Roberts Leonardo Roever Sharon Rosenberg Myrna Rosenfeld Ann Rosenthal Catharine Ross Charles Rosser David Roth Anita Sabichi Joshua Safer Hiroshi Saito Nathan Sandbo Paul Sanders Robert Sargis Akinori Sato Amr Sawalha Amnon Schlegel Paul Schmidt Bryan Schneider Andreas Schwingshackl Sudhir V.