We previously reported a cross-sectional association between the presence of human herpesvirus 8 (HHV-8) serum antibodies and screen-detected prostate cancer in men living in Tobago. In the same study population, we examined the association between HHV-8 seropositivity and incident prostate cancer discovered at later screenings.In 40-81 year-old men without prostate cancer discovered at initial digital rectal examination (DRE) and prostate-specific antigen (PSA) screening, a case-cohort design measured the association between baseline HHV-8 seropositivity (modified immunofluorescence assay for antibodies against HHV-8 lytic antigens) and incident prostate cancer detected at DRE and PSA screenings three or five years later.vs. 9.9% seropositive; crude odds ratio (OR) 3.96, 95% confidence interval (CI) 1.53-10.2; age-adjusted OR 2.42, 95% CI 0.91-6.47). HHV-8 seropositivity did not increase incident prostate cancer risk (age-adjusted hazard ratio (HR) 0.88, 95% CI 0.46-1.69).Analyses included 486 unique individuals, 96 incident prostate cancer cases, and 415 randomly selected subjects representing an at-risk cohort. By design, the random sub-cohort contained 25 incident prostate cancer cases. In the sub-cohort, the frequency of HHV-8 seropositivity increased across age groupings . HHV-8 seropositivity was higher in men with elevated (≥ 4.0 ng/mL) than men with non-elevated PSA at initial screening . Co-occurrence of HHV-8 seropositivity and PSA elevation may explain cross-sectional association between HHV-8 and PSA screen-detected prostate cancer. Neisseria gonorrhoeae, Chlamydia trachomatis, human papillomavirus (HPV) type 18, and Treponema pallidum (syphilis)  measures of unadjusted and age-adjusted association between HHV-8 seropositivity measured at baseline (Wave 1) and prostate cancer detected later in time, at Wave 2 or Wave 3 [We used the chi-square test to evaluate 1) the statistical significance of differences between at-risk men with incomplete r Wave 3 . These mvs. 26.0% ≥ 60 years), smoking history (48.5% vs. 39.6%), personal cancer history (1.3% vs. 0.3%), Wave 1 PSA ≥ 4 ng/mL (13.5% vs. 5.5%), and Wave 1 DRE (64.7% vs. 76.3% negative and 20.0% vs. 10.3% missing).Table vs. 5.5% PSA ≥ 4 ng/mL), and more frequently positive Wave 1 prostate cancer screening (43.8% vs. 16.9% DRE or PSA positive). Case and sub-cohort HHV-8 seropositivity rates were 17.7% and 11.1%, respectively. When compared with 40-49 year-old sub-cohort men (3.5% HHV-8 seropositive), HHV-8 seropositivity was higher in 50-59 year-old sub-cohort men (13.6% HHV-8 seropositive) and higher yet in ≥ 60 year-old sub-cohort men (22.9% HHV-8 seropositive). HHV-8 seropositivity rates were lower in sub-cohort men with a history of smoking than those without (7.1% vs. 13.9%) and higher in sub-cohort men with a history of benign prostatic hypertrophy than those without (24.0% vs. 10.5%). HHV-8 seropositivity increased with Wave 1 PSA . HHV-8 seropositivity was higher in men with elevated (≥ 4.0 ng/mL) than men with non-elevated PSA . HHV-8 seropositivity was higher in sub-cohort men with a positive than in men with a negative Wave 1 prostate cancer screen result (20.0% vs. 9.3% seropositive).Wave 1 HHV-8 serologic status was available for 415 (93.9% of 442) men in the sub-cohort and for 96 (88.1% of 109) men in the case group . Table vs. 3.5% and 50-59 years: 10.8% vs. 13.6%), except in the oldest age group (≥ 60 years: 27.7% vs. 22.9%). In men with a non-elevated (< 4 ng/mL) Wave 1 PSA, the HHV-8 seropositivity rate was higher in the case group (17.1% vs. 9.9%). In men with an elevated (≥ 4 ng/mL) Wave 1 PSA, however, the HHV-8 seropositivity rate was lower in the case group (19.2% vs. 30.4%). In the two age sub-groups with appreciable HHV-8 seropositivity, age-specific HHV-8 seropositivity rates were not consistently higher or lower in case than sub-cohort men with non-elevated Wave 1 PSA (50-59 years: 11.5% vs. 13.7% and ≥ 60 years: 28.1% vs. 20.4%) and consistently lower in case than sub-cohort men with elevated Wave 1 PSA (50-59 years: 9.1% vs. 12.5% and ≥ 60 years: 26.7% vs. 41.7%).Table Table Our previous study used an immunofluorescence assay to measure HHV-8 antibodies in 138 prostate cancer cases and in 140 age-matched controls . HHV-8 se.g., PSA ≥ 4 ng/mL, age-adjusted HR 0.39, 95% CI 0.10-1.63; Table A positive association between HHV-8 seropositivity and prevalent prostate cancer in a cross-sectional study  and an iFour comparative studies of HHV-8 and prostate cancer have appeared ,11,26,27Analyses restricted to the sub-cohort showed strong association 1) between HHV-8 seropositivity and increasing age, a result also seen in Tobago women  and manyStudy strengths include unique population and setting (predominantly African ancestry Tobago residents ) and a cOur prospective study could not demonstrate an association between HHV-8 seropositivity and incident prostate cancer. However, analyses uncovered a strong relationship between elevated HHV-8 seropositivity and PSA. The HHV-8 association previously observed with prevalent prostate cancer may signify enhanced detection of prostate cancer possibly caused by the effects of HHV-8 on PSA. In this context, the association we observed between HHV-8 seropositivity and PSA elevation deserves further study.HHV-8: human herpesvirus 8; DRE: digital rectal examination; PSA: prostate-specific antigen; OR: odds ratio; CI: confidence interval; HR: hazards ratio; HPV: human papillomavirus; PLCO: Prostate Lung Colorectal, and Ovarian Cancer Screening Trial.The authors declare that they have no competing interests.ACM participated in study design, data analysis and interpretation, prepared a first draft of the manuscript, and helped revise the final manuscript. FJJ completed immunofluorescence assays and helped revise the final manuscript. CHB conceived the study, acquired data, provided study coordination, and helped revise the final manuscript. JWW selected analytic methods and directed statistical analysis. ALP acquired data and provided study coordination. JLW participated in study design, data analysis and interpretation and helped revise the final manuscript. All authors read and approved the final manuscript.


To determine the nosocomial acquisition rate of ESBL-E among patients and healthcare workers (HCWs) during an epidemic (March 2009 to Nov 2010) in an orthopaedics ward at HUG.Universal screening made by anal swab of all patients on admission and every 2 weeks if screening remained negative. 49 samples were collected from 41 HCW and 60 environmental samples were analysed. Molecular typing was performed on all ESBL-E isolates. If there was more than 97.5% similarity, strains were considered identical.Between March 2009 and November 2010, 1’531 admissions occurred to the orthopaedic ward . Among 565 anal swabs, ESBL-E were detected in 204 samples from 45 patients.E. coli (n=39), Klebsiella pneumoniae (n=10), Enterobacter spp (n=8), Citrobacter spp (n=2), Morganella morganii (n=2), and Proteus vulgaris (n=1). Two different ESBL-E strains were detected in 6 patients, and 3 others carried three distinct isolates. The ESBL-E transmitted were E. coli (14 patients), K. pneumoniae (3 patients) and both in 2 patients.The ESBL-E found were Identical ESBL-E species with epidemiological links were found in 25 cases. Only 9 of these were attributable to the unit. Most positive patients (96% [43/45]) were colonized asymptomatically with ESBL-E.Among HCWs, 6 samples (12%) were positive. Transmission was only observed between patients, not HCWs.None of the environmental samples revealed presence of ESBL-E.Transmission of ESBL-E strains was only observed between patients. No transmission between HCWs and patients occurred. HCW screening and environmental sampling is not useful during ESBL-E carriage outbreaks.E. coli.The main ESBL-E transmitted was E. coli-ESBL carriers.ESBL-E transmission can occur in units with extended length of stay, questioning the new Swiss policy of abandoning contact precautions for None declared


In the Phase III, randomised, open-label ODIN trial, treatment-experienced HIV-1-infected adults with no screening DRV resistance-associated mutations received DRV/r 800/100mg qd or DRV/r 600/100mg bid (both arms + ≥2 NRTIs). At Week 48, 72.1% qd vs 70.9% bid patients achieved HIV-1 RNA <50 copies/mL , confirming non-inferiority of DRV/r qd. The relationship between DRV PK and efficacy and safety following treatment with DRV/r is explored.0h) and exposure  using a population pharmacokinetic model. Relationships between PK parameters and efficacy  were assessed using ANCOVAs. Relationships between PK parameters and occurrence of adverse events of interest and laboratory lipid abnormalities were evaluated using descriptive statistics.Sparse blood sampling for PK evaluations was taken at Weeks 4, 8, 24 and 48 to determine DRV trough concentrations (C0h was 1896 (184-7881) ng/mL for DRV/r qd and 3197  ng/mL for DRV/r bid. Median (range) AUC24h for DRV/r qd was 87,788  ng.h/mL and 109,401  ng.h/mL for bid. No relevant relationships were observed between DRV PK and efficacy: changes from baseline in HIV-1 RNA log10 copies/mL at Week 48 for pooled data by DRV AUC24h quartile ranges  were -2.06, -2.22, -2.19, and -2.08 log10 copies/mL, respectively. The % patients achieving HIV-1 RNA <50 copies/mL by these quartile ranges were 82.0%, 88.5%, 82.6% and 76.5% (observed data), respectively. In a logistic regression analysis adjusting for baseline viral load, AAG levels and number of sensitive NRTIs in the optimised background regimen, there were no relevant relationships between PK and virological response. No apparent relationships were observed between DRV PK and occurrence of rash-, cardiac-, GI-, liver-, lipid- and glucose-related AEs or laboratory lipid abnormalities.PK data were available for 280 DRV/r qd patients and 278 bid patients. Median (range) C0h and AUC24h compared to DRV/r 600/100mg bid; however, comparable efficacy between DRV/r qd and bid confirmed adequate DRV concentrations were achieved following qd dosing. No relevant relationships were observed between DRV PK and efficacy or safety at Week 48.Dosing with DRV/r 800/100mg qd resulted in lower C


Tricholepidion gertschi is the sole extant representative of the family Lepidotrichidae. Its phylogenetic position is of special interest, since it may provide crucial insights into the early phenotypic evolution of the dicondylian insects. However, the phylogenetic position of T. gertschi is unclear. Originally, it was classified among silverfish (Zygentoma), but various alternative relationships within Zygentoma as well as a sistergroup relationship to all remaining Zygentoma + Pterygota are discussed, the latter implying a paraphyly of Zygentoma with respect to Pterygota. Since characters of the head anatomy play a major role in this discussion, we here present the so far most detailed description of the head of T. gertschi based on anatomical studies by synchrotron micro-computer tomography and scanning electron microscopy. A strong focus is put on the documentation of mouthparts and the anatomy of the endoskeleton as well as the muscle equipment. In contrast to former studies we could confirm the presence of a Musculus hypopharyngomandibularis (0md4). The ligamentous connection between the mandibles composed of Musculus tentoriomandibularis inferior (0md6) is also in contact with the anterior tentorium. Phylogenetic analysis of cephalic data results in monophyletic Zygentoma including T. gertschi. Zygentoma are supported by the presence of a set of labial muscles originating at the postocciput, presence of an additional intralabral muscle, and four labial palpomeres. Character systems like the genitalic system, the mating behaviour, the segmentation of the tarsi, the overall body form, and the presence of ocelli which were proposed in other studies as potentially useful for phylogenetic reconstruction are evaluated.The relic silverfish  Trichlepidion gertschi occurs only in the coastal region of northern California. The species is characterized by a number of peculiarities with respect to all other extant silverfish species (= Euzygentoma) such as the presence of ocelli (in addition to compound eyes), 5-segmented tarsi [T. gertschi is the sister species to all other dicondylians (Zygentoma + Pterygota), sister species to all other Zygentoma, or a subgroup within Zygentoma . Moleed tarsi -7 and moed tarsi -13 disagT. gertschi is crucial to understand the evolution of several morphological characters in the stem lineage of Dicondylia, e.g. presence of a proventriculus [However, the phylogenetic position of triculus , sperm ctriculus ,21, the triculus ,14 and ttriculus  includintriculus .T. gertschi to remaining Zygentoma [T. gertschi with a strong focus on the documentation of mouthparts, endoskeleton and muscle equipment. We show that characters of the cephalic morphology indeed provide information on a sistergroup relationship of T. gertschi and the remaining studied Zygentoma.Available cephalic data did not help thus far to resolve the phylogenetic relationships of ygentoma ,14. Thissynchrotron radiation micro-computer tomography (SR-μCT), so that they could be used to complement the character matrix , Thermobia domestica  (Lepismatidae), Lepisma saccharina Linneaus, 1758 (Lepismatidae), and Atelura formicaria Heyden, 1855 (Nicoletiidae). The outer anatomy of T. gertschi was furthermore investigated with scanning electron microscopy (SEM).All specimens were fixed in Bouin's solution  and inveSR-μCT was done using the recommendations of Betz et al.  and the http://www.blender.org). Both software packages are distributed under the general public license (GPL). Tables and figures were edited with GIMP ver. 2.8, Inkscape ver. 0.48 and Scribus ver. 1.4.1 . A 3D model of the head of T. gertschi is available  the specimen was transferred in a series of steps into 100% ethanol, critical point dried , and sputter coated (Model Anatech Hummer VII). Microscopy was performed on a Hitachi S-2460 N scanning electron microscope using a rotatable sample holder . The terMachilis germanica was selected as the outgroup. Only unambiguous changes were mapped on the optimal trees. Character numbers and states are given in brackets using the following syntax: (character number : character state). The character matrix is derived from Blanke et al. [Parsimony analyses of 139 cephalic characters (see Appendix) and Bremer support (BR) calculations were carried out with TNT  using 1,e et al.  and is be et al. . Please 2. Among them, numerous (>500/100 μm2) small tubercles on the exoskeleton, possibly sensorial in function, cover the entire head : insertion directly anterior of 0md1 (muscle "spt" of Chaudonneret [0te2): the insertion in between the muscle bundles of 0md1 supports homologisation with the muscle "spot" of Chaudonneret [0te3): O, anterior side of the dorsal tentorial arm; I, frons near the dorsal part of the antennal base. M. posterotentorialis (0te4): absent. M. tentoriotentorialis longis (0te5): O, ventrolaterad on the anterior corpotentorium; I, mesad on the posterior tentorium. M. tentoriotentorialis brevis (0te6): O, anterior tentorium, along the gap towards the posterior tentorium; I, posterior tentorium, along the gap towards the anterior tentorium.Musculature: M. tentoriofrontalis posterior (donneret ); O, at donneret ; O, at tThe convex labrum Figures  is cover0lb1): O, mesally on the epistomal ridge; I, mesally on the inner basal wall of the labrum. M. frontoepipharyngalis (0lb2): absent. M. epistoepipharyngealis (0lb3): this muscle can easily be confused with the 0lb2. The origin of 0lb3 lies clearly only on the epistomal ridge. O, laterally on the epistomal ridge; I, basal epipharyngeal wall. M. labralis transversalis (0lb4): absent. M. labroepipharyngealis (0lb5): O, basal labral wall; I, basal wall of epipharynx. M. labrolabralis (0lb6): O, mesobasal labral wall in between the two bundles of 0lb5; I, medioapical area of labrum.Musculature: M. frontolabralis : O, mesally on the corpotentorium; I, anterior margin of the scapus. M. tentorioscapalis posterior (0an2): O, in the posterior part of the corpotentorium; I, posterior basal margin of the scape. M. tentorioscapalis lateralis (0an3): O, at the anterior base of the dorsal tentorial arms; I, dorsal basal margin of the scape. M. tentorioscapalis medialis (0an4): O, at the dorsal tentorial arms directly over 0te1; I, dorsal basal margin of the scape. M. frontopedicellaris (0an5): absent. M. scapopedicellaris lateralis (0an6): O, broadly on the dorsolateral base of the scape; I, dorsolateral base of the pedicellus. M. scapopedicellaris medialis (0an7): O, ventrolateral base of the scape; I, ventrolateral base of the pedicel. M. intraflagellaris (0an8): absent. M. interampularis (0ah1): absent. M. ampulloaortica (0ah2): absent. M. ampullopharyngealis (0ah3): absent. M. ampullofrontalis (0ah4): absent. M. frontofrontalis (0ah5): absent.Musculature: M. tentorioscapalis anterior  reaches into the lumen of the mandible directly posterad the mandibular ridge Figure . The twoThe mola is almost formed like a right-angled triangle in lateral view Figure , with th0md1): O, dorsal parts of the head, anterior of the postoccipital ridge and on this ridge; one muscle bundle also posterior of the postoccipital ridge; I, tendon originating from the proximal part of the posterior mandibular edge. M. craniomandibularis externus anterior (0md2): O, gena, anterior of the compound eye; I, tendon originating from the proximal part of the anterior mandibular edge, directly lateral to the anterior articulation complex. M. craniomandibularis externus posterior (0md3): O, directly posterior of the compound eye, with several bundles also at the postoccipital ridge; I, tendon originating from the anterior mandibular edge near the posterior articulation. M. hypopharyngomandibularis (0md4): O, small sclerite close to the loral arm of the hypopharynx; I, proximal inner side of the anterior wall of the mandible. M. tentoriomandibularis lateralis superior (0md5): O, ventrally at the anterior tentorial arm; I, anterior mandibular rim between 0md2 and 0md3. M. tentoriomandibularis lateralis inferior (0md6): O, the whole inner wall of the mandible except for the region near the incisivi and mola; I, in the same region of the other mandible and with a few muscle bundles also at the ventral anterior area of the corpotentorium. M. tentoriomandibularis medialis superior (0md7): O, at the ventral base of the anterior tentorial arms; I, proximal of the posterior articulation at the posterior mandibular rim. M. tentoriomandibularis medialis inferior (0md8): O, at the transition of the corpotentorium and the anterior tentorial arm below 0md7; I, mediodorsal wall of the mandibular cavity.Musculature: M. craniomandibularis internus  is three times longer than wide in overall shape Figure . The carThe stipes is composed of a narrow basistipes and a much larger mediostipes bearing the palpus, galea and lacinia Figure . The whoThe palpus is five-segmented and densely covered with trichoid sensilla. The first segment is one third as long as the second one. The third one is slightly longer than the second one, the fourth and fifth are as long as the second one. Each segment is slightly thinner than the preceding one. The fifth segment bears distally six special sensilla formed by a basal cylindrical segment densely covered with microtrichia and four to six tubular extensions on the tip of the cylindrical base Figures . These sThe galea is sickle-shaped Figure , distall0mx1): O, laterally at the postoocipital ridge; I, basal cardinal process. M. craniolacinialis (0mx2): O, distal of 0mx1 at the postoocipital ridge; I, cuticular tendon at the basal edge of lacinia together with 0mx6. M. tentoriocardinalis (0mx3): O, at the lateral part of the posterior tentorium; I, inner wall of the cardo. M. tentoriostipitalis anterior (0mx4): O, ventral on the corpotentorium; I, at the posterior stipital rim. M. tentoriostipitalis posterior (0mx5): O, lateral on the corpotentorium; I, at the basal inner wall of the stipes. M. stipitolacinialis (0mx6): O, posterior wall of the stipes, basal to the cardostipital ridge; I, basal proximal edge of lacinia, at a common cuticular tendon with 0mx2. M. stipitogalealis (0mx7): O, posterior wall of the stipes, basal to the cardostipital ridge next to 0mx6; I, basal edge of galea. M. stipitopalpalis externus (0mx8): O, posterior wall of the stipes, opposite of the palpus; I, posterior rim of the first palpomere of the maxillary palpus. M. stipitopalpalis medialis (0mx9): O, medially at the posterior wall of the stipes; I, ventral edge of palpomere 1. M. stipitopalpalis internus (0mx10): O, posterior inner wall of the stipes, opposite of the palpus; I, anterior rim of the first palpomere of the maxillary palpus. M. stipitalis transversalis (0mx11): O, outer stipital wall, near the palpus; I, inner stipital wall, near the palpus. M. palpopalpalis maxillae primus (0mx12): O, basal edge of palpomere 1; I, basal edge of palpomere 2. M. palpopalpalis maxillae secundus (0mx13): O, mesal edge of palpomere 2; I, mesal edge of palpomere 3. M. palpopalpalis maxillae tertius (0mx14): O, basal edge of palpomere 3; I, basal edge of palpomere 4; M. palpopalpalis maxillae quartus (0mx15): unclear.Musculature: M. craniocardinalis : O, posterior side of the postoccipital ridge; I, proximal area of the glossal base. M. postoccipitoglossalis lateralis (0la2): O, posterior side of the postoccipital ridge, right next to 0la1; I, dorsolateral area of the glossal base. M. postoccipitoparaglossalis (0la3): O, posterior side of the postoccipital ridge, lateral of 0la1 & 0la2; I, distal base of the paraglossa. M. postoccipitopraementalis (0la4): O, posterior side of the postoccipital ridge, right next to 0la1 & 0la2; I, inner proximal wall of the prementum. M. tentoriopraementalis (0la5): O, lateral area of the posterior tentorium; I, laterobasal edge of prementum. M. tentorioparaglossalis (0la6): O, lateral area of the posterior tentorium, right next to 0la5; I, paraglossa, close to the labial palpus. M. tentorioglandularis (0la7): O, lateral posterior area of the corpotentorium; I, labial gland. M. submentopraementalis (0la8): O, medially on the postmentum; I, mediobasal edge of prementum. M. postmentomembranus (0la9): unclear. M. submentomentalis (0la10): absent. M. praementoparaglossalis (0la11): O, distal on the basal edge of the prementum; I, basal edge of paraglossa. M. praementoglossalis (0la12): O, more mesally on the basal edge of the prementum, right next to 0la11; I, basal edge of glossa. M. praementopalpalis internus (0la13): O, mesally on the prementum; I, anterior basal edge of labial segment 1. M. praementopalpalis externus (0la14): O, mesally on the prementum, right next to 0la13; I, posterior basal edge of labial segment 1. M. praementomembranus (0la15): O, anterolateral area of the postmentum; I, anteromedial area of postmentum. M. palpopalpalis labii primus (0la16): O, mediobasal edge of labial palpomere 1; I, medial and distal edge of palpomere 2. M. palpopalpalis labii secundus (0la17): O, mediobasal edge of palpomere 2; I, basal edge of the palpomere 3.Musculature: M. postoccipitoglossalis medialis : O, frons, near the antennal base; I, oral arms of the suspensorial sclerites. M. tentoriooralis (0hy2): O, anterior tentorial arm, near the anterior tentorial pit; I, one muscle bundle on the oral arms of the suspensorial sclerites, one bundle at the lateral buccal wall: both bundles are well separated from 0hy1. M. craniohypopharyngealis (0hy3): O, posterior tentorial arms; I, suprasalivarial sclerite. M. postoccipitalohypopharyngealis (0hy4): O, posterior wall of the postoccipital ridge, together with 0la1 & 0la2; I, hypopharyngeal fulcrum. M. tentoriosuspensorialis (0hy5): O, anterior margin of the posterior tentorium; I, suspensorium of the hypopharynx. M. postmentoloralis (0hy6): O, anterior part of the postmentum; I, loral arm of the hypopharyngeal suspensorium. M. praementosalivaris anterior (0hy7): O, distolateral wall of the prementum, close to the labial palpus; I, lateral wall of salivarium. M. praementosalivaris posterior (0hy8): O, medially on the basal part of the prementum; I, posterior wall of salivarium. M. oralis transversalis (0hy9): unclear. M. loroloralis (0hy10): O, loral arm of suspensorial sclerite; I, loral arms of the suspensorial sclerites on the other side. M. lorosalivarialis (0hy11): O, hypopharyngeal suspensorium; I, loral arm of the hypopharynx. M. hypopharyngosalivaris (0hy12): O, loral arm of the hypopharynx, right next to 0hy11; I, salivarial orifice. M. anularis salivarii (0hy13): unclear.Musculature: M. frontooralis : two distinct muscle bundles. O, postclypeus; I, roof of the cibarium. M. clypeobuccalis (0bu1): O, clypeus, near the epistomal ridge; I, roof of the bucca. M. frontobuccalis anterior (0bu2): O, frons dorsal of the epistomal ridge; I, dorsal buccal wall. M. frontobuccalis posterior (0bu3): O, more posterior than 0bu2 on the frons; I, dorsal buccal wall, posterior of 0bu2. M. tentoriobuccalis lateralis (0bu4): absent. M. tentoriobuccalis anterior (0bu5): O, anteriormost part of the corpotentorium between the anterior tentorial arms; I, ventral wall of the bucca, directly behind the anatomical mouth. M. tentoriobuccalis posterior (0bu6): O, laterally on the dorsal wall of the corpotentorium; I, lateral wall of the foregut at height of the 0ph1. M. verticopharyngealis (0ph1): O, frons right next to the 0te4; I, dorsal wall of the foregut, posterior to the supraoesophagial ganglion. M. tentoriopharyngealis (0ph2): O, laterally on the dorsal wall of the corpotentorium right next to 0bu6; I, ventral wall of the foregut, beneath 0ph1. M. postoccipitopharyngealis (0ph3): absent. M. anularis stomodaei (0st1): ring muscle layer that covers the entire foregut. M. longitudinalis stomodaei (0st2): longitudinal muscle layer covering the entire foregut, right next to 0st1.Musculature: M. clypeopalatalis , presence of M. labroepipharyngealis (0lb5), M. verticopharyngealis (0ph1), M. tentoriopharyngealis (0ph2) and the five-segmented maxillary palpus.Generally, the monophyly of Dicondylia and Pterygota is well supported by molecular and morphological data ,41 even The monophyly of winged insects is strongly supported  was considered absent [Tricholepidion) exhibit an origin of this muscle exclusively on the tentorium. Our phylogenetic analysis corroborates monophyletic Zygentoma despite the inclusion of the mandible ligament in the character matrix (character 69) with high support . Euzygentoma and T. gertschi possess a remarkable set of extrinsic labial muscles originating from the postoccipital region and extending dorso-ventrally through the whole head into the labium. Archaeognatha and Pterygota clearly do not possess this set of labial muscles [gertschi and Euzygentoma, possess four labial palpomeres (103:3). Also, the intralabral muscle equipment is characterized by an additional muscle, the M. epistoepipharyngalis . In the present analysis the low number of ommatidia  is a homoplastic character since Grylloblattodea also show reduced eyes [Galloisiana yuasai [T. gertschi as sister to Euzygentoma.The position of ygentoma ,18, as sygentoma ,16, or aygentoma ,19 withid absent ,14 and dd absent ,44,45. Id absent ,44,45, w muscles ,44,46. Tced eyes  which hoced eyes ). A M. la yuasai . Except Tricholepidion as sistergroup to Odonata with low support while Giribet [Tricholepidion as sister taxon to Euzygentoma + Pterygota with low support. All other molecular works supported monophyletic Zygentoma [With few exceptions most molecular studies advocate monophyletic Zygentoma. Based on secondary structure alignment of the 18S unit Kjer  recovere Giribet , using aygentoma ,4,6,7.T. gertschi and Lepismatidae [T. gertschi Dallai et al. [T. gertschi resembles the ancestral state of insects with a 9 + 9 + 2 axonemal pattern and accessory tubules with 16 protofilaments. The sperm pairing in T. gertschi is a true fusion between two spermatozoa along the entire sperm head region, which is different from sperm aggregations in other Zygentoma [T. gertschi  in smatidae . Zrzavý smatidae  considersmatidae ). In a di et al. ,21 discoygentoma . Characteognatha ). The oveognatha ) and higeognatha .T. gertschi include similarities in the mating behaviour of T. gertschi and Lepismatidae [T. gertschi and some Nicoletiidae [Petrobiellus and Mesomachillis species [T. gertschi. The widening of the apical labial palpus segment is paralleled in males of several Machilidae and Meinertellidae  and, heT. gertschi, since these occur as well in several pterygote taxa and the phylogenetic significance is therefore unclear. Zrzavý [T. gertschi, it is conceivable that five-segmented tarsi already existed in the stem lineage of Dicondylia. Engel [Also, we interpret the five-segmented tarsi  not as a. Zrzavý  considera. Engel  even cona. Engel ).T. gertschi in its own family Tricholepidiidae because the extinct type species of the Lepidotrichidae, Lepidotrix pilifera Silvestri, 1912, might be more closely related to the Euzygentoma than to T. gertschi due to the apparent absence of ocelli [T. gertschi clearly possesses three ocelli, we consider this a weak argument for this classification, since loss of ocelli occurred several times within Dicondylia, e.g. in Xenonomia (= Notoptera + Mantophasmatodea), Phasmatodea [L. pilifera is mandatory. As for the head  we partThe authors declare that they have no competing interests.AB, BW and BM designed the study, AB and FW conceived the experiments. AB and FW conducted the SRμCT, AB the SEM and phylogenetic analysis. AB, MK and BW carried out the analysis of the raw data. AB, MK, BW, and BM wrote the manuscript. All authors read, revised and approved the manuscript.List of characters used for phylogenetic reconstruction0. Orientation of head: (0) orthognathous; (1) prognathous or slightly inclined; (2) hypognathous1. Number of ocelli: (0) 0; (1) 2; (2) 3.2. Compound eyes: (0) composed out of more than 80 ommatidia; (1) less than 80 ommatidia;3. Distance between eyes: (0) less than their own width; (1) greater than their own width; (2) eyes fused at single point; (3) eyes broadly fused along an eye seam4. Shape of vertex: (0) flat, not developed into large protuberance; (1) conical, or developed into a large transverse ridge5. Epicranial or coronal suture: (0) present; (1) absent6. Parietal ridge: (0) absent; (1) present.7. Postoccipital ridge: (0) present; (1) absent.8. Subgenal ridge: (0) absent; (1) present9. Pleurostomal ridge and circumocular ridge: (0) not in contact; (1) partly in contact10. Interantennal ridge: (0) absent; (1) present11. Shape of frons: (0) flat when seen from lateral; (1) outwardly bulged when seen from lateral12. Distinct convexity ventrad the antennal bases: (0) absent; (1) present13. Scutellum: (0) absent; (1) present14. x-shaped median apodeme on the frontal region: (0) absent; (1) present15. Clypeus: (0) not subdivided; (1) subdivided into ante- and postclypeus16. Postclypeus: (0) not enlarged; (1) enlarged17. Anteclypeus: (0) membranous; (1) sclerotised18. Adult mouthparts: (0) with function; (1) without function19. Oval sclerotization of labral base: (0) absent; (1) present.20. Tormae: (1) absent; (0) present21. Mesal extension of tormae: (0) present; (1) absent22. M. epistoepipharyngealis (0 lb3): (0) present; (1) absent23. M. labroepipharyngealis (0 lb5): (0) present; (1) absent24. M. labrolabralis (0 lb6): (0) present; (1) absent25. Insertion of antennae: (0) close to the anterior mandibular articulation with the pleurostomal and circumantennal ridges in contact (where applicable); (1) distinctly separated from the anterior mandibular articulation, pleurostomal and circumantennal ridges not in contact.26. Antennifer: (0) present; (1) absent27. Length of pedicel and scapus: (0) pedicel longer than scapus; (1) scapus longer than pedicel; (2) scapus and pedicel equal in length28. Oval scerite in membrane connecting scapus and pedicellus: (0) absent; (1) present.29. Size of first flagellomere: (0) not enlarged; (1) first flagellomere more than twice as long as second one.30. Antennal stridulatory organ: (0) absent; (1) present31. Areas of origin of antennal muscle 0an1: (0) anterior tentorial arms only; (1) anterior tentorial arms and tentorial bridge; (2) on dorsal tentorial arms only; (3) on dorsal arms and tentorial bridge; (4) anterior and dorsal tentorial arm.32. Areas of origin of antennal muscle 0an2: (0) anterior tentorial arms only; (1) anterior tentorial arms and tentorial bridge; (2) on dorsal tentorial arms only; (3) on dorsal arms and tentorial bridge; (4) tentorial bridge only; (5) dorsal and anterior tentorial arms.33. M. tentorioscapalis lateralis (0an3): (0) present; (1) absent34. M. tentorioscapalis medialis (0an4): (0) present; (1) absent35. Circumesophageal vessel ring branching off the dorsal aorta posterior to the brain: (0) present; (1) absent36. Ostia of dorsal vessel: (0) lips always present; (1) ostia with and without lips (excurrent ostia).37. Position and number of excurrent ostia within a segment: (0) one ventrolateral pair; (1) ventromedian.38. Antennal circulatory organs in adults: (0) present; (1) absent39. Antennal vessel wall: (0) uniform; (1) bipartite40. Contractibility of antennal ampulla: (0) absent (non-pulsatile); (1) present (pulsatile).41. M. interampullaris (0ah1): (0) absent; (1) present42. M. ampulloaorticus (0ah2): (0) absent; (1) present43. M. ampullopharyngealis (0ah3): (0) absent; (1) present44. M. ampullo-frontalis (0ah4): (0) absent; (1) present45. Connection of antennal ampulla to supraoesophageal ganglion: (0) absent; (1) present46. Oval nuclei in tissue connecting the antennal ampulla and supraoesophageal ganglion: (0) absent; (1) present47. Anterior and posterior tentoria: (0) seperated; (1) merged48. Transverse mandibular tendon: (0) present; (1) absent49. Processes of the anterior tentorial apodemes extending into the lumen of the mandibular base: (0) absent; (1) present50. Corpotentorium: (1) elongated; (0) slim.51. Apophyses on the anterior surface of the corpotentorium: (0) absent; (1) present52. Secondary anterior tentorial bridge (“perforation of the corpotentorium"): (0) absent; (1) present.53. Lateral lobes on the anterior tentorial arms: (0) absent; (1) present54. Cuticular dorsal tentorial arms: (0) absent; (1) present55. Trabeculae tentorii of posterior tentorial arms (0) present; (1) absent56. M. tentoriofrontalis posterior (0te1): (0) present; (1) absent57. M. posteriotentorialis (0te4): (0) present; (1) absent58. M. tentoriotentorialis longus (0te5): (0) present; (1) absent59. M. tentoriotentorialis brevis (0te6): (0) present; (1) absent60. Numbers of incisivi on the left mandible: (0) 2; (1) 3; (2) 5; (3) 0; (4) 1; (5) 461. Numbers of incisivi on the right mandible: (0) 2; (1) 3; (2) 4; (3) 5; (4) 0; 5 (1)62. Armament on the mesal side of the left mandible: (0) without teeth or ridges; (1) one tooth; (2) three ridges63. Dorsal cutting edge of the left mandible: (0) notched; (1) smooth64. Mandibular postmola: (0) absent; (1) present65. Anterior mandibular joint: (0) absent; (1) present66. Anterior mandibular joint: (0) cuticular hardening on the mandibular depression; (1) channel-joint (2) ball-and-socket joint67. Anterolateral part of the anterior mandibular articulation : (0) present; (1) absent68. Posterior mandibular joint: (0) cylinder-shaped (1) ball-and-socket joint69. Mandibular ligament: (0) present; (1) absent.70. M. craniomandibularis externus anterior (0md2): (0) present; (1) absent71. M. hypopharyngomandibularis (0md4): (0) present; (1) absent72. M. tentorio-mandibularis lateralis superior (0md5): (0) present; (1) absent73. M. tentorio-mandibularis medialis superior (0md7): (0) present; (1) absent74. Cardo: (0) present; (1) absent75. Division of stipes into basistipes and mediastipes: (0) present; (1) absent76. Galea: (0) present; (1) absent77. Distal field of trichomes on the galea: (0) undivided; (1) divided; (2) just a U-shaped seam78. Connection of lacinia and galea: (0) separated; (1) fused79. Shape of lacinia: (0) sickle-shaped; (1) chisel-shaped; (2) truncate; (3) short claw80. Mesally directed setae on lacinia: (0) present; (1) absent81. Lacinia: (0) free; (1) in galeal cavity82. Lacinial incisivi: (0) present; (1) absent83. Number of incisivi on lacinia: (0) 3; (1) 2; (2) 1; (3) more than 384. Dentisetae on lacinia: (0) present; (1) absent85. Proximal apodeme on the lacinia: (0) absent; (1) present86. Galeolobulus: (0) absent; (1) present87. Maxillary palpus: (0) 5-segmented; (1) 4-segmented; (2) 1-segmented; (3) 3-segmented; (4) 6-segmented; (5) 7-segmented88. Orientation of maxillary palpi: (0) ventrally oriented; (1) anteriorly or dorsally directed89. 0mx7: (0) present; (1) absent90. M. palpopalpalis maxillae primus (0mx12): (0) present; (1) absent91. Postmentum: (0) not subdivided; (1) subdivided into submentum and mentum92. Angle between submentum and mentum: (0) less than 60° or absent; (1) more than 60°93. Curvature of submentum: (0) absent; (1) curved in lateral view94. Median longitudinal tunnel of labium: (0) absent; (1) present95. Median cleft of prementum: (0) absent; (1) present96. Labium: (0) paraglossa and glossa seperated; (1) paraglossa and glossae completly fused97. Glossa: (0) present; (1) reduced98. Number of glossae: (0) 2; (1) 1;99. Number of paraglossae: (0) 2; (1) 1;100. Shape of paraglossa: (0) cylindrical, as wide as thick; (1) flat, wider than thick; (2) palpus-like.101. Relative length of paraglossae and glossae: (0) about equally long; (1) paraglossae twice as long or longer102. Orientation of labial palpi: (0) anterior or lateral; (1) ventral or posterior103. Number of labial palpomeres: (0) 3; (1) 1; (2) 2; (3) 4104. Shape of labial palpi: (0) approximately round in cross section; (1) dorsoventrally flattened105. Length of labial palpi: (0) longer than glossae; (1) about as long as the glossae106. Moveable hooks of labial palpi: (0) absent; (1) present107. M. postoccipitoglossalis medianus (0la1): (0) present; (1) absent108. M. postoccipitoglossalis lateralis (0la2): (0) present; (1) absent109. M. postoccipitoparaglossalis (0la3): (0) present; (1) absent110. M. postoccipitoprementalis (0la4): (0) present; (1) absent111. 0la5: (0) present; (1) absent112. Origin of M. tentoriopraementalis inferior 0la5 (M.29): (0) ventral apodeme; (1) posterior tentorial arms; (2) posterior tentorial arms (posttentoria) and postocciput.113. M. tentorioparaglossalis (0la6): (0) present; (1) absent114. Origin of M. tentorioparaglossalis (0la6): (0): tentorium; (1) basal edge of prementum115. M. tentorioglandularis (0la7): (0) present; (1) absent116. M. submentopraementalis (0la8): (0) present; (1) absent117. M. submentopraementalis (0la8): (0) one component; (1) two components118. M. postmentomembranus (0la9): (0) present; (1) absent119. M. submentomentalis (0la10): (0) absent; (1) present120. M. praementoparaglossalis (0la11): (0) present; (1) absent121. M. praementoglossalis (0la12): (0) present; (1) absent122. M. praementopalpalis internus (0la13): (0) present; (1) absent123. M. praementopalpalis externus (0la14): (0) present; (1) absent124. Hypopharynx overlapping paraglossae and glossae 0) absent; 1) present125. Shape of hypopharynx: (0) slope like; (1) distinctly flattened126. Superlinguae: (0) present; (1) absent127. Salivary glands and ductus: (0) present; (1) absent128. Connection of salivary ducts: (0) connected before opening, Y-shaped; (1) open separately129. M. frontobuccalis lateralis (0hy2): (0) present; (1) absent130. M. craniohypopharyngealis (0hy3): (0) present; (1) absent131. M. postmentoloralis (0hy6): (0) present; (1) absent132. M. praementosalivaris posterior (0hy8): (0) absent; (1) present133. M. lorosalivarialis (0hy11): (0) present; (1) absent134. 0hy12: (0) present; (1) absent135. M. frontobuccalis posterior (0bu3): (0) present; (1) absent136. M. tentoriobuccalis lateralis (0bu4): (0) absent; (1) present137. 0bu5: (0) present; (1) absent138. M. tentoriobuccalis posterior (0bu6): (0) present; (1) absent.139. Origin of M. tentoriobuccalis posterior 0bu6 (M.50): (0) anterior and/or posterior bridge, (1) pretentoriaHomologization of the muscular terminology with other authors. Abbreviations: +, muscle present ; -, muscle absent;/, muscle not dealt with by the author; ?, unclear homology.Click here for fileCharacter state matrix in excel format together with short descriptions of the charactes used: (?) refers to a missing or unclear character state, (-) to inapplicable characters.Click here for fileCharacter state matrix in nexus format: (?) refers to a missing or unclear character state, (-) to inapplicable characters.Click here for fileT. gertschi3D model of the head of . Please use the open source software Blender (http://www.blender.org) to view the model.Click here for fileImage stack of transversal slices through the head of T. gertschi packed in the "avi" movie format for easy browsing through the stack.Click here for fileComplete tree (strict consensus) showing all taxa. Character numbers above, character states below the nodes.Click here for file


In “Probable Tiger-to-Tiger Transmission of Avian Influenza H5N1,” by Roongroje Thanawongnuwech et al., an error occurred. The GenBank accession nos. for HA and NA gene initiated from influenza A virus (A/Tiger/ Thailand/CU-T3/04) are AY842935 and AY842936.http://wwwnc.cdc.gov/eid/article/11/5/05-0007_article.htm.The corrected article appears online at We regret any confusion these errors may have caused.


S,6S,2R)-9,13-dimethyl-5-methylene-3-oxatricyclotrideca-9,12-diene-4,11-dione], C15H16O3, is a guanolide isolated from Artemisia douglasiana. The fused-ring system contains a seven-membered ring that adopts a chair conformation, a fused planar cyclopentenone ring and a five-membered lactone ring fused in envelope conformation. The absolute structure determined by X-ray analysis agrees with that previously assigned to this compound by NMR studies  and also with that of leucodine, a closely related guaianolide .Dehydroleucodin [systematic name: (1dero 1972. Tetrah al. 1988. J. Nat. DOI: 10.1107/S1600536811048938/bg2432Isup2.hkl            Structure factors: contains datablock(s) I. DOI: 10.1107/S1600536811048938/bg2432Isup3.mol            Supplementary material file. DOI: 10.1107/S1600536811048938/bg2432Isup4.cml            Supplementary material file. DOI:  crystallographic information; 3D view; checkCIF report            Additional supplementary materials:


Errors were introduced in the preparation of this article for publication: incorrect symbols were inserted in the legends of Tables S2, S3, S6, S7, and S8. The corrected legends are:Table S1. White-tailed Deer RRL Contig Table (3.66Mb XLS)Table S2. White-tailed Deer RRL Informative blastn Hits Table S3. White-tailed Deer RRL Putative SNPs Table S4. White-tailed Deer RRL Functional Annotation (1.07 Mb XLS)Table S5. White-tailed Deer RRL plus RSL (Pooled) Contig Table (7.99 Mb XLS)Table S6. White-tailed Deer RRL plus RSL (Pooled) Informative blastn Hits Table S7. White-tailed Deer RRL plus RSL (Pooled) Putative and Validated SNPs Table S8. White-tailed Deer RRL plus RSL (Pooled) Mitochondrial SNP Table Table S9. White-tailed Deer RRL plus RSL (Pooled) Functional Annotation (2.71 Mb XLS)


HIV-infected patients have a higher risk of developing cancer than the general population. Kaposi's sarcoma (KS), non-Hodgkin's lymphoma (NHL), primary CNS lymphoma (PCL) and invasive cervical cancers are considered AIDS-defining. An increased incidence in recent years, however, has been reported also for other malignancies after the introduction of HAART.We performed a case-control study to characterize all HIV-infected patients with both AIDS and non-AIDS-defining neoplasms observed among all consecutive patients followed at the Infectious Diseases Unit of Pescara General Hospital, since 1991 through 2012. All cases were matched with equinumerous controls without neoplasia homogeneous for age, sex and AIDS diagnosis.Out of 626 patients consecutively assisted since 1991, 57 cases of malignancy (9.1%) were observed. Of these, 45 (79.0%) occurred in males; mean age was 43.6±9.3 years; 49 (86.0%) patients were diagnosed with AIDS. Tumors observed were: NHL, 17 (29.8%); SK, 13 (22.8%); HCC, 5 (8.8%); CPL, 6 (10.5%); Hodgkin's lymphoma, 4 (7.0%); solid tumors, 12 (21.1%), including 1 AIDS-defining tumor . Among these, 37 (66.1%) patients died; of them 14 (37.8%) had non-AIDS cancers. Cases were well matched with the 55 controls for sex (p=0.9), age (p=0.6) and AIDS diagnosis (p=0.6). In comparison with controls, CD4 nadirs were not different (153±151 in controls vs 136±154 cells/mmc), while CD4 at tumor diagnosis were very different between controls (463±283 cells/mmc) and cases . Among patients with malignancies, those who died had a non-significant reduction in CD4 counts (p=0.14); seemingly irrelevant were smoking status (p=0.9), working ability (p=0.4), HCV coinfection (p=0.4). Surprisingly, in patients co-infected with HBV, including HBsAg negative, antibody-positive subjects, tumors were significantly more frequent .Factors potentially relevant for carcinogenesis in the prolonged survival patients of the HAART era may include HBV coinfection in spite of the lack of active biochemical activity (HbsAg negative) in the majority of coinfected patients. The potential relevance of this finding deserves prompt assessment in a larger multicentric cohort.


The third author's name appears incorrectly in the citation. The correct citation is: Talman V, Tuominen RK, Boije af Gennäs G, Yli-Kauhaluoma J, Ekokoski E (2011) C1 Domain-Targeted Isophthalate Derivatives Induce Cell Elongation and Cell Cycle Arrest in HeLa Cells. PLoS ONE 6(5): e20053. doi:10.1371/journal.pone.0020053


She was born small for gestational age with no catch-up growth. Congenital anomalies including right dysplastic kidney and large secundum atrial septal defect were present. She had delayed development with microcephaly and dysmorphism, including triangular facies, epicanthic folds, low set ears, micronagthia, and brachydactyly. Ophthalmological assessment showed astigmatism, myopia, and left exotropia requiring surgical correction. Audiology assessment showed bilateral mild conductive hearing loss. Thyroid function, morning cortisol, serum calcium and renal function tests were normal. Metabolic disease workup including lactate, plasma for amino acid, urine metabolic screen, VLCFA, transferrin isoelectrofocusing and clotting profile were normal. CT and MRI brain were normal. Serum IGF-1 at 13 years old was 62nmol/L (+ 0.5SD). Growth hormone study with glucagon showed peak growth hormone of 32mg/L. Bone age was 12 years at chronological age of 12-year-10month. Radiograph of both hands showed brachydactyly but no proximal implantation of 1st digit. Genetic study show normal karyotype, but MLPA and FISH later confirmed heterozygous terminal deletion of 15q26.2 with the genetic defect compatible with IGF-1 receptor mutation. Growth hormone therapy was refused by the patient and mother. Breast development started at 12-year-4month and menarche started at 13-year-5month of age. The growth spurt was absent with peak growth velocity of only 5.5cm/year. On the latest follow-up at 13-year-9month of age, her height was 128.8cm (-4.7SDS).A 5-year-9month old Chinese girl presented with severe growth retardation, height SDS -4.17 and body weight SDS -2.37. The mid-parental height was 151.2cm (3Our patient displayed typical phenotypic features of IGF-1 receptor mutation of heterozygous deletion of 15q26.2 with severe growth retardation. The condition could potentially benefit from growth hormone treatment according to recent literatures [


Other studies have reported high rates of depression and anxiety among human T-lymphotropic virus type 1 (HTLV-1) infected subjects, and have even suggested that HTLV-I causes psychiatric disease.We interviewed HTLV-I, HTLV-II and demographically similar HTLV seronegative blood donors with the Mini-International Neuropsychiatric Interview (MINI). Prevalences of major depression and generalized anxiety disorder in each group were calculated and compared to published U.S. population data. Adjusted odds ratios (aOR) and 95% confidence intervals (95% CI) controlling for educational achievement, alcohol intake and self-reported health status were calculated with multivariate logistic regression.Major depression was diagnosed in 5 (5.4%) of 93 HTLV-I positive subjects  and 17 (6.6%) of 256 HTLV-II positive subjects , compared to 12 (2.1%) of 585 HTLV seronegative blood donors. The prevalence of major depression among infected subjects was comparable to the 6.7% prevalence in the U.S. general population. Generalized anxiety disorder was diagnosed in 5 (5.4%) HTLV-I positive subjects  and 12 (4.7%) HTLV-II positive subjects (OR = 1.65 95% CI 0.68-4.01), compared to 15 (2.6%) seronegatives and 3.1% in the U.S. general population.We observed slightly higher prevalence of major depression and generalized anxiety disorder among HTLV-I and HTLV-II subjects that was not significantly elevated after controlling for health status and other confounding variables. Comparison to U.S. population data suggested that these findings are in part explained by a “healthy blood donor effect” among our controls.


Improving trunk appearance is important for scoliotic patients. Selecting an appropriate rater is vital for effectively measuring this outcome. This study investigates whether a four-week intensive scoliosis-specific exercise programme results in improved patient body image and how this varies between patients, physiotherapists and an external scoliotic rater.82 patients  with IS and mean age 30.79 years (Range 10-81) were treated with a four-week intensive scoliosis-specific physiotherapy course (ScolioGold). Patients, 2 blinded physiotherapists and a blinded scoliotic rater rated patients’ body-image before and after treatment. Body-image was assessed using a 0-10 scale, for 5 elements .Mean total scores before treatment were; patients 28.51 (SD8.76), physiotherapists 22.94 (SD6.01) and external rater 20.55 (SD7.27) and after treatment were; patients 15.46 (SD7.40), physiotherapists 13.73 (SD5.88) and external rater 6.61 (SD4.10). Differences in patients (P), physiotherapists (T) and external rater(E) body-image scores were found to have statistically significantly improved after treatment using Wilcoxon-signed rank . ICC scores between P&T, P&E and T&E were; fair (0.28), slight (0.19) and moderate (0.58) before treatment and fair (0.34), fair (0.28), moderate (0.59) after treatment.Statistically significant improvements between pre-post treatment scores substantiate intensive exercise methods (ScolioGold), in the treatment of IS-related negative body image. Significant variation between patients’, physiotherapists’ and external rater’s scoring highlight the need for patients to rate body-image due to the subjectivity of this outcome measure, to ensure we adopt a client-centred care approach in our treatment goals to improve patient body-image.


There was an error in the title. The correct title is: HIV-1 Tropism Determination Using a Phenotypic Env Recombinant Viral Assay Highlights Overestimation of CXCR4-Usage by Genotypic Prediction Algorithms for CRF01_AE and CRF02_AG. The correct citation is: Mulinge M, Lemaire M, Servais J-Y, Rybicki A, Struck D, et al. (2013) HIV-1 Tropism Determination Using a Phenotypic Env Recombinant Viral Assay Highlights Overestimation of CXCR4-Usage by Genotypic Prediction Algorithms for CRF01_AE and CRF02_AG. PLoS ONE 8(5): e60566. doi:10.1371/journal.pone.0060566.


Therefore, many individuals are capable of mitigating the presence of autoantibodies and avoiding clinical disease. The objective of this study was to investigate unique features of SLE patients compared with autoantibody-positive (aAbn = 790) were screened by multiplex, bead-based assays for autoantibodies against: dsDNA, chromatin, ribosomal P, SS-A/Ro, SS-B/La, Sm, Sm/RNP, RNP, SCL-70, Jo-1, and centromere B. Sera from aAb+ individuals, matched aAb- controls and SLE patients were tested for 52 cytokines using multiplex bead-based assays and ELISAs. Hierarchical clustering was performed and Kruskal-Wallis tests with Dunn's multiple comparisons were compared including a false discovery rate. Immune cell phenotyping and phospho-flow cytometry was performed on peripheral blood mononuclear cells from aAb+ and aAb- healthy individuals. Unpaired t tests and Mann-Whitney tests were performed.Individuals  and matched aAb- healthy controls and SLE patients were selected for further analysis. While aAb+ healthy individuals displayed some similar cytokine patterns to SLE patients, they also displayed a suppressed cytokine profile that included decreased T-cell cytokines (IFNγ (P < 0.05), IL-5 (P < 0.05), IL-17F (P < 0.01)), decreased B-lymphocyte stimulator levels (P < 0.05), and increased IL-1 receptor antagonist levels (P < 0.001). An increased percentage of B cells was found in aAb+ healthy individuals compared with aAb- healthy controls (P = 0.039) that consisted of an increased percentage of memory B cells (P = 0.034) and a decreased percentage of transitional B cells (P = 0.028). Compared with aAb- healthy controls, B cells from aAb+ healthy individuals showed significantly increased pSTAT1 and pSTAT3 in response to IFNα stimulation (P = 0.037 and P = 0.040), increased pSTAT1 in response to IFNγ stimulation (P = 0.018), and increased pSTAT3 in response to IL-21 stimulation (P = 0.041). CD4+ T cells from aAb+ healthy individuals showed decreased pSTAT3 in response to IFNγ and IL-2 stimulation (P = 0.018 and P = 0.005). IFNα, IFNγ and IL-6 stimulation significantly increased pSTAT signaling in monocytes from aAb+ healthy individuals.Of the screened individuals, 57 individuals were positive for at least one autoantibody (7.2%), with 33.3% being Native American, 57.9% European American, 8.8% African American, and 89.5% female. European American aAb+ healthy individuals exhibit features of inflammation and loss of immune tolerance, they are capable of suppressing these responses by regulatory mechanisms probably no longer functional in patients with autoimmune disease.Although aAb


There was an error in the third subheading of the Results section ("African-Americans and Caucasians"). The correct sentence is: Single locus tests of association in the African-Americans identified seven significant allelic associations at IL12B polymorphisms rs3212227 (p = 0.002), rs2421047 (p = 0.008), rs2288831 (p = 0.008), rs10631390 (p = 0.001), rs3212220 (p = 0.003), rs6894567 (p = 0.007), and rs17860508 (p = 0.002) and three significant genotypic associations at rs3212227 (p = 0.05), rs10631390 (p = 0.05) and rs6894567 (p= 0.03) (Table 2b).”


Jatropha curcas leaf extracts.Drug-resistant HIV, a major global concern, warrants the development of novel anti-virals as alternative and inexpensive therapy. In the current study, we isolated potentially drug-resistant HIV and assessed previously unreported anti-viral activity of In vitro micro-co-culture was employed for virus isolation followed by drug susceptibility assays to determine resistance to Azidothymidine (AZT) and Lamivudine (3TC).Jatropha curcasleaves were extracted using Soxhlet apparatus. Methanolic (ME) and aqueous (AE) extracts were chosen for further study. Secondary metabolites were detected by High-Performance Thin Laye rChromatography and in vitro cytotoxicity established by MTT assay. Anti-viral activity was evaluated by p24 inhibitionin post- and pre-infection interaction studies.50 values ranging from 0.001418-82.73 µM AZT and 2.645-15.35 µM 3TC.Seven HIV isolates were obtained (isolation rate: 23.33%) with drug IC50 values were 32.07 mg/mL AE and 35.5 mg/mL ME.Tannins, flavonoids, saponins were detected in AE and flavonoids, saponins in ME while CC50 values were ranging from 0.0255-0.4137 mg/mL AE and 0.00073-0.1278 mg/mL ME; pre-infection studies (1 isolate) showed 100% p24 inhibition by ME and 97.19% p24 inhibition by AE at 25 mg/mL each.In post-infection studies (4 isolates), ICJatropha curcas leaf extracts showed effective anti-viral and probable entry inhibition activity against potentially drug-resistant HIV, which has not been reported earlier. We conclude that Jatropha curcasis a good candidate for anti-HIV therapy with further research.HIV isolates potentially resistant to AZT/3TC were obtained; genotypic drug resistance is being ascertained.


Significance of blood glucose (BG) control in ICU patients, especially in terms of mortality reduction, has been recognized in recent years. However, the relationship between BG profile and the severity, as well as BG target, is not clearly elucidated. A preliminary study was performed in order to clarify the relationship between BG profile and the severity of ICU patients.r) between the abovementioned SOFA scores and BG parameters were calculated using two-dimensional and linear regression analysis .Forty-seven patients were studied. The following parameters were calculated during first week after ICU admission. (1) Mean and maximum value of SOFA scores . (2) Mean, standard deviation, maximum, minimum, and difference of BG levels , respectively). BG levels were measured basically every 6 hours with capillary blood. (3) Correlation coefficients ((1) rt and rl (rt/rl) between SOFAmax and BG parameters: BGsd (0.48/0.36), BGmax (0.47/0.33), BGd (0.47/0.35), BGm (0.30/0.22), BGmin (0.21/0.36). (2) (rt/rl) between SOFAm and BG parameters: BGsd (0.45/0.33), BGmax (0.45/0.28), BGd (0.45/0.30), BGm (0.28/0.17), BGmin (0.17/0.29).(1) Variable and maximum BG levels during the first week , rather than mean and minimum BG levels , were related to the severity. (2) Suppression of the higher variable and maximum BG levels was considered to link to better outcome. (3) On the other hand, part of the severe patients seemed to have the lowest of those variable and maximum BG levels, judging from two-dimensional or parabolic correlations between those BG parameters and SOFA scores.


Reasons for screen failures are evaluated for three phase 1 HIV vaccine clinical trials recruiting healthy low-risk participants at the Perinatal HIV Research Unit: SAAVI102/HVTN073 and SAAVI103/HVTN086  and IAVIB003/HVTN091 (Ad26 and Ad35 ENV vaccines). Recruitment strategies involved a pre-screening programme, clinics and community outreach.Protocol-specific eligibility was determined using assessments of understanding, risk behaviour, medical history, physical examination, blood and urine testing, and for HVTN073 and 086, electrocardiograms. Descriptive analysis and multivariate logistic regression of age, trial group and gender were performed.Between June 2009-2012, 225 participants, median age 22 years(IQR:20-25) were screened. Overall 53% were ineligible, 60% of females vs. 51% of males (p=0.2). Site screening-to-enrolment ratios for 073, 086 and 091 were 2.1:1, 2.3:1 and 1.7:1 respectively. Medical abnormalities contributed 59% (n=70) of ineligibility reasons, chiefly urine abnormalities , abnormal ECG (n=12), raised liver enzymes (n=10), raised blood pressure (n=9), low white cells (n=8) and hepatitis B (HBsAg+ve) or C (anti HCV+) (n=7). Other criteria excluded 41%(n=49) e.g. incomplete screening before enrolment closure (n=16), high-risk sexual behaviors (n=15), inability to comply with protocol (n=11), enrolment in another study (n=3), substance abuse , and poor understanding (n=2). In multivariate analysis, increasing age  predicted ineligibility but gender did not . HVTN073&086 participants were more likely to be ineligible than HVTN091 .Screen failures in phase 1 vaccine trials in Soweto provide young people opportunities for care, especially through blood pressure, urine, risk behaviour and hepatitis B/C screening. Older participants and those in protocols stipulating ECG criteria were more likely to fail screening.


Gillisia limnaea Van Trappen et al. 2004 is the type species of the genus Gillisia, which is a member of the well characterized family Flavobacteriaceae. The genome of G. limnea R-8282T is the first sequenced genome (permanent draft) from a type strain of the genus Gillisia. Here we describe the features of this organism, together with the permanent-draft genome sequence and annotation. The 3,966,857 bp long chromosome (two scaffolds) with its 3,569 protein-coding and 51 RNA genes is a part of the  Genomic Encyclopedia of Bacteria and Archaea project. T (= DSM 15749 = LMG 21470 = CIP 108418) is the type strain of the species Gillisia limnaea . The. TheG. ln 4.9 µm , which i strains -34. MotiT are iso-C15:0, anteiso-C15:0, iso-C15:1, iso-C16:0, C17:0 2-OH, iso-C17:0 3-OH, iso-C17:1 ω9c, anteiso-C17:1 ω9c and summed feature 3 (containing iso-C15:0 2-OH and/or C16:1 ω7c) [T.The principal cellular fatty acids of strain R-8282 Genomic Encyclopedia ofBacteria andArchaea project [This organism was selected for sequencing on the basis of its phylogenetic position , and is  project . The gen project  and the G. limnaea strain R-8282T, DSM 15749, was grown in DSMZ medium 514 (BACTO Marine Broth) [et al. 2009 [e Broth)  at 20°C.al. 2009  for optial. 2009 .The genome was sequenced using a combination of Illumina and 454 sequencing platforms. All general aspects of library construction and sequencing can be found at the JGI website . PyroseqGenes were identified using Prodigal  as part The genome consists of two scaffolds with 3,558,876 bp and 407,981 bp length, respectively, with a G+C content of 37.6% . Of the G. limnaea R-8282T revealed the presence of three rhodopsin genes related to proteorhodopsin  and xanthorhodopsin  protein-encoding sequences, whereas a third rhodopsin protein sequence  seems to be truncated. Another finding was a set of genes involved in β-carotene biosynthesis, together with a gene encoding a β-carotene 15,15'-monooxygenase , an enzyme that oxidatively cleaves β-carotene into two molecules of retinal, which is necessary for rhodopsin function. PRs and XRs are photoactive transmembrane opsins that bind retinal and which belong to the microbial rhodopsin superfamily [E. coli cells for ATP synthesis [Salinibacter ruber M31T [Bacteria [Archaea [Genome analysis of erfamily . When exerfamily . This prynthesis  as well ynthesis . In contynthesis ,52, thatber M31T ,54. Its ber M31T , resultiBacteria ,57 or ba[Archaea .Flavobacteriaceae  [Krokinobacter sp. 4H-3-7-5 (AEE18495) [Dokdonia [The gene encoding the putative XR (Gilli_2340) of strain R-8282HQ04368)  and KrokEE18495) , which wDokdonia ,66 , indicating that Gillisia sp. strain CBA3202 does not belong to the species G. limnaea.Interestingly, no rhodopsin-encoding sequence could be detected in the genome sequence of  CBA3202 , which w CBA3202 . Digital CBA3202  between Bacteroidetes phylum were frequently found attached to aggregates [T several genes were detected that are thought to be involved in gliding motility (gldA (Gilli_1140), gldB (Gilli_2923), gldC (Gilli_2942), gldD (Gilli_1840), gldE (Gilli_1841), gldF (Gilli_3447), gldG (Gilli_3446), gldH (Gilli_2158), gldI (Gilli_0258), gldJ (Gilli_1638), gldK (Gilli_2747), gldL (Gilli_2748), gldM (Gilli_2749), gldN (Gilli_2750), espA (Gilli_3049), espB (Gilli_3050), remB (Gilli_2697), sprA (Gilli_2693) and sprE (Gilli_2130)). This observation indicates the possible gliding motility of strain R-8282T, but has never been reported in literature.Compared to free-living bacteria, representatives of the gregates  and durigregates ,71. Theygregates ,73. In s


There was an error in the title.The correct version of the title is: Specific Inhibition of the Redox Activity of Ape1/Ref-1 by E3330 Blocks Tnf-α-Induced Activation of Il-8 Production in Liver Cancer Cell LinesThe correct citation is: Cesaratto L, Codarin E, Vascotto C, Leonardi A, Kelley MR, et al. (2013) Specific Inhibition of the Redox Activity of Ape1/Ref-1 by E3330 Blocks Tnf-α-Induced Activation of Il-8 Production in Liver Cancer Cell Lines. PLoS ONE 8(8): e70909. doi:10.1371/journal.pone.0070909


Eradicating cHCV is necessary for the subsequent management of patients with HIV and every HIV/HCV co-infected patient should be considered for treatment. We describe differences between cHCV mono-infected and cHCV/HIV co-infected patients in baseline factors and outcome of cHCV-treatment with peginterferon alfa 2a + RBV in the worldwide largest cHCV cohort.Noninterventional prospective multicenter German cohort, started January 2008 and still recruiting. Interim analysis of cHCV patients, stratified for cHCV mono-infection and cHCV/HIV co-infection. The results are based on a cross-sectional analysis of all available data in April 2010.2, naïve/relapse/non-responder/re-infection: 86.4/3.8/4.5/5.3(CI), 88.0/6.1/5.3/0.6 (MI) %, source of infection (>1 answer possible): iv drug use 25.2(CI), 44.9(MI) %, sexual transmission 60.7 (CI), 4.1(MI)%, other 8.0 (CI), 24.0 (MI), unknown 13.1(CI), 33.0 (MI)%. 86.4 % of the co-infected patients received antiretroviral HIV-treatment (ART), 66.2 % of them had an HIV-RNA level below 50 copies/mL, median CD4-cells/µ count was 502. From those patients who finished treatment, 52.9% of the CI-Group and 67.7% of the MI-Group completed the planned course. Reasons for discontinuation (>1 answer possible) were non-response  and patient request . Other reasons were tolerability  and compliance issues .Treatment response rates, stratified by genotypes, were already available regarding RVR and EVR  and 4.993 cHCV mono-infected (MI). Main baseline- characteristics: 85.9% were GT1/4/5/6 patients in the CI-Group and 63.4% in the MI-Group, age was 41.0 (CI), 42.0 (MI) yrs, 89.7 (CI), 62.9 (MI)% were male, BMI was 22.8 (CI), 24.9 (MI) kg/mIn this preliminary analysis HCV/HIV co-infected patients seemed to respond similar according to RVR and EVR in GT1/4/5/6 as HCV-mono infected patients on HCV-treatment. Treatment discontinuation due to non-response and patient request was much more common in the co-infected group. Other reasons for discontinuation like tolerability and compliance are equal in both arms.A more detailed analysis, in particular the influence of the HIV-ART on HCV-therapy outcome, may help interpreting these data. An updated analysis will be presented.


Radical prostatectomy (RP) is frequently responsible for erectile dysfunction (ED). Post-RP patients often show insufficient response or treatment failures to PDE5 inhibitor therapy. This study was undertaken to evaluate the acute effects of the soluble guanylate cyclase (sGC) stimulator, BAY 60-4552 and vardenafil administered alone or in combination on erectile responses to electrical stimulation of the cavernous nerve (ES-CN) in rats with cavernous nerve (CN) crush injury-induced ED.Male Sprague-Dawley rats underwent laparotomy  or bilateral CN crush injury (n=57). After 3 weeks of recovery, erectile function was evaluated in urethane-anesthetized rats following ES-CN at different frequencies. The acute effects of intravenous (iv) injection of vehicle, vardenafil 0.03 mg/kg, BAY 60-4552 0.03 mg/kg or 0.3 mg/kg, or a BAY 60-4552 0.03 mg/kg + vardenafil 0.03 mg/kg combination were evaluated in CN crushed rats.Bilateral CN crush injury followed by a 3-week recovery period decreased erectile responses to ES-CN by about 50%. In CN crushed rats, both iv vardenafil 0.03 mg/kg and BAY 60-4552 at the tested dosings (0.03 or 0.3 mg/kg) increased erectile responses to ES-CN to the same extent: ΔICP/MAP at 10Hz ES-CN was 20.9± 1.3 % after iv vehicle, 25.3± 3.3 % (P<0.001) after iv vardenafil, and 26.3± 4.9 % and 26.6± 5.2 % after BAY 60-4552 0.03 mg/kg (P<0.01) and 0.3 mg/kg (P<0.001) respectively. The combined iv administration of vardenafil and BAY 60-4552 in CN crushed rats exerted additive effects and totally restored erectile responses to ES-CN equivalent to sham rats .The present study supports the concept that the combined administration of a sGC stimulator, BAY 60-4552 and vardenafil provides additive beneficial effects. Thus this combination could become a novel treatment option in ED patients with cavernous nerve injury showing insufficient response or treatment failures to PDE5 inhibitors.


AbstractNazeris Fauvel collected from Nabanhe Nature Reserve, Yunnan Province, are described under the names of Nazeris nabanhensis sp. n. and Nazeris caoi sp. n. The male sexual characters are described and illustrated. A key to the Nazeris species of Yunnan is provided. A map of the collecting sites is given.Two new species of the genus  Nazeris Fauvel (1873: 298) can be readily distinguished from other Paederinae by the labrum having four teeth at the front margin and the bi-lobed 4th tarsal segments. Up to the present, 51 species and subspecies of Nazeris have been recorded from China. Yunnan is a mountainous province located in Southwest China, from PageBreakwhich nine species of Nazeris have been described: Nazeris zhangi Watanabe & Xiao (1993: 130) from “Yu’an-shan near Kunming City”, Nazeris giganteus Watanabe & Xiao (1997:2) and Nazeris daliensis Watanabe & Xiao (1997: 7) from “Diancang shan Mts., Dali shi”, Nazeris alpinus Watanabe & Xiao (1997: 5) from “Mt. Yulongxue shan, Lijiang County”, Nazeris jizushanensis Watanabe & Xiao (1997: 9) from “Mt. Jizu Shan, Binchuan County”, Nazeris baihuaensis Watanabe & Xiao (2000: 312), Nazeris ishiianus Watanabe & Xiao (2000: 319) and Nazeris nomurai Watanabe & Xiao (2000: 316) from “Gaoligong Shan Mts., Baoshan area”, Nazeris huanxipoensis Watanabe & Xiao (2000: 318) from “Huanxipo, Tengchong Xian”. Only two species have become known from the three countries adjacent to Yunnan : Nazeris coomani Jarrige (1948: 40) (redescribed by Nazeris odzisan Watanabe (1996: 1) from “Mt. Tam Dao, Vinh Phu Prov.” (Vietnam).The genus Nazeris nabanhensis sp. n. and Nazeris caoi sp. n. The male sexual characters of the two new species are described and illustrated. A map .Nazeris species was not examined. The characters used in comparative remarks and keys are according to descriptions of ; postocular portion 1.96 times as long as eye length; punctation coarse, dense, and umbilicate; interstices reduced to narrow ridges. Antennae slender; relative length of each segment from 1 to 11: 42.0 : 15.0 : 29.0 : 23.0 : 22.5 : 22.0 : 19.0 : 17.0 : 15.5 : 14.0 : 20.0; relative width of each segment from 1 to 11: 12.0 : 7.5 : 6.0 : 6.0 : 6.0 : 6.0 : 6.0 : 6.0 : 6.0 :7.5 : 7.5.convex, oval, longer than wide (length/width = 1.20), narrower (pronotum/head = 0.93) and shorter (pronotum/head = 0.94) than head; prosternum with strong longitudinal median carina, which disappears behind anterior margin. Elytra shorter than wide (length/width = 0.91), distinctly shorter (elytra/pronotum = 0.74) and slightly narrower (elytra/pronotum = 0.97) than pronotum.PageBreakdian lobe in dorsal view tri-lobed, median part cone-shaped, two outer parts acute at apices, with little agnail in each outer side near apex; dorso-lateral apophyses slightly curved inward, distinctly widened near apex, extending beyond apices of median lobe.elongate, tergites without any microsculpture. Seventh sternite  trapezoiSeventh and 8th sternites simple. The other characters are similar to those of male.Nazeris daliensis Watanabe (1997: 7) from Yunnan Province in appearance, but it can be distinguished from the latter by the following characters: elytra slightly narrower than pronotum ; depth of excision of male 8th sternite nearly half of middle length of sternite ; apical part of median lobe of aedeagus in dorsal view tri-lobed . The new species can be distinguished from Nazeris coomani Jarrige (1948: 40) from Vietnam by head with umbilicate punctation (in Nazeris coomaniPageBreak punctation of head simple) and distinguished from Nazeris odzisan Watanabe (1996: 1) from Vietnam by elytra shorter than wide (in Nazeris odzisan elytra longer than wide); dorso-lateral apophyses of aedeagus extending beyond apices of median lobe (in Nazeris odzisan not extending to apices of median lobe).The new species is similar to The specific name is derived from the name of the type locality: Nabanhe Nature Reserve.urn:lsid:zoobank.org:act:3B251645-1B6B-4388-ACEC-4E5B42C4A858PageBreakParatypes 1 male, same data as holotype; 1 female, Jinghong City, Nabanhe Nature Reserve, Bengganghani, 1,900m, 1. V. 2009, Hu Jia-Yao & Yin Zi-Wei leg. SHNUC.CHINA: Holotype: Yunnan Prov.: male, Jinghong City, Nabanhe Nature Reserve, Bengganghani, 1,930m, 14. XI. 2008, Hu Jia-Yao & Tang Liang leg. Body length: 6.1–6.4 mm; forebody length: 3.3–3.6 mm. elongatesuborbicular, slightly longer than wide (length/width = 1.07); postocular portion 2.14 times as long as eye length; punctation coarse, dense, and umbilicate; interstices reduced to narrow ridges. Antennae slender; relative length of each segment from 1 to 11: 42.0 : 13.5 : 30.0 : 23.0 : 21.0 : 21.0 : 19.0 : 18.0 : 18.0 : 16.0 : 22.0; relative width of each segment from 1 to 11: 10.5 : 7.0 : 6.5 : 6.0 : 5.5 : 6.0 : 5.5 : 5.5 : 6.0 :6.5 : 7.0.PageBreak strong longitudinal median carina, which disappears behind anterior margin. Elytra slightly shorter than wide (length/width = 0.97), distinctly shorter (elytra/pronotum = 0.80) and slightly narrower (elytra/pronotum = 0.97) than pronotum.convex, oval, longer than wide (length/width = 1.19), narrower (pronotum/head = 0.88) and shorter (pronotum/head = 0.98) than head; prosternum withelongate, tergites without any microsculpture; densely and coarsely punctate. Seventh sternite  distinctSeventh and 8th sternites simple. The other characters are similar to those of male.Nazeris nabanhensis sp. n. from the same locality, but can be distinguished from the latter by the following PageBreakcharacters: postocular part more than twice as long as longitudinal diameter of each eye ; median lobe of aedeagus in dorsal view bi-lobed (in Nazeris nabanhensis tri-lobed); dorso-lateral apophyses of aedeagus not extending to apices of median lobe (in Nazeris nabanhensis extending beyond apices of median lobe). The new species can be distinguished from Nazeris coomani Jarrige (1948: 40) from Vietnam by head with umbilicate punctation (in Nazeris coomani punctation of head simple), and distinguished from Nazeris odzisan Watanabe (1996: 1) from Vietnam by elytra shorter than wide (in Nazeris odzisan elytra longer than wide); median lobe of aedeagus in dorsal view bi-lobed (in Nazeris odzisan not lobed).The present new species is similar in appearance to The species is named in honor of Mr. Guanghong Cao of Nabanhe Nature Reserve, who helped us a lot during field work.


There was an error in the citation. The correct citation is: Aka JA, Lin S-X (2012) Comparison of Functional Proteomic Analyses of Human Breast Cancer Cell Lines T47D and MCF7. PLoS ONE 7(2): e31532. doi:10.1371/journal.pone.0031532


The fifth author's name was spelled incorrectly. The correct name is: Max Schelker. The corrected citation is:Raue A, Schilling M, Bachmann J, Matteson A, Schelker M, et al. (2013) Lessons Learned from Quantitative Dynamical Modeling in Systems Biology. PLoS ONE 8(9): e74335. doi:10.1371/journal.pone.0074335In equation 7, many additional factors of 2 were added incorrectly. Please see the correct equation 7 here: In equation 8, '2A_0' should only read 'A_0.' Please see the correct equation 8 here:


Neonatal mice developed neurological disease and pulmonary dysfunction after an infection with a mouse-adapted human Enterovirus 71 (EV71) strain MP4. However, the hallmark of severe human EV71 infection, pulmonary edema (PE), was not evident.To test whether EV71-induced PE required a proinflammatory cytokine response, exogenous pro-inflammatory cytokines were administered to EV71-infected mice during the late stage of infection.After intracranial infection of EV71/MP4, 7-day-old mice developed hind-limb paralysis, pulmonary dysfunction, and emphysema. A transient increase was observed in serum IL-6, IL-10, IL-13, and IFN-γ, but not noradrenaline. At day 3 post infection, treatment with IL-6, IL-13, and IFN-γ provoked mild PE and severe emphysema that were accompanied by pulmonary dysfunction in EV71-infected, but not herpes simplex virus-1 (HSV-1)-infected control mice. Adult mice did not develop PE after an intracerebral microinjection of EV71 into the nucleus tractus solitarii (NTS). While viral antigen accumulated in the ventral medulla and the NTS of intracerebrally injected mice, neuronal loss was observed in the ventral medulla only.Exogenous IL-6, IL-13, and IFN-γ treatment could induce mild PE and exacerbate pulmonary abnormality of EV71-infected mice. However, other factors such as over-activation of the sympathetic nervous system may also be required for the development of classic PE symptoms. Enterovirus genus of Picornaviridae family. In general, EV71 infections are mild, such as hand, foot, and mouth disease and herpangina in young children. However, central nervous system (CNS) infections with life-threatening pulmonary and cardiac complications have occurred [Enterovirus 71 (EV71), a highly neurotropic, positive-sense single-stranded RNA virus, belongs to the occurred .Pulmonary edema (PE) and subsequent rapid onset cardiopulmonary failure are hallmarks of EV71 induced mortality . EV71-inOur previous studies showed that a mouse-adapted EV71 strain, EV71/MP4, could experimentally infect laboratory mice via oral (p.o.), intramuscular, and intracranial (i.c.) inoculation routes, resulting in CNS infection and death . Clinica7 PFU/ml. MP4 strains were tested by monoclonal antibodies for EV71 (mAb3324), EV71/coxsackievirus A16 (mAb3323), coxsackievirus A24 (mAb3302), coxsackievirus B3 (mAb3306), echovirus 9 (mAb3313), PV type 1 (mAb3331), PV type 2 (mAb3332), and PV type 3 (mAb3335)  using indirect immunofluorescence staining of infected RD cell cultures, and RT-PCR using specific primers for EV71. HSV-1/KOS, a clinical isolate strain of human simplex virus-1 (HSV-1)  was grown in Vero cells.Rhabdomyosarcoma (RD) cells  were maintained in Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal bovine serum, 2 mM L-glutamine, penicillin and streptomycin. Vero cells (ATCC) were maintained in DMEM containing 5% newborn calf serum, penicillin and streptomycin. Mouse-adapted EV71 strain MP4  was prop5 PUF/mouse) or HSV-1/KOS (2 × 102 PFU/mouse) through the fontanelles using a 26-gauge needle. Control mice were given culture medium. To systemically increase proinflammatory cytokine levels, mice were intraperitoneally (i.p.) injected at three days post-inoculation with recombinant mouse IL-6, IL-13, and IFN-γ   2 or 3 times within 48 h. Control mice were given bovine serum albumin (BSA). Mice were observed twice daily for clinical signs and mortality. Lung function and body weight monitored daily for one week. Lung weight/body weight analysis, histopathology, and immunohistochemistry were performed after these experiments. For i.c. microinjection, EV71/MP4 was bilaterally microinjected into the nucleus tractus solitarii  of 8-week-old ICR mice in a volume of 0.2 μl (3 × 107 PFU/ml) over 10 min through a 27-gauge stainless steel cannula connected to a 10-μl Hamilton syringe  driven by an injection pump . Mice were observed twice daily for clinical signs and mortality for 5 days. Clinical disease was scored as follows: 0, healthy; 1, ruffled fur and hunchbacked appearance; 2, wasting; 3, limb weakness; 4, limb paralysis; 5, moribund and death. The Institutional Animal Care and Use Committee approved all animal protocols.Specific-pathogen-free, 7-day-old ICR mice  were i.c. injected with 10 μl of EV71/MP4 . Readings were collected for 3 min after 3 min of resting in the chamber.After anesthetization with pentobarbital sodium , blood was collected after axilla dissection. The levels of IL-6, IL-10, IL-13, and IFN-γ in serum and noradrenaline in plasma of EV71-infected mice were determined using ELISA kits  and a noradrenaline EIA kit , respectively according to the manufacturer's instructions. The detection limits for IL-6, IL-10, IL-13, IFN-γ, and noradrenaline were 15.6, 31.25, 62.5, 31.25, and 0.027 pg/ml, respectively.Changes in vascular permeability in lungs were determined by measuring the increment of wet lung weight. Individual lung lobes were removed, blot-dried on gauze, and weighed using a balance with accuracy to 0.0001 gram. Data were expressed as the ratio of total wet lung weight to body weight.Animals were perfused with isotonic saline containing EDTA. The whole brains and lungs were removed and weighed. Half of the tissues were immersion fixed in 10% buffered formalin for 48 h, bisected, embedded in paraffin, and stained with hematoyxlin and eosin (H & E) or Nissl stain. The remaining tissue samples were frozen in a liquid nitrogen-cold hexane bath in 100% OCT compound . All samples were stored at -70° C until assayed.The presence of EV71 virions in cryosections of frozen tissues  was visualized by a previously described method [U tests. The results are expressed as means ± standard errors of the means (S.E.M.). A P value of < 0.05 was considered significant.The clinical scores, lung weight/body weight ratio, and numbers of EV71-positive and NeuN-positive cells were analyzed using either the nonparametric one-way analysis of variance (ANOVA) or Mann-Whitney 5 PFU/mouse), 7-day-old mice did not gain weight and developed clinical symptoms with diffuse emphysema but no evidence of PE in the lung , IL-13 (0.15 μg/mouse), and IFN-γ (0.8 μg/mouse) to mice 3 days after an i.c. inoculation of EV71 (two doses within 48 h). At this time the animals developed mild clinical symptoms with the presence of virus in the CNS. All the mock-infected BSA-treated mice gained weight normally Figure  without P = 0.0054, Figure P = 0.0318, Figure 2 PFU/mouse) prior to the administration of IL-6, IL-13, and IFN-γ. HSV-1 is a neurotropic virus and its infection is known to cause diffuse encephalitis in mice, mainly in tissues of the cerebrum and cerebellu [Weight loss in EV71-infected mice resulted in increased lung weight/body weight ratios, as compared with non-infected control mice . Immunostaining showed that EV71-positive cells accumulated at the ventral medulla (VM) over time Figure  and 4B. In the course of the development of a mouse model of human EV71 infection, we demonstrated that EV71 could spread from the gastrointestinal tract or muscle to and accumulate in the CNS, especially in the brainstem of mice after different routes of inoculation . FollowiClinical findings showed that increases in serum IL-1β, IL-6, IL-10, IL-13, TNF-α, and IFN-γ were associated with PE development in EV71 patients . In thisBased on the distribution of viral antigens and viral genomic sequences, EV71 is likely propagated throughout the CNS via motor pathways . Our preSurprisingly, PE did not developed in adult mice after a direct inoculation of EV71 to the NTS, an area known to contribute to the development of PE in rats upon injury ,25. In oBesides an over-stimulated proinflammatory response, sympathetic excitement has been proposed as another mechanism involved in the development PE in EV71 patients , other aCollectively, we demonstrated that IL-6, IL-13, and IFN-γ over-stimulation exacerbated pulmonary dysfunction and clinical symptoms, and provoked a mild PE in EV71-infected mice. A synergistic proinflammatory cytokine response and damage to specific brain regions, or more precisely specific neuronal cells, may be necessary for the development of EV71-induced PE.BSA: bovine serum albumin; EV71: Enterovirus 71; HSV-1: herpes simplex virus-1; PIF: peak of inspiratory flow; PEF: peak of expiratory flow; LC: Locus coeruleus; MRI: magnetic resonance imaging; MV: minute volume; NTS: nucleus tractus solitarii; PV: poliovirus; PE: pulmonary edema; TV: tidal volume.The authors declare that they have no competing interests.SWH participated in the design of the study, carried out the animal studies, performed the statistical analysis, and drafted the manuscript. YPL participated in the design of the study. YTH carried out the immunostaining studies. CHL carried out the intracerebral microinjection studies. JIC participated in design and coordinate the immunostaining studies. HYL participated in the design of the study. IJS participated in the design of the study. CKY conceived of the study, and participated in its design and coordination and helped to draft the manuscript. All authors read and approved the final manuscript.Figure 1S. Intracranial inoculation of EV71 resulted in CNS infection, clinical disease, and emphysema in mice. Seven-day-old ICR mice (n = 24) were intracranially inoculated with or without EV71/MP4 strain (4 x105 PUF/mouse). Body weight (A) and clinical disease (B) were then monitored daily after infection. Lung tissues were collected for general morphological analysis (H & E stain) . Clinical disease was scored as followed: 0, healthy; 1, ruffled hair, hunchbacked or reduced mobility. 2, wasting; 3, limb weakness. 4, limb paralysis. 5, death. Bars: 1.0 mm. Note moderate emphysema but not pulmonary edema was observed in the EV71-infected mice (arrowheads).Click here for fileFigure 2S. Exogenous IL-13 treatment exacerbated pulmonary dysfunction in EV71-infected mice. Seven day-old ICR mice (n = 12) were intracranially inoculated with EV71 (4 × 105 PFU/mouse) followed by an intraperitoneal injection IL-13 at days 3 and 4 post inoculation. Change in pulmonary functions of mice were monitored daily. Ctrl: culture medium; BSA: bovine serum albumin; PIF: peak of inspiratory flow; PEF: peak of expiratory flow; MV: minute volume; TV: tidal volume. Data represent means ± S.E.M. *, P < 0.05 and **, P < 0.01.Click here for file


Lipoic acid (LA) stimulates production of an immunomodulatory molecule, cAMP, that may have therapeutic benefit in multiple sclerosis (MS). The study sought to determine the bioactivity of two forms of oral LA, racemic (R/S-LA) and R-LA, to identify factors that may improve the therapeutic effectiveness of LA in MS.Participants met the following criteria: age 18-70 years and a definite multiple sclerosis diagnosis. Consenting participants were randomized to 2 groups: R/S-LA (n=20) or R-LA (n=8). Blood was collected at baseline, 5, 10, 15, 30, 60, 90, 120, 180, 240, and 300 minutes after ingestion of a single 1200 mg LA dose. Bioactivity was determined by measuring immune cell cAMP levels (pmol/mg) at baseline and 240 minutes post ingestion. Group differences were analyzed by repeated measures analysis of variance (cAMP) and t-test (pharmacokinetics).For R/S-LA, mean baseline cAMP levels were 8.6 (SE 0.83) pmol/mg protein, which increased to 14.1 (SE 1.7) 240 minutes post-ingestion. For R-LA, baseline cAMP levels were 5.7 (SE 0.54), which decreased to 4.7 (SE 0.41) 240 minutes post-ingestion. The mean change in cAMP levels were different between groups, p<0.01. The two groups showed no differences in serum LA levels at 240 minutes (p=0.29), but showed a difference in the mean AUC (min*mcg/ml): R/S-LA is 681.8 (SE 83.4) and R-LA is 389.5 (SE 43.9) (p<0.01). Tmax (minutes) between groups differed: R/S-LA was 81.0 (SE 8.9) and R-LA was 13.1 (SE 2.7); p<0.001.At 1200 mg oral dose and comparable serum LA levels at T240, R/S-LA showed higher cAMP levels compared to R-LA. Since R-LA had an earlier Tmax, it is plausible that increases in cAMP may have occurred at earlier undetected time-points. This pilot study warrants further investigation as differences between R-LA and R/S-LA in bioactivity and pharmacokinetics would impact clinical trial design and patient care.


Elevated signal intensity (SI) in T2w images is often designated as area-at-risk (AAR) following acute/sub-acute MI. While AAR has been qualitatively associated with reductions in wall thickening (WT), quantitative information between the two is not available -3. QuantIn an animal model, quantify the:1) Effect of SI threshold on estimating AAR,2) Reduction in WT with AAR at increasing SI thresholds, and3) Correlation between AAR and percent scar.Acquisition Protocol: Basal, mid, and apical slices in short axis orientation were obtained in a pig (n=14) AMI model (LAD occlusion) at 3.0T :a) Cine SSFP: TR/TE/α = 3/1.5 ms/45°; acquired temporal resolution: 12 ms.b) Delayed enhancement MRI (DE-MRI): 10 min after 0.2 mmol/kg of contrast, scar was visualized using a gated IR-TFE sequence with inversion delay (TI) adjusted to null normal myocardium.c) Dual-IR T2W imaging (BB): Effective TE/TR: 80 ms/2*RR interval; TSE readout.Data Analysis: Myocardial region was manually segmented from cine, DE-MRI, and BB images Figure  using MA1) Normalized wall thickness (nWT) per segment = (WTES - WTED)/( WTED), where ED = End-Diastole, ES-End-Systole.2) Segmental scar burden, defined as ratio of pixels designated as scar to total number of pixels in each segment of DE-MRI. Scar pixel is one with SI > [mean + 5*Standard Deviation (SD) of normal remote myocardium].3) Segmental AAR, defined as regions in BB images with SI > mean + n*SD of normal remote myocardium .1) As a share of total myocardium, AAR burden was significantly higher (43 to 57 %) than scar burden (30 %) (Table 2) Spatially, AAR overlapped, and extended beyond scar regions.3) Reduction in segmental nWTwas lower in AAR regions that did not overlap scar region compared to those segments that did(108 ± 36 % vs 91 ± 29 %, Figure In sub-acute AMI, AAR is significantly larger than scar. In non-overlapping regions of AAR and scar, nWT, while diminished compared to normal remote myocardium, is significantly better than in regions of scar.NA


The word "Hydroxypropyl" is misspelled in the article title. The correct title is: Enhancement of Naringenin Bioavailability by Complexation with Hydroxypropyl-β-Cyclodextrin.The correct citation is: Shulman M, Cohen M, Soto-Gutierrez A, Yagi H, Wang H, et al. (2011) Enhancement of Naringenin Bioavailability by Complexation with Hydroxypropyl-β-Cyclodextrin. PLoS ONE 6(4): e18033. doi:10.1371/journal.pone.0018033Hydroxypropyl is also misspelled in the fifth sentence of the abstract. The fifth sentence should read: Hydroxypropyl-β-cyclodextrin (HPβCD), specifically, increased the solubility of naringenin by over 400-fold, and its transport across a Caco-2 model of the gut epithelium by 11-fold.


Topiramate is the only approved oral preventive drug for chronic migraine (CM). However, we usually use other preventive drugs of prevention of frequent episodic migraine. Zonisamide is a neuromodulator that has showed efficacy in prevention of CM.To evaluate the efficacy of zonisamide after three months of therapy in CM patients (IHS-2006 criteria) that present inefficacy/intolerance/contraindication to topiramate, sodium valproate, â-blocks and flunarizine.Doses ZNS: 50-200mg. Primary end-point: Number of migraine days-NMD: Ineffective response-Inef(reduction of days<50%), good-G(50-75%), excellent-Exc(>75%). Secondary end-points: number of migraine episodes-NME; number of headache days-NHD; drug overuse; consumption of triptans and NSAIDs; EVA and MIDAS score, effective mean dose of ZNS, adverse events.We prospectively included 27 patients (May 2011-May 2012), 85.2% women. Twelve patients (44.4%) presented 16 adverse events (100% mild). Four of them-14.8% left the therapy. NMD, in the 23 patients who finished the three months follow-up, was Exc-39.1%, G-43.5%, and Inef-17.4%; NME was Exc-30.4%, G-43.5%, and Inef-26.1%; and NHD was Exc-34.8%, G-39.1%, and Inef-26.1%. Drug overuse disappeared in 47.8% of overusers. The consumption of triptans and NSAIDs decreased 54.3%, and 65.7%. The EVA score decreased 3.7 points (56.2%), and MIDAS scale score decreased 14.6 points (48.7%). Effective mean doses of ZNS: 106.6mg/night.Zonisamide presents a good profile of efficacy (70.3% of responses) and an acceptable tolerance. It could be a useful therapeutic option in CM patients intolerants, refractory, or with contraindications for topiramate, and the other drugs preventive drugs of migraine.


The proposed contrast-enhanced first-pass perfusion cardiovascular MR (CMR) protocol integrates some recent technical MRI advances towards quantitative analysis of perfusion CMR images: fast multi-slice pulse sequence , robust To evaluate an integrated first-pass perfusion cardiovascular MR (CMR) protocol designed to determine absolute contrast-agent concentrations in blood and tissues.1 shortening expected in blood and wall. First-pass perfusion CMR was performed in 7 volunteers . A signal-to-concentration model was applied to calculate Gd-DTPA concentrations in blood and tissues [1 relationship based on Bloch equation in the center of k-space. Gd-DTPA concentrations were calculated assuming: fast water exchange condition [1=3.8L.mmol-1.s-1[1 measured with a multi-point SR fit. TurboFLASH imaging parameters included: FOV=350mm×315mm, slice thickness=8mm, matrix=160×144, in-plane resolution=2.2mm×2.2mm, TE/TR=1.2/2.4ms, flip angle 10°, temporal resolution=114ms, tSENSEx3, centric k-space trajectory, and receiver bandwidth=1008Hz/pix. Total image acquisition time was 523ms for the acquisition of 4 slices, namely aortic root and SA base, mid, and apex levels, with respective TD values 50-164-278-393ms. Contours for the blood and left ventricle were drawn manually, and the myocardium was divided into 6 (base-mid) or 4 (apex) standard segments.A multi-slice saturation recovery (SR) pulse sequence with sequential SR time delays (TD) after a non-selective saturation pulse  was impl tissues ,5. A proondition , longituRepresentative images at peak contrast in blood and myocardium are shown Fig.The proposed integrated first-pass perfusion CMR protocol at 3T produced AIF and myocardial wall Gd-DTPA concentrations consistent with previously published results. Future work includes evaluation of the integrated protocol in cardiac patients.


Biventricular size and function have been studied extensively in patients after tetralogy of Fallot (TOF) repair, but little is known about atrial size and function. The atria play a crucial role in ventricular filling during diastole, and abnormalities in atrial size and function may reflect ventricular diastolic dysfunction. Diastolic dysfunction may precede systolic dysfunction and may therefore play an important role in the early detection of ventricular dysfunction.We assessed bi-atrial size and function in patients after TOF repair, and evaluated relationships with biventricular systolic and diastolic function, and clinical parameters.51 patients (21±8 years) and 30 healthy controls (31±7 years) were included and underwent magnetic resonance imaging. Patients also underwent exercise testing, and biomarker assessment. Bi-atrial and biventricular size, systolic and diastolic function were assessed from time-volume curves (figure 2 (patients) vs. 28±8 ml/m2 (controls), p=0.001); RA reservoir function, RA early emptying fraction, and the RA early-to-late-emptying ratio (E/A ratio) were decreased (RA E/A ratio: 1.1±0.5 (patients) vs. 1.9±0.9 (controls), p<0.001). Patients had larger right ventricular (RV) volumes, lower biventricular ejection fraction and prolonged biventricular deceleration time (Dt) (RV Dt: 0.24±0.10 (patients) vs. 0.13±0.04 (controls), p<0.001). Left atrial (LA) maximal volume and LA early emptying fraction were decreased. Left ventricular (LV) E/A-filling ratio was increased (LV E/A-ratio: 4.2±3.7 (patients) vs. 2.7±1.3 (controls), p=0.008).In patients, right atrial (RA) minimal volume (min.vol.), RA pump function, and RA late emptying fraction were increased (RA min.vol.: 34±8 ml/m2 slope: 32±4 (patients with EDFF) vs. 28±6 (patients without EDFF), p=0.014). Patients with abnormal RA emptying (reservoir function <30% and pump function >24%) had higher NT-proBNP levels  vs. 7±7 pmol/l , p=0.002) and worse exercise capacity. RA min.vol. was positively associated with RV end-diastolic volume .Patients with end-diastolic forward flow (EDFF) had larger RA and RV size, higher RA pump function (RA pump function: 27±8% (patients with EDFF) vs. 20±7% (patients without EDFF), p=0.003), higher N-terminal prohormone brain natriuretic peptide (NT-proBNP) levels, and higher ventilatory response to carbon dioxide production (VE/VCOIn TOF patients with good clinical condition and moderate RV dilatation, abnormal bi-atrial function and abnormal biventricular diastolic function is common. Abnormal RA emptying was associated with impaired clinical outcome, as was the presence of EDFF. These parameters, together with RA enlargement, could serve as useful markers for clinically relevant RV diastolic dysfunction.This research was funded by the Netherlands Heart Foundation: grant 2006B095.


ICU patients (ptes) account for a large proportion of HI. Its epidemiology allow us to identify key issues and prioritize interventions. We determined the incidence of HI in ICU in Uruguay and described specific locations, dispositive-associated rates and microorganisms.A national surveillance system for HI was implemented in 2006; prospective surveillance was performed using NNISS criteria. It is mandatory, to record online and send their data to the Ministry of Health. Data are audited and results published annually.S. aureus , A. baumanii , Ps. aeruginosa  and K. pneumoniae .We present 2010 results of medical-surgical ICUs. 53 hospitals reported. 13611 ptes were surveyed (99541 ptes-days). 2340 HI episodes were reported (density of incidence rate (ID) 23.5/1000 ptes-days and cumulative incidence 17.2%). Ventilator-associated pneumonia (VAP) (34%), bronchitis (B) (28%), catheter-associated urinary tract infection (CAUTI) (21%) and central-line associated bacteremia (CLAB) (8%) were the main infectious sites. VAP ID was 14.2/1000 ventilator-days (dispositive utilization (DU) 0.5, secondary bacteremia (SB) 5.3% and contributor mortality (CM) 19.7%), CLAB ID was 1.9/1000 catheter-days  17.7%) and CAUTI ID was 5.8/1000 catheter-days  3.7%, (CM) 5.1%). Microorganisms were Respiratory tract infections are the main problem. ICUs predominance of Gram Negative Bacilli in these infections may suggest the importance of exogenous sources. VAP and CAUTI rates are also high, diminish its incidence is priority for the national program.None declared.