As elimination is approached, fewer and fewer infections will occur, perhaps making natural boosting of a protective immune response a less impactful attribute of a product’s TPP. Furthermore, expression in the human increases the possibility that immune selection will lead to the proliferation

of escape mutants. Additional data are therefore needed to support KPT-330 datasheet whether endemic boosting should be a critical attribute of an ideal SSM-VIMT. The clinical development plan (CDP) and the basis of regulatory approval for an SSM-VIMT will likely be different from those applied to pre-erythrocytic and blood-stage malaria vaccines due to the methods in which vaccine effect will be established at the level of the community rather than the individual. In 2010, the major points of discussion on CDP/regulatory pathway were on the acceptability to regulatory authorities of a vaccine acting via delayed clinical benefit, the appropriate CDP and regulatory pathway, including the potential need for a cluster randomized trial (CRT), and the required level of efficacy. A Y-27632 supplier critical

outcome of the 2010 MVI TBV workshop was that the US Food and Drug Administration (FDA) indicated that there is no legal bar to prevent a vaccine such as an SSM-TBV from being considered for licensure in the context of their review process. The FDA has the authority to license biological products that are demonstrated to be “safe, pure, and potent” (Section 351 of the Public Health Service Act & Section 505(b) of the Food, Drug, and Cosmetic Act), regardless of whether the disease occurs in the United States [23]. This feedback has encouraged the malaria vaccine development community to consider product development pathways for vaccine approaches exclusively targeting

parasite transmission from human to Metalloexopeptidase mosquito. In 2012, moreover, the report on the MALVAC meeting states, “great progress has been made in recent years with a general acceptance in malaria vaccine circles that the issue of community benefits for TBV is not a major hurdle for clinical or regulatory pathways” [24]. The challenge moving forward will be to further define both the CDP and regulatory pathways and seek specific feedback from regulators, such as the FDA, European Medicines Agency, or another stringent regulatory authority. Another important outcome of the VIMT research agenda-setting meetings and consultations was the preliminary definition of two potential clinical development pathways for an SSM-VIMT (Fig. 1). One involves a large-scale, Phase 3 efficacy trial, which, in the case of an SSM-VIMT, has been proposed by regulators to be a CRT to demonstrate vaccine impact on incidence of infection in the community.

v.) injection of docetaxel by tail vein injection

2×/week, C-DIM-5 and C-DIM-8 indicate 30 min exposure of mice to 5 mg/ml nebulization on alternate days respectively. C-DIM-5 + doc and C-DIM-8 + doc indicate 30 min exposure of mice to 5 mg/ml nebulized C-DIM-5 and C-DIM-8 on alternate VE-822 order days respectively plus intravenous injection of doc 2×/week. The estimated total deposited amount of inhaled drug (D) for the ambient air was calculated by the following formula: D=CC-DIM×V×DI×T,D=CC-DIM×V×DI×T,where CC-DIM = concentration of C-DIM in aerosol volume (C-DIM-5; 48.9 μg/l, C-DIM-8; 51.6 μg/l) estimated as the amount of C-DIM received from each port of the inhalation assembly. V = volume of air inspired by the animal during 1 min (1.0 l min/kg); DI = estimated

deposition index (0.3 for mice), and T = duration of treatment in min (30 min). Under these conditions, the total deposited dose of aerosol formulations of C-DIM-5 and C-DIM-8 were 0.440 mg/kg/day and 0.464 mg/kg/day respectively. Tissue homogenates from excised lung tumor were lysed on ice using RIPA buffer (G-Biosciences, St. Louis, MO). Total protein content was determined by the BCA method of protein estimation according to manufacturer’s protocol. The protein samples (50 μg) were separated on a Mini-PROTEAN® TGX™ gel (Bio-Rad, Hercules CA) and blotted onto nitrocellulose membranes as previously described (Ichite et about al., 2010). The blots were then AZD2281 nmr probed with primary antibodies

targeting cleaved caspase8, cleaved caspase3, PARP, cleaved PARP, survivin, NfkB, p21, Bcl2, TR3 and β-actin (as loading control). Following incubation of membranes with HRP-conjugated secondary antibodies, chemiluminescent signal detection of proteins of interest was aided by autoradiography following exposure to SuperSignal West Pico Chemiluminescent Substrate (Thermo Fisher Scientific Inc, Rockford, IL). Blots were quantified by densitometry with the aid of ImageJ (rsbweb.nih.gov/ij/) and the results presented as means of protein/β-actin ratio with SD. Total RNA from lung tissue homogenate was extracted using Trizol reagent per manufacturer’s protocol (Invitrogen, Carlsbad CA) and converted to complementary DNA using SABiosciences’ RT2 First Strand Kit. The gene expression of a panel of 84 genes representing six biological pathways implicated in transformation and tumorigenesis was profiled using the Mouse Cancer PathwayFinder RT2 Profiler™ PCR Array. The array included five controls including GAPDH and β-actin as housekeeping genes. Amplification was performed on an ABI 7300 RT-PCR and data analysis done with a PCR Array Data Analysis Software (SA Biosciences, Valencia CA). Apoptosis detection on paraffin-embedded the lung sections was carried out using the DeadEnd™ Colorimetric Apoptosis Detection System (Promega, Madison, WI) following the manufacturer’s protocol.

They were acclimatized

to animal house facilities for seven days and were maintained under standard condition (Temperature 25 ± 2 °C, 12-h light: 12-h dark cycle) throughout the experimentation. The animals were fed with standard pellet diet (Nutrivet life science, HDAC inhibitor Pune, M.S., India) and water was supplied ad-libitum. The studies were carried out as per the CPCSEA guidelines and after approval of the Institutional Animal Ethical Committee (Ref.No.: BVDUMC/443/2012-2013). Rats were randomly selected and divided into six groups of six animals each. The inter and intra group weight difference was below 20%. Hepatotoxicity was induced in rats by orally feeding 1000 mg/kg b.w. acetaminophen suspended in water. The dose of satwa was finalized on the basis of the earlier studies carried out in the laboratory. The treatment protocol, as mentioned below, was followed: Group I: Control (n = 6); received feed and water normally for 15 days The animals were observed daily for any signs of discomfort and/or infection. After 15 days of continuous treatment, animals were fasted overnight, blood was collected by retro-orbital puncture and animals were humanely sacrificed. Liver was

excised immediately, washed in saline, weighed and stored in 10% neutral buffered formalin for histological analysis. Blood was allowed to clot at R.T. for 30 min and serum was collected after centrifugation at 2000 rpm for 15 min. Marker enzymes of liver damage (serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT) and alkaline phosphatase (ALP)), total bilirubin,

total Cholesterol, HDL Cholesterol, total Triglycerides were estimated click here using not commercial kits (Coral clinical system, Goa, India). LDL Cholesterol (mg/dL) was estimated by using the formula: (Total Cholesterol – HDL Cholesterol) – triglycerides/5 and VLDL Cholesterol was estimated by using the formula: Triglycerides/5. Paraffin-embedded liver tissues were cut at 4 μm and stained with hematoxylin-eosin. The slides were examined under microscope and photographed. Results are presented as Mean ± Standard Error (SE). Dunnett Multiple Comparison Test and one way Analysis of Variance (ANOVA) was done to estimate the statistical significance between groups. In the present study, comparative hepatoprotective potential of T. cordifolia, T. sinensis and Neem-guduchi Satwa were evaluated by assessing activities of serum enzymes SGOT, SGPT, ALP and total bilirubin. The animals of paracetamol treated group showed elevated levels of SGOT, SGPT, ALP and bilirubin, as compared with normal control group ( Table 1). The results of comparative hepatoprotective potential of T. cordifolia, T. sinensis and Neem-guduchi Satwa on paracetamol treated rats indicate differential activity of three different species in hepatoprotection. T. cordifolia was found to have a specific action on maintaining lipid profile. The experimental group treated with T.

The incidence rate in the under six months age group may have been an underestimation if many hospitalisations for acute gastroenteritis occurred in the first six weeks of life. There was no active follow up, only passive surveillance of hospitalisations of study participants. Participants may have moved from the area or died at home, and thus no longer be contributing to the total follow

up time, yet it was assumed that these participants had contributed the full 5 years of follow up time. This would have led selleck screening library to underestimation of incidence rates as the denominator would be inflated. Although CHBH is the referral hospital for all local clinics in Soweto, there is a chance that selleck inhibitor some participants may have consulted

a private practitioner and had an admission at a private hospital. There is also the possibility that those with very severe acute gastroenteritis may have died in the community before arriving at the hospital. These cases would not have been identified as an episode of acute gastroenteritis and included in the numerator in incidence calculations but would have contributed to total person time, leading to an underestimation of the number of admissions for severe acute gastroenteritis and the incidence rates. There were no stool samples collected on admission and so no stool identification of pathogens was possible. As a result the true proportion of

severe acute gastroenteritis caused by rotavirus could not be determined. Despite these limitations the results provide unique information on disease burden estimates in HIV-infected children Acute gastroenteritis is an important cause of hospitalisation in South Africa, especially in children under 2 years of age and those with concomitant HIV infection. The estimated risk of hospitalization for rotavirus associated acute gastroenteritis is two out fold greater in HIV-infected compared to HIV-uninfected children, despite rotavirus being identified in a lower proportion of acute gastroenteritis cases in HIV-infected children. The introduction of rotavirus vaccine, proven to be safe, immunogenic and efficacious in both HIV-infected and uninfected children, into the national immunisation program is likely to decrease the overall burden of severe acute gastroenteritis regardless of HIV infection status. Ongoing surveillance for rotavirus disease as well as a case control study to determine the effectiveness of the vaccine in routine use are currently underway in South Africa. Conflict of Interest Statement: The Phase 3 trial on which this secondary analysis is based was funded by Wyeth. SM has been a paid temporary-consultant /expert board member for Pfizer, GSK, Merck, and Novartis, and has been paid for speaking engagements by Pfizer and GlaxoSmithKline.

The AERRS was calculated as follows: AERRS=β(1−p)AERRS=β(1−p)where β is the annual growth rate of people aged 16–60 and p was the annual vaccination compliance. This analysis was performed using Matlab 7.0 (The Mathworks Inc., USA). There were 12,457

HFRS cases and 725 deaths reported in Hu County between 1971 and 2011. The HFRS cases were reported each year, with the incidence ranging from 9.53/100,000 in 2005 to 300.57/100,000 in 1984. The mortality rate ranged from 0 in 1995, 1996, 1999 and 2010 to 24.91/100,000 in 1979. A fluctuating but distinctly declining trend of annual HFRS incidence and mortality rate was identified between 1971 and 2011 (incidence: Cochran–Armitage trend test Z = −34.38, P < 0.01; mortality rate: Z = −23.44, P < 0.01). The HFRS vaccination program Ku-0059436 supplier in Hu started in 1994, with the vaccination compliance ranging from 4.55% in 1994 to 83.67% in 2010. A distinctly increasing trend of annual HFRS vaccination compliance was identified for the study years (Cochran–Armitage trend test Z = 1621.70, P < 0.01) ( Fig. 1). When the

maximum temporal cluster size was 20% of the study period, the most likely temporal cluster of HFRS epidemic between 1971 and 2011 fell within a window encompassing 1983–1988 click here (relative risk (RR) = 3.44, P < 0.01), with the average incidence of 151.41/100,000. When the maximum temporal cluster size was 30%, 40% or 50% of the study period, the most likely temporal cluster fell within a window encompassing 1979–1988 (RR = 3.18, P < 0.01), with the average incidence of 125.54/100,000 ( Table 1). There was a negative correlation between the annual HFRS incidence and vaccination compliance in Hu with the lagged year from −5 to also 5. The cross correlation was significant when the lagged year was 1 or 2, with the cross correlation coefficient equal

to −0.51 and −0.55, respectively, and the standard error equal to 0.24 and 0.25, respectively (Table 2). The time series of annual HFRS cases in Hu between 1971 and 2011 generated a peak in power around five during 1976–1988, indicating a five year cyclical fluctuation of HFRS epidemic during this period (Fig. 2B–D). After 1988, this peak disappeared and was replaced by more aperiodic dynamics. Although not significant, a relative peak in power was detected at approximately fifteen years during 1988–2011 in the HFRS time series (Fig. 2D). The vaccination compliance increased after 1994 and the annual effective recruitment rate of susceptible individuals declined after 1988 (Fig. 2D). HFRS cases among Japanese soldiers in northeast China were reported in the early 1930s [28]. The most serious epidemic of HFRS ever recorded in China occurred in the 1980s, with 696,074 HFRS cases reported during this outbreak [1].

While the peer-assisted learning framework encouraged students to work with and learn from each other, the responsible clinical educator had supervisory responsibilities Cytoskeletal Signaling inhibitor of minimising risk to patients and students, providing formative and summative feedback and assessment, and providing appropriate education/guidance. The traditional model involved delivery of supervision according

to the usual practice of the clinical educators when supervising pairs of students. This was not standardised but was characterised by supervisor feedback to learners and individualised learning activities including supervised practice, reflective learning and assessment. Peer-assisted learning activities were

not scheduled or facilitated. Outcome measures were defined a priori and completed by blinded assessors of clinical performance outcomes (who were not part of the investigative team), clinical educators and students (ie, self assessment). It was not possible to blind students or clinical educators to group allocation due to clear differences in the structure of the two education models. The primary outcome measure was the Assessment of Physiotherapy Practice, scored by blinded outcome assessors, supervising clinical educators, and students at the end of each 5-week placement. The Assessment of Physiotherapy Practice instrument is designed to monitor longitudinal evaluation of physiotherapy student performance in the clinical environment and has been shown to be reliable, with Selleck GSK J4 an ICC (2,1) of 0.92 (95% CI 0.84 to 0.96).22 It has been validated against a range of other indicators (eg, stability in hierarchy of item

difficulty, global rating scores) when applied by clinical educators who assessed students during at least 4 weeks of clinical placement.23 The Assessment of Physiotherapy Practice comprises 20 items in seven key areas that map to the core competencies specified in the Australian Standards for Physiotherapy.24 Montelukast Sodium Each item is rated on a 5-level scale from 0 (infrequently/rarely demonstrates performance indicators) to 4 (demonstrates most performance indicators to an excellent standard). The total Assessment of Physiotherapy Practice score ranges from 0 to 80, with a higher score representing better performance. The standard error of measurement for the Assessment of Physiotherapy Practice was low and the minimal detectable change at 90% confidence was 7.9.23 Whilst the Assessment of Physiotherapy Practice ratings by the supervising clinical educator and the students were longitudinal, the blinded outcome assessors completed the Assessment of Physiotherapy Practice following a half-day observation of each student within the final 3 days of their placement.

The reviewers extracted post-intervention sample sizes, means, and standard deviations (SD) for the experimental and control groups. The authors were contacted to provide additional information if necessary. The analyses were performed using RevMan 5. In each study, the effect size for the intervention

was calculated by the difference between the means of the experimental and control groups at the end of the intervention. If the outcome was measured on the same scale, the weighted mean difference (WMD) and 95% confidence interval (CI) were calculated. Otherwise, the standardised mean difference (SMD) and 95% CI were calculated. Data were pooled using a fixed effect MLN8237 purchase model and heterogeneity was calculated using a Chi-square test (χ2). A random effect model was used to re-analyse data when significant heterogeneity was noted.

Publication bias was investigated by using the funnel plot (Leandro, 2005). The search was performed on October 1, 2009. After screening the titles and abstracts, ten studies met the Selleck BKM120 inclusion criteria (Beckers et al 2008, Cider et al 1997, Delagardelle et al 2002, Feiereisen et al 2007, Haykowsky et al 2005, Mandic et al 2009, Pu et al 2001, Selig et al 2004, Tyni-Lenné et al 2001, Williams et al 2007a). Two studies (Selig et al 2004, Williams et al 2007a) had overlapping subjects, and the one with larger sample size was included (Selig et al 2004). Two other studies were excluded because of incomplete data (Delagardelle of et al 2002, Haykowsky et al 2005). The study by Feiereisen and colleagues also consisted of resistance training and control

groups that were excluded due to lack of control group randomisation (Feiereisen et al 2007). We included one study (Barnard et al 2000) through searching reference lists of one review article (Volaklis and Tokmakidis, 2005) (Figure 1). Tables 1 and 2 summarise the characteristics of the included studies. Quality: The methodological quality of the eight included trials ranged from 4 ( Barnard et al 2000) to 7 ( Beckers et al 2008, Mandic et al 2009, Pu et al 2001) on the PEDro scale ( Table 1), with a mean of 5.7 out of 10 (SD 1.2). No trials blinded participants or therapists, while four trials blinded assessors, seven had 85% or greater retention rates, and all reported between-group differences with point estimates and measures of variability. Participants: Most of the included studies had predominantly male participants with stable chronic heart failure and mean ages ranging from 55 to 65 years. Only one study recruited only women ( Pu et al 2001), with participants aged a mean of 77 years. New York Heart Association classifications ranged from I to III and left ventricular ejection fraction was approximately 40% in most studies.

23 (0.99, 1.50) and TT (aGMR 1.36 (1.04, 1.80). Both associations showed a marked interaction with maternal albendazole treatment (interaction p-values 0.02 and 0.001, respectively), being evident only in the albendazole-placebo group (cCFP aGMR 1.57 (1.19, 2.00) and TT aGMR 1.99 (1.35, 2.97)). No consistent associations were observed for other species. Maternal BCG scar was associated

with a markedly lower infant IL-5 and IL-13 responses to cCFP (aGMR 0.76 (0.61, 0.94) and 0.80 (0.64, 1.00)) and a somewhat lower IFN-γ response (aGMR 0.87 (0.70, 1.09)). An increasing number of doses of maternal tetanus immunisation during the pregnancy was associated with increased infant IFN-γ (aGMR 1.44 (1.16, 1.79)) and IL-13 (1.22 (1.01, 1.46)), and AZD6738 a weak increase in IL-5 (aGMR 1.19 (0.97, 1.44)) responses to TT. Female infants had broadly lower responses for both cCFP and Alpelisib TT,

with aGMRs for each cytokine response ranging from 0.69 to 0.86 (Table 1, Table 2, Table 3 and Table 4). Associations for anthropometric variables were somewhat variable; after adjustment for confounding, associations remained for the IL-13 response for TT and IL-10 response to cCFP, which both showed increased responses for higher scores: IL-13 for TT, birth weight aGMR 1.43 (1.09, 1.89), weight-for-age z-score at one year, 1.13 (1.01, 1.28), height-for-age z-score at one year 1.13 (1.01, 1.26); IL-10 for CFP, height-for-age z-score at one year, 1.08 (1.00, 1.17). Current malaria parasitaemia was strongly associated with reduced IFN-γ, IL-5 and IL-13 responses for cCFP (aGMR 0.49 (0.28, 0.80), 0.41 (0.30, 0.60) and 0.46 (0.29, 0.75) respectively), and for TT (aGMR 0.47 (0.25, 0.85), 0.32 (0.21, 0.53) and 0.50 (0.26, 0.93) respectively), and with a reciprocal increase in IL-10 responses for TT (aGMR 2.38 (1.48, 3.80)).

Previous episodes of malaria during infancy showed weaker effects, but a high number of episodes was associated with a reduced IL-5 response to cCFP (aGMR 0.84 (0.76, 0.95)) and an increased IL-10 response to TT (aGMR 1.18 (1.03, 1.34)). Associations with infant HIV status differed for cCFP and TT. For cCFP, HIV-exposed-uninfected infants through showed no difference in response compared to HIV-unexposed infants, but HIV-positive infants showed markedly lower IFN-γ, IL-5 and IL-13 responses (aGMR 0.06 (0.02, 0.23), 0.37 (0.25, 1.00) and 0.20 (0.09, 0.53) respectively), and higher IL-10 responses (aGMR 2.19 (1.56, 3.15)). For TT, both HIV-exposed-uninfected infants, and HIV-infected infants, showed impaired IFN-γ, IL-5 and IL-13 responses: HIV exposed-uninfected, aGMR 0.57 (0.35, 0.94), 0.51 (0.33, 0.82) and 0.61 (0.39, 0.95); HIV-infected, aGMR 0.35 (0.11, 1.13), 0.16 (0.10, 0.52) and 0.09 (0.04, 0.27); there was no effect on the IL-10 response.

Second, it should give us a better understanding of our patients and their needs. Third, these benefits will help to give us a competitive advantage in the health-care marketplace. Jones and Hush (2011) highlight the undoubted importance of undergraduate (including graduate-entry)

physiotherapy programs. However, it is also important that postgraduate education reflects the same aims. Speaking personally, a postgraduate degree in Pain Management has revolutionised the way I treat all patients. There is a common misconception that the pain sciences, or indeed www.selleckchem.com/products/sch-900776.html a pain management approach, are only for those involved in treatment of chronic pain sufferers. Nothing could be further from the truth. The biopsychosocial model of pain has been championed in recent years. This model enables clinicians (either as an individual or in a multidisciplinary team) to perform a formulation of any person who is experiencing pain. A formulation

examines all three domains of a person in pain (the biological body processes, the psychological background and response, and the environment in which the person lives) and suggests how those domains inter-relate to lead to the outcome of the experience of pain. It is not that physiotherapists have all the skills in each of these areas. However, such an approach enables us to accept that there may be lots of contributors to the pain being experienced by that person in front of us. Such a process of formulation click here is almost intuitive in chronic pain due to the frequency of significant psychological and social concomitants to the pain. However, a similar diagnostic process is also essential in all acute situations, as it is common for there to be issues such as belief structures, anxiety, family or work situations, that impact on the experience of pain. Failure to identify these factors will lead to us not doing as good a job as we might. Since JJ Bonica first championed the multidisciplinary

environment in assessing and treating Resveratrol people with chronic pain, the unique contribution of different professions to the understanding of pain treatment has grown. Jones and Hush (2011) emphasise this multidisciplinary aspect of pain education. Clinicians from other disciplines have so much to offer to help us understand more fully the complexity of pain. Few courses offer an opportunity to actually learn with and from each other. The formal postgraduate study program with which I am involved (the postgraduate degree program in Pain Management, Sydney Medical School, The University of Sydney) is one of the few that provide such an environment. I would encourage all physiotherapists to brush up on their pain science, both basic and clinical, as well as training clinicians of the future.

PCV-7 has been shown in many studies to be highly immunogenic and effective against IPD [5], [15], [16] and [17], with the vaccine efficacy of 97.4% against vaccine serotypes in the US [5]. In the large trial in South Africa and Gambia, the efficacy of PCV-9 was 83% and 77% against IPD caused by vaccine serotypes [18] and [19]. Twice as many IPD cases were indirectly prevented due to herd immunity after the PCV-7 implementation in the US [8]. Due to serotype specific efficacy of the vaccine, serotype coverage of IPD implies and predicts the efficacy of the vaccine. In this region, the serotype coverage of 70.3% by PCV-7 in IPD in children under five years of age in our study was less than the 78% coverage found in Singapore

[15], but higher than in a study in China in 2008 which found 63.6%, 64.8% and 79.6% coverage by PCV-7, PCV-10 and PCV-13, respectively [20].

The serotype coverage of IPD isolates by PCV-7 in children ≤14 years VEGFR inhibitor old in Taiwan was 85%, somewhat higher than in our study [21]. WHO reported the overall serotype coverage of PCV-7 ranged from 60 to 85% worldwide [22]. There has been a concern about the increased proportion of nonvaccine serotypes reported in the US and Spain after introduction of PCV-7 vaccination program [8], [23] and [24]. The widely use of PCV-7 may contributed to the emergence of nonvaccine serotypes, especially serotype 19A [8], [23] and [24]. However, a study in Korea reported an increase in serotype 19A even before the introduction Non-specific serine/threonine protein kinase of PLX4032 molecular weight PCV-7 [25]. It is probable that both selective vaccine pressure and clonal spread were contributing factors to the circulating serotypes in the community. In Thailand, we reported the serotype coverage of PCV-7, PCV-9, PCV-11, and PCV-13 of 73.9%, 77.4%, 77.4%, and 87.8%, respectively, in children younger than 5 years of age during 2001–2005 [11]. The serotype coverage found in this study was somewhat lower than that report, but was still within the 95% confidential interval. Although PCV-7 has been available in Thailand since June 2006, the vaccine has been

used mainly in private settings with an estimated 55,000 doses sold each year, representing less than 5% of children <5 years of age. This low vaccine uptake did not seem to affect the serotype distribution in this relatively small study. The top seven serotypes of invasive isolates found in our study were different in rank of order and frequency (%) in each age groups, as well as whether the sites were sterile or non-sterile. Although the top seven serotypes of isolates from sterile sites in children younger than 5 years of age were not completely match with other studies reported earlier in Thailand [11], [26], [27] and [28], they were quite consistent. The common serotypes found in those and our studies were 6B, 14, 19A, 19F, 23F. The PCV that included all these serotypes, i.e. PCV-13, would be the most appropriate for large scale use in Thailand.