Another study [Rektorova et al. 2005] assessed the cognitive functions of 41 PD patients in treatment with levodopa before and after 8 months of an add-on therapy with pramipexole or pergolide: any difference was found between cognitive performance at the baseline and after the therapy with dopamine agonists. A similar finding was reported by a study [Relja and Klepac, 2006] that evaluated a sample of 16 medicated PD patients during 12 months of treatment: patients treated with levodopa alone and patients receiving

pramipexole as add-on therapy to Inhibitors,research,lifescience,medical levodopa did not cognitively differ at the baseline and at the follow-up neuropsychological assessment. Table 2. Studies investigating chronic cognitive effects of levodopa and dopamine agonists in PD. The order is chronological. These findings preliminary showed that: (1) chronic dopaminergic Tanespimycin molecular weight stimulation at least do not have Inhibitors,research,lifescience,medical negative mid-term effects on cognitive functions of PD patients; (2) levodopa and dopamine agonists do not have differential mid-term effects on cognitive functions of PD patients. In these studies patients

were followed only for brief periods (from 6 months to 2 years), while dopaminergic drugs may be taken by PD patients for many years: this suggests that the long-term Inhibitors,research,lifescience,medical effect of chronic dopaminergic stimulation with levodopa or dopamine agonists on cognitive functions of PD patients is actually almost unknown. Discussion This article aimed at reviewing Inhibitors,research,lifescience,medical empirical

evidence on the cognitive effects of dopaminergic drugs in PD. The study of cognition in patients with PD is of particular interest because the spatiotemporal progression of dopamine depletion during the course of the disease provides a special model for assessing dopaminergic effects on neural systems with differential baseline dopamine levels. The interaction between degrees Inhibitors,research,lifescience,medical of dopamine depletion (dorsolateral versus orbital frontostriatal circuits; left hemisphere versus right hemisphere) and different dopamine replacement therapies may produce different cognitive profiles at different stages of the disease: this complex clinical picture could partially Org 27569 explain why findings of studies on cognitive functions of PD patients are usually heterogeneous also within the same cognitive domain. Considering different possibilities of empirical investigation of cognitive effects of dopaminergic drugs in PD in relation to drug (levodopa or dopamine agonist), temporal interval (acute or chronic) and cognitive domain, we found that empirical evidence is almost focused on acute effects of levodopa administration on prefrontal executive functions.

It was proposed that the A-CPR unit would assist during CPR because the number of selleck inhibitor Paramedics at the scene at rural cardiac arrest is often less than metropolitan areas [12]. This study was undertaken to compare the rates of survival to hospital between C-CPR and A-CPR in adults following OHCA in this setting. Methods Study design This study used a matched case–control method (1 case: 4 controls where available [min 2, max 4 controls]) [13] using prospectively Inhibitors,research,lifescience,medical collected case data matched to Victorian Ambulance Cardiac Arrest Registry (VACAR) data. The VACAR database contains

case data on all OHCA attended by Emergency Medical Services (EMS) in the state of Victoria, Australia. All adult (>18years of age) OHCA cases using the A-CPR (AutoPulse®, Zoll Medical Corporation, Chelmsford, Inhibitors,research,lifescience,medical MA, USA) were matched to cases receiving C-CPR. All cases were matched by known predictors of survival [14]; age (+/− 5years), gender, response time (defined as ‘at patient’ – ‘call received’ time,+/− 5 minutes), presenting cardiac rhythm (VF / VT / PEA / Asystole), and the presence of bystander CPR. Paramedics were trained to commence manual chest compressions whilst setting up the A-CPR device and to apply the device Inhibitors,research,lifescience,medical with minimal interruption to chest compressions. All controls were selected

from regional settings similar to those of the A-CPR trial sites. The primary outcome Inhibitors,research,lifescience,medical measure was survival to hospital (defined as pulse on arrival to hospital in the absence of chest

compressions). The Monash University Human Research Ethics Committee approved the study. Setting The A-CPR was introduced into three mixed urban / rural settings of Ambulance Victoria. The three settings were the provincial city of Geelong (population 208,139), and the townships of Shepparton (population 58,870) and Mildura (population 45,703). The regions employ Inhibitors,research,lifescience,medical a two-tier response system comprising Advanced Life Support (ALS) paramedics who have a range of advanced life support skills (laryngeal mask airway, intravenous adrenaline, intravenous fluids) and Mobile Intensive Care Ambulance (MICA) paramedics who are authorised to perform endotracheal intubation and administer a range of cardiac drugs, including adrenaline, amiodarone and atropine. (see http://www.ambulance.vic.gov.au) The responding skill set is determined by a computerised call taking and dispatch system (Advanced Medical Priority Dispatch System, Salt Lake all City, Utah), and dispatches the closest and most appropriate resource based on the nature of the case. A-CPR devices were placed on ambulance vehicles staffed by ALS paramedics, MICA paramedics, or mixed ALS/MICA paramedic crews as these vehicles were more likely to arrive first at scene. Statistical analysis Continuous data was reported as medians (IQR) due to non-parametric distribution, and frequencies are expressed as percentages.

The study also explored whether adenoma diagnosis might represent a ‘teachable moment’ (Lawson and Flockie, 2009), and how this moment might be better utilised as a prevention opportunity. Prospective participants aged 50–74 and living within Tayside, Scotland, who had undergone adenoma removal within the last three months were identified retrospectively from hospital records and invited to participate in a focus group. All patients were advised of the study through a letter of introduction sent by the colorectal nurse specialist responsible for screening. This letter was then followed two weeks later by a written

invitation from the research team. Those interested were telephone screened for BMI (> 25 kg/m2) and availability. Recruitment selleck chemicals llc Autophagy Compound Library was from a mix of urban and rural populations and a range of social backgrounds, as assessed by the Scottish Index of Multiple Deprivation (SIMD) which defines deprivation at the postcode level on the basis of income, employment, health, education, skills, housing, geographical access and crime (Scottish Government,

2009). Written informed consent was obtained prior to the focus groups. A discussion guide was developed containing open-ended questions around key areas including experiences of adenoma diagnosis and treatment, understanding of adenoma and its relationship to lifestyle and disease, and how participants

would feel about being offered advice and support for making behaviour changes, particularly in relation to healthy eating, physical activity and weight loss. Focus groups were moderated by an experienced researcher and digitally audio-recorded with participants’ consent. Recorded discussions were transcribed and a thematic analysis was conducted. The approach drew on both the deductive and inductive approaches to thematic analysis (Braun and Clarke, 2006): themes relating to the pre-specified research questions (for example, attitudes towards receiving lifestyle advice) were actively sought in the data, whilst further themes Cell press evolved from the coding process itself (for example, the perceived contradiction between receiving an all-clear message during inhibitors screening and then being offered advice for lifestyle change). Ethical approval was given by NHS Tayside’s Committee on Medical Research Ethics. In total, 135 men and women were invited to take part. CRC screening nurses provided a list of the most recent 105 eligible participants, 31 females and 74 males, of whom 8 females and 22 males agreed to be contacted. A further 30 were subsequently invited, including purposive over-sampling of females to improve representation of women in the study. Of these 135, 38 agreed to be contacted.

Assays based on monoclonal antibodies (mAb) and lectins have shown that expression of Tn in breast cancer is associated with high grade ductal carcinomas [3,75,77]. Its expression was found to significantly predict a shortened 5-year disease free survival, a positive lymph node status and increased combined histological stages [75]. Another study found that Tn antigen expression detected by Tn-specific

Inhibitors,research,lifescience,medical Vicia villosa lectin (VVL-B4) in ovarian cancer was correlated with increased malignancy, metastatic progress and low patient survival [2]. Increased Tn antigen expression is also correlated with metastatic potential and poor prognosis in cervical cancers [78,79]. Nevertheless, the mechanisms linking Tn antigen expression to cancer progression still remain unknown. Tn on MUC1 was shown to be bound by the macrophage galactose-type lectin on macrophages and dendritic cells [80] and Tn presence may enable the tumor to escape immunosurveilance [81]. Beside its aberrant function the genetic basis causing

Inhibitors,research,lifescience,medical Tn appearance on O-glycoslyated proteins is still under investigation. It is becoming evident that the loss of functional COSMC is one molecular explanation for the increased Tn expression on human cancer cells [82]. COSMC is an essential chaperone for correct protein O-glycosylation and loss of COSMC is associated with loss of T-synthetase and increase in Tn antigen [83]. In cervical cancer a deletion Inhibitors,research,lifescience,medical of functional Inhibitors,research,lifescience,medical allele (LOH) leads to complete absence of COSMC and increased expression of Tn and sTn [82]. Early pioneering work by Springer and colleagues reported experiments for long-term anti-carcinoma vaccination and treatment of breast cancer [84] without delivering additional proof. Tn expression has been linked to tumor progression and targeted cancer treatment which has been used for anti-cancer vaccination and

treatment of breast cancer [64]. Carbohydrates alone do generally not activate T lymphocytes and have therefore reduced immunogenicity [85]. Inhibitors,research,lifescience,medical The increased immunogenicity can be achieved by linking Tn to carrier protein such as selleck compound keyhole limpet haemocyanin (KLH) [86], MUC1 peptide [87,88], most or the use of immunological adjuvants such as saponin [89], forming glycoconjugates to generate anti-glycan antibodies. A pilot study in a cohort of epithelial ovarian, fallopian tube, and peritoneal cancer showed an induced prevalently IgM-antibody response to a heptavalent vaccine including Tn and Tn-MUC1. Only Tn-MUC1 revealed both IgM and IgG response [90]. These observations are in concordance with another more recent study where natural anti-glycan antibodies were detected using a glycopeptide array [25]. This clearly indicates recognition of Tn by the cognate immune system. Despite the chemical simplicity of Tn antigen, its antigenetic structure is considered to be rather complex and recent data suggest that Tn antigen antibody binding capacity is determined by the peptide context of Tn antigen [91].

The European Resuscitation Council (ERC), the American Heart Association (AHA) and other international emergency medical organisations published their guidelines for cardiopulmonary resuscitation in 2005 and 2010 [1,8-10]. As a reasonable compromise between maximised periods of uninterrupted ECC, interposed ventilations and rescuer fatigue the recommended compression-ventilation ratio (CVR) for adults was changed #selleck chemicals keyword# from 15:2 to 30:2 in 2005 [4]. Subsequent studies comparing the two CVRs gave conflicting results. While participants of one study claimed 30:2 to be more exhausting, other

investigators found that the quality of ECC did not decrease with the 30:2 ratio during a 10-minute, single-rescuer scenario [11,12]. The aim of this prospective, randomised, manikin-based, Inhibitors,research,lifescience,medical cross-over study was to investigate the impact

of the rescuers’ physical fitness, biometry and gender on the quality of ECC using CVRs of 15:2 and 30:2. Furthermore, we aimed to determine objective parameters of physical fitness that reliably predict the quality of ECC. Methods Study participants After obtaining the approval of the Ethics Committee of the Medical Faculty of the Georg-August-University, Göttingen, we recruited, prior to the publication of the updated guidelines for cardiopulmonary resuscitation in 2010, 30 male and 10 female volunteers with written informed consent from Inhibitors,research,lifescience,medical the Göttingen Fire Department (paramedics) and the Göttingen University Hospital (intensive-care nurses and physicians) to this exploratory study. All participants were competent in Basic Life Support (BLS) Inhibitors,research,lifescience,medical and certified Advanced Life Support (ALS) providers. No

participant was taking cardiovascular or respiratory medications, had recently underone a surgical intervention, had suffered any cardiopulmonary disease or had any other cause of limited physical endurance. Part I: Physical fitness test The physical fitness of all Inhibitors,research,lifescience,medical participants was evaluated by two different consecutively performed ergometric endurance tests two days before the ECC trials. First, a cycle ergometry (ERG 551, Bosch, Stuttgart, Germany) test was used following a protocol with a stepwise increase of physical strain every three minutes that started Phosphoprotein phosphatase at 50 watts and was increased by 50-watt steps up to a minimum strain of 150 watts. If the participant’s heart rate (HR) did not reach 100 beats per minute (bpm) at the end of the 150-watt step, a fourth step of 200 watts was added. Depending on the HR at the 50 – 150 – (or 200-) watt steps, a final maximum step was individually defined in order to reach a HR of 170 bpm. The pedal rate had to be kept constant at 50-60 revolutions/min. The workload required to reach a HR of 170 was determined as the personal watt capacity (PWC170), which represents a validated standard parameter for physical fitness in sport physiological investigations [13,14].

two-minute frames in study [12]) or by the lack of subgroup analyses. Indeed, the reduction of ECC depth over time in Jantti’s study failed to reach significance level but showed an analogous tendency (p = 0.079). According to the participants’ subjective perception, 30:2 was more exhausting but was also rated as more comfortable.

This confirms the subjective evaluation of participants by Deschilder et al. [11]. Our findings may be attributed to the frequency of interruption of ECC by interposed ventilations. The model There is an ongoing discussion as to Inhibitors,research,lifescience,medical whether standard resuscitation manikins and manikin-based scenarios may sufficiently reflect clinical reality [31]. First, in contrast to a linear relation Inhibitors,research,lifescience,medical in manikins, there is a rather non-linear relation between compression depth and force to be applied to the human chest [32]. Secondly, rescuers, although physically capable of performing effective ECC, may refrain from performing correct ECC because of fear of injuring the patient, particularly when the patient’s chest is rather stiff. Nevertheless, controlled investigations on the technical quality of ECC related to variable conditions are usually performed on resuscitation manikins [6,12,33,34]. Their mechanical properties facilitate training and assessment

of the characteristics of chest compression, decompression and rate [35]. Factors that do have an impact on the quality of ECC, such as BMI, Inhibitors,research,lifescience,medical physical fitness and gender remain the

same irrespective of the depth-force relation. Furthermore, the average force needed to compress a patient’s elastic chest to the recommended minimum Inhibitors,research,lifescience,medical depth of 38 mm has been determined to be 27.5 ± 13.6 kg [32]. The force-depth relation of the manikin used in this study (32.5 kg for 38 mm) accurately reflects this clinical reality. Moreover, the stressful setting of a clinical resuscitation could distract healthcare providers from focusing their attention on the correct performance of ECC, hence physical fitness and biometric parameters may selleck kinase inhibitor unconsciously influence the quality Inhibitors,research,lifescience,medical of ECC even more. Limitations We are aware of the limited number of female participants, which Thiamine-diphosphate kinase may have prevented us from gaining significance levels of p < 0.05 in several tests and may have caused a bias in evaluating the entire cohort. However, gender-based analyses revealed parallel results for male and female rescuers. As our cohort consisted of professional healthcare providers, our results may differ from those found among laypersons. Furthermore, our participants only imitated rescue breaths, and fatigue during actual CPR with correctly provided rescue breaths or during continuous ECC (e.g. in the context of hands-only CPR or during continuous ECC with a secured airway) might therefore be different, Moreover, our study was performed prior to the publication of the updated 2010 guidelines, and the correct compression depth was therefore defined as 38-51 mm according to the 2005 guidelines.

2 The syndromal heterogeneity of the diagnostic constructs makes it impossible to demonstrate a potential

syndromal specificity of a drug. Historically, drugs have been developed empirically on the basis of clinical observations. The discovery of chlorpromazinc for the treatment of schizophrenia in the early fifties by Delay and Deniker,3 and of imipramine for depression a few years later by Kuhn4 are such examples. On the other hand, new psychopathological syndromes have been identified by observant clinicians who recognized the unique actions of psychotropic drugs like clomipramine for the treatment of specific disorders such as obsessive-compulsive disorder (OCD)5 or imipramine for panic disorders.6,7 Unlike other medical Inhibitors,research,lifescience,medical conditions, the etiology and pathophysiology of psychiatric disorders

remain unknown. This is true despite the recent advances in the understanding of the function Inhibitors,research,lifescience,medical of the central nervous system (CNS) and in the field of biological psychiatry. Neurotransmitter imbalances in some areas of the CNS as well as neuroanatomical and neurophysiological abnormalities have been hypothesized to explain most of these psychiatric disorders, but this hypothesis has failed to be conclusively demonstrated. However, as no rational alternative explanation has been advanced for these disorders, the current pharmacological approach to Inhibitors,research,lifescience,medical the treatment of psychiatric disorders is based Inhibitors,research,lifescience,medical on trying to restore the observed dysfunction of central neurotransmitters. Since the ICD-10 and DSM-IV classifications are based on clinical descriptions, they neglect biochemical and physiological

abnormalities that are involved in the pathogenesis of disorders. The increasing knowledge of transmitter function in relation to behavioral selleck chemicals pharmacology has suggested links to numerous psychiatric conditions. This “pathophysiological approach” to Inhibitors,research,lifescience,medical the development of new treatments is oriented more toward behavioral abnormalities than toward nosological syndromes. Pathophysiological approaches allow transnosological treatment because particular symptoms can occur in many different psychiatric disorders. Behavioral abnormalities can be attributed to increased or decreased neuronal activity, and sometimes to alterations of specific transmitter receptors. This points to a role for functional pharmacology, which implies that, rather than nosological categories, one should treat basic disturbances in cognitive functions, click here impulse control, perception, information processing, and mood regulation. Since in many cases monotherapy is insufficient to adequately treat the different nosological categories, naturalistic clinical practice requires that most patients be treated according to their symptoms with more than one drug.2 The need for such multiple-drug therapy is due to many factors, such as multiple syndromes, comorbidity, and different target symptoms like negative and positive symptoms in schizophrenia.

Minor intellectual deficits are present in many patients in contrast with CDM and childhood onset DM1. Avoidant, obsessive-compulsive and passive-aggressive personality features have also been

reported (24, 25). Nocturnal apnoeic episodes and daytime sleepiness are a common manifestation. Gastrointestinal tract involvement covers irritable bowel syndrome, symptomatic gall stones and gamma-glutamyltransferase elevations. Finally, endocrine abnormalities include testicular atrophy, hypotestosteronism, insulin resistance with usually mild type-2 diabetes, thyroid dysfunction. Late-onset/asymptomatic DM1 In late-onset or asymptomatic #learn more keyword# patients (with low number of CTG repeats), only limited features are found on clinical and paraclinical assessment. Myotonia, weakness and excessive daytime sleepiness are rarely present. Before DNA tests became Inhibitors,research,lifescience,medical available, there were many examples of incorrect ascertainment, even when using markers such as EMG evidence of myotonia and slitlamp examination for the characteristic cataracts (26). In late-onset patients, the search for cataracts is helpful for identifying the transmitting person. Myotonic Dystrophy type 2 Clinical features The prevalence of DM2 is not well established, but estimated

to be similar to DM1 in European populations (27). In DM2 there Inhibitors,research,lifescience,medical are no distinct clinical subgroups although initially different phenotypes of DM2 were described: DM2/PROMM and PDM (5-7). The most important discrepancy between DM1 and DM2 is absence of a congenital or early-onset form in DM2 (12, 28) and the clinical presentation is a more continuum from early adult-onset Inhibitors,research,lifescience,medical severe form to very late–onset mild Inhibitors,research,lifescience,medical symptoms (paucisymptomatic). Clinically based ascertainment of DM2 patients is even more difficult because of the large phenotypic variability and a large number of individuals with milder symptoms who remain undiagnosed. Moreover, milder phenotypes with

prominent myalgia may easily be misdiagnosed as fibromyalgia (29) and patients with onset of slowly progressive proximal muscle weakness after age 70 years may not be referred before for neuromuscular investigations. Further evidence that a large proportion of DM2 patients may be undiagnosed came from a recent study which indicate that co-segregation of heterozygous recessive CLCN1 mutations in DM2 patients is higher than expected (30). In DM2 patients with co-segregating CLCN1 the severity of myotonia appear to be more evident either clinically or on EMG, thus these patients could be more easily identified and diagnosed than DM2 patients without the modifier allele. Consequently the majority of DM2 patients remains undiagnosed even in clinical centers with considerable experience with DM2.

EGFP-expressing cells in the monocyte populations were analyzed by gating using FlowJo software. The dromedary camel fibroblast cell line Dubca (ATCC® CRL-2276™) cells were seeded at 3 × 105 cells/well in a 24-well plate and infected with 10 MOI of Ad5.EGFP. At 24 h after infection, flow cytometry of cells was analyzed using LSRII and FlowJo software. For statistical analysis, the one-way analysis of variance and Tukey’s test were performed using Prism software (San Diego, California, USA). Results were considered statistically significant when the p value was <0.05. Symbols *, **, ***, and **** are used to indicated the P values <0.05, <0.005,

<0.001, <0.0001, respectively. E1/E3 deleted human type 5 adenoviral vector was used to insert the full-length

S and extracellular domain S1 of the codon-optimized inhibitors MERS-S open reading frames to generate Ad5.MERS-S and Ad5.MERS-S1 adenoviral vectors Tyrosine Kinase Inhibitor Library concentration (Fig. 1A). To detect MERS S protein expression of recombinant adenoviral candidate vaccines, A549 cells were infected with AdΨ5, Ad5.MERS-S, or Ad5.MERS-S1 and incubated with pooled selleck compound library day 28 sera from Ad.MERS or control immunized mice. Immunocytochemical analysis showed expression of MERS S protein in A549 cells infected with either Ad5.MERS-S or Ad5.MERS-S1, while no expression was detected in the mock and AdΨ5-infected cells. These same sets of infected cells were not stained with pooled sera from mice immunized with AdΨ5 (data not shown). Furthermore, cells transduced with Ad5-encoding full-length MERS-S showed a plaque-like structure, which may have resulted from syncytium formation due to MERS full length S protein expression, while the soluble form of MERS S1 protein, which was detected intracellularly (presumably 3-mercaptopyruvate sulfurtransferase before secretion), showed no syncytium formation (Fig. 1B). Both the Ad5.MERS-S- and Ad5.MERS-S1-immunized mice developed MERS-S-specific antibodies, measured as reactivity on A549 cells transfected with pAd using flow cytometry, while no specific antibody response was detected in serum samples from control animals inoculated with AdΨ5 or with pre-immunized naïve mouse sera (Fig. 2). Specific response was slightly higher

in mice immunized with Ad5.MERS-S than in mice immunized with Ad5.MERS-S1 (76.9% vs. 65.9% positive cells). These data suggest that adenoviral vaccines expressing MERS-S and MERS-S1 were able to induce S-specific antibodies. Sera from mice collected every week after i.n. boosting with 1 × 1011 v.p. of Ad5.MERS-S, Ad5.MERS-S1, or control AdΨ5 respectively, were tested for S protein-specific IgG2a and IgG1 immunoglobulin isotypes, indicating a Th1- or Th2-like response, respectively, by ELISA. Both IgG1 and IgG2a were detected as soon as one week after the first immunization. The induction of MERS-S-specific IgG1 and IgG2a antibodies were comparable between immunized groups. As shown in Fig. 3A, more significantly different IgG1 responses (Th-2) were observed in the sera of mice vaccinated with Ad5.MERS-S1 (**P < 0.

HPV 16 cLIA, (b) HPV 16 PsV NAb vs. HPV 16 TIgG, (c) HPV 18 PsV NAb vs. HPV 18 cLIA and (d) find more HPV 18 PsV NAb vs. HPV 18 TIgG. Abbreviations: GMT, geometric mean titre; PsV NAb, pseudovirus neutralizing antibody; cLIA, Merck competitive Luminex immunoassay; TIgG, Merck total IgG Luminex immunoassay; NT100, PsV NAb 100% neutralization endpoint; NT90, PsV NAb 90% neutralization endpoint; NTpartial, PsV NAb partial neutralization endpoint. Table 2 shows the proportions of subjects inhibitors seropositive for HPV 16 and 18 for the three assays through to 36 months post-vaccine. At baseline, 0.1% of PsV NAb NT100 negative subjects were HPV 16 cLIA seropositive and none were HPV 18 cLIA seropositive,

whereas 10.8% and 27.5% respectively were baseline TIgG seropositive. At month 36, HPV 16 antibodies remained detectable in all subjects by selleck products all three assays. In contrast, beginning at 18 months post-vaccine, HPV 18 antibodies could not be detected by cLIA in a proportion of subjects, and by month 36, 13.6% overall of subjects had no detectable HPV 18 cLIA antibodies. When stratified by study group, HPV 18 cLIA seropositivity at 36 months was 85.9% for 2-dose girls (Group 1), 95.3% for 3-dose girls (Group 2) and 79.4% for 3-dose adults (Group 3) (1 vs. 2 p = 0.11; 1 vs. 3 p = 0.51; 2 vs. 3 p < 0.01). The TIgG assay detected HPV 18 antibodies in most subjects and all subjects were PsV NAb

seropositive (NTpartial endpoint) at 36 months. HPV 16 NT100 GMTs for 2-dose girls were similar to those for 3-dose girls through to 36 months (Table 3), and both 2- and 3-dose girls had HPV 16 NT100 GMTs approximately 2- to 3-fold higher than 3-dose adults at all time points. either For HPV 18, NT100 GMTs were similar for both 2- and 3-dose girls at 7 months, and both groups had higher GMTs than 3-dose adults. At 18, 24 and 36 months, HPV 18 GMTs for 2-dose girls were about 2-fold lower than those for 3-dose girls, but at 36 months, GMTs for 2-dose girls remained similar to those for 3-dose adults. Responses measured

by the cLIA and TIgG assays showed similar patterns. NT90 and NTpartial GMTs for both HPV 16 and 18 were consistently 2- to 8-fold higher respectively than the corresponding NT100 GMTs (Table 3 and Supplementary Fig. 2). Supplementary Fig. II.   HPV 16 and HPV 18 PsV NAb GMTs by study group to month 36. Box plots of month 7 to month 36 PsV NAb (NT100, NT90 and NTpartial) GMTs for HPV 16 and HPV 18 by study group. (a) HPV 16 PsV NAb NT100, (b) HPV 16 PsV NAb NT90, (c) HPV 16 PsV NAb NTpartial, (d) HPV 18 PsV NAb NT100, (e) HPV 18 PsV NAb NT90 and (f) HPV 18 PsV NAb NTpartial. Abbreviations: GMT, geometric mean titre; PsV NAb, pseudovirus neutralizing antibody; cLIA, Merck competitive Luminex immunoassay; TIgG, Merck total IgG Luminex immunoassay; NT100, PsV NAb 100% neutralization endpoint; NT90, PsV NAb 90% neutralization endpoint; NTpartial, PsV NAb partial neutralization endpoint.