Moreover, a dose dependent increase in

Paclitaxel in vivo the Na+/K+ ratio was also found. The increase in electrolyte excretions with the ethanolic extract (at both doses) was less than that found with furosemide ( Table 2). There are few reports on the diuretic activity of the Geraniaceae species. One study reported use of the aqueous extract of Geranium robertianum L in conditions requiring increased diuresis, such as cystitis, oliguria, urethritis, pyelonephritis, hypertension and gout. 10 The diuretic effect of the orally administered ethanolic extract of Geranium seemannii Peyr. was evaluated in normal adult male Wistar rats and compared with that produced by furosemide, a loop diuretic widely used in clinical practice. Diuresis has two components: an increase in urine volume (water secretion)

and a net loss of solutes (i.e., electrolytes) in the urine. These processes may result from suppression of renal tubular reabsorption of water and electrolytes into the blood stream. Administration of the Geranium seemannii Peyr. extract showed a significant increase in urine output and electrolyte excretion (p < 0.001) in a dose dependent manner ( Table 1 and Table 2), indicating the possibility of intrinsic and causal action, possibly receptor-mediated. Some herbs induce diuresis by stimulating the thirst center in the hypothalamus and thereby enhancing fluid intake.18 and 19 Some plants elicit diuresis due to their high salt content.20 Such nonspecific mechanisms are unlikely to be involved in the effect of the test compound, in spite of the high Na+ level in 3-deazaneplanocin A cost urine, because the extract of G. seemannii Peyr. did not alter the osmolarity or specific gravity of urine. Thus, the diuretic effect is not related to an osmotic mechanism. Furthermore,

osmotic diuretics are inactive when administered orally, and for this reason are usually administrated intravenously. 20 The diuretic effect of G. seemannii these Peyr. is also unlikely to be due to an impairment of the action of an antidiuretic hormone, because such impairment causes polyuria with low osmolarity. The reference drug furosemide showed a marked increase in urine volume and in urinary excretion of Na+ and Cl−, with a similar pattern as that found with the ethanolic extract of Geranium seemannii Peyr. ( Table 1 and Table 2), suggesting a similar mechanism of action in both cases. Furosemide, like other loop diuretics, acts by inhibiting NKCC2, the luminal Na+-K+-2Cl− symporter in the thick ascending limb of the Henle loop. It also abolishes the corticomedullary osmotic gradient and blocks negative as well as positive free water clearance. 21 and 22 By inhibiting the transporter, the loop diuretics reduce the reabsorption of NaCl in the kidney and also diminish the lumen-positive potential that derives from K+ recycling. This electrical potential normally drives divalent cation reabsorption in the loop. Thus, by reducing this loop potential, diuretics induce an increase in Mg2+ and Ca2+.

Randomisation allocated 101 participants to an accelerated intervention incorporating early therapeutic exercises (exercise group) or a standard protection, rest, ice, compression, and elevation intervention (standard group). Interventions: During

the first week after baseline both groups received written advice on using ice and compression. The exercise group also undertook 20 minutes of exercises three times a day focused on increasing ankle range of movement, activation and strengthening of ankle musculature, and restoring sensorimotor control. In the following four weeks a standardised treatment consisting of ankle rehabilitation exercises was provided to both groups. Outcome measures: The primary outcome was subjective ankle function assessed by the lower extremity functional scale (0–80) Afatinib order at weeks 1 to 4. Secondary outcomes assessed were: pain at rest and pain with activity with 10-cm visual analogue scales, swelling by a modified version of the figure of eight method, and physical activity by a physical activity logger. Ankle function by the Karlsson score and rate of reinjury were also assessed at 16 week follow-up. Results: 15 of the 101 patients dropped out during the trial, 11 in the

exercise group and 4 in the standard group. An effect was found in favour of the exercise group with the lower extremity functional scale (0–80) at week 1 (MD 5.3, 98.75% selleck kinase inhibitor CI 0.3 to 10.3) and week 2 (MD 4.9, 95% CI 0.3 to 9.6). In addition, the exercise group was more active in the first week as measured by time spent

walking (0.4 hours per day, 95% CI 0.2 to 0.6). No between-group differences were observed for pain at rest, pain why with activity, or swelling. At 16 weeks there were no significant differences between the groups in the Karlsson score or reinjury rate (2 in each group). Conclusion: An accelerated exercise protocol during the first week after ankle sprain improved ankle function and early return to weight bearing activity. Between-group difference in time spent walking per day calculated by CAP editors This study is the first to describe the effect of early mobilisation in combination with the standard PRICE (Protection, Rest, Ice, Compression, Elevation) treatment after an acute ankle sprain using a randomised controlled trial where, instead of rest, the intervention group performed therapeutic exercises aimed at increasing ankle movement, as well as static strengthening and stretching exercises (Knight 1995). The main finding was a significant improvement in short-term ankle function for those completing the exercise protocol during the first week following an ankle sprain. It is worth noting that the size of the effect (expressed as change in the lower extremity functional score from baseline to week 1) was smaller than the change of 9 points nominated as the clinically important change.

The difference observed between the release profiles of F1, F2, F3 and F4 was statistically significant (P < 0.05). Thus, PEO 303 was observed to be a suitable polymer for developing the sustained release matrices for aceclofenac. Formulations F2 (PEO N60K) and F4 (PEO 303) release the drug over a period of 12 h by swelling and subsequently eroding. 7 The similarity in the release profiles of commercial sustained release tablet and the developed formulations was compared by calculating the similarity factor (f2).8 The f2 values, when compared with Hifenac

SR, were observed to be 54.43, 62.72, 55.61 and 44.23 for formulations F5, F6, F7 & F8 respectively. The release showed less similarity when compared with Hifenac SR. Some amount of PEO 303 in the tablets was replaced with Polyox N60K at 10% (F9), 20% (F10) and 30% (F11) in formulation http://www.selleckchem.com/products/MK-2206.html F6 by keeping the total polymer percent at 28% to get the comparable release profile (higher similarity (f2) value). SCR7 in vitro The drug release was increased from the formulations in the order

of F9 < F10 < F11 (Fig. 4). Formulation, F10 showed higher similarity factor 77.68 when compared to F9 (68.23) and F11 (62.04). The mechanism of aceclofenac release was analyzed by using an empirical equation proposed by Ritger and Peppas.9 The release exponent “n”, was in the range of 0.513–0.795 for all the matrix tablets, indicating non-Fickian (anomalous) diffusion as the release mechanism. The time required for 50% of the drug to be released much (T50 h), of the prepared formulations, increased as the PEO amount increased, in all the formulations ( Table

2). In the formulations F9, F10 and F11, the T50 value is decreased by increasing the Polyox N60K. This is the expected pattern in release profile because a part of high molecular weight PEO 7 × 106 was replaced with low molecular weight PEO 7 × 106. The T50% values of all the formulations tested were in the range of 9.25–17.5 h. The T50 value of formulation F10 (13.9 h) was very close to the T50 value of Hifenac SR (14.1 h), indicating that both exhibited the same in vitro performance. The drug release from the formulation F10 is fast at initial hours when compared to Hifenac SR ( Fig. 5) but the difference in drug release is not more than 5% at any time point. The similarity in release profiles is confirmed by the similarity factor of 77.68. The formulation F10 was optimized to test for in vivo bioavailability study along with Hifenac SR. The formulation F10 was containing the polymer at 28% to the total tablet weight and containing high molecular weight PEO 7 × 106 at 80% combining with low molecular weight 2 × 106 at 20% in the total polymer amount. The pharmacokinetic evaluation indicated that aceclofenac from formulation F10 and from Hifenac SR was released slowly and absorbed over long periods of time.

Both the number of re-assortant strains and the high proportion of mixed infections are indications of the variety of sources from which children are likely to acquire infections. Of rotavirus-positive specimens, some remained untypeable for both G type and P types. Possible explanations include too few virus particles with intact RNA in the stool specimens,

the viruses not being recognized by the primer sets, and the viruses not belonging to genotypes included in the primer set. Since the study protocol was set up to capture acute gastroenteritis cases reporting to only one clinic in each of the study sites and there was no active effort to look for and log every case of diarrhea reporting to the Cytoskeletal Signaling inhibitor hospital and attached health centers, there is a possibility that the estimation of the number of acute diarrhea cases in the study age group is lower than the actual number of cases. Additionally, this manuscript may have possibility of potential bias due to buy Z-VAD-FMK under reporting of severe rotavirus-positive diarrhea

due to inclusion of two low rotavirus-positive seasons (April 2011–July 2011 and April 2012–July 2012) and only one high rotavirus positive season (August 2011–March 2012). In summary, this study highlights the high prevalence of rotavirus gastroenteritis in India, the higher severity of rotavirus disease than that of other diarrheal diseases, and the circulation of Dipeptidyl peptidase a diverse range of rotavirus strains, including several uncommon and emerging strains like G9 & G12. This study report has generated geographically representative data to inform public health policy in India. With the prospect of rotavirus vaccine introduction in the Indian EPI Schedule

in the near future, the importance of rigorous surveillance to monitor disease and strains before and after vaccine introduction cannot be overemphasized. We are grateful to the subjects who volunteered to participate in this research study. Funding: This study was funded by a research grant from Shantha Biotechnics Limited. Conflicts of interest: All the authors except Saluja T, Prasad R, Gujjula R, Rao R and Dhingra MS were the Principal Investigators of the study at their respective study sites. All the Principal Investigators declared that they had no financial interests in the manufacturer but received research grant to undertake the study. Saluja T, Prasad R, Gujjula R, Rao R and Dhingra MS are employed by Shantha Biotechnics Limited and were involved in planning, analyzing and interpreting the study. “
“Rotavirus is the leading cause of diarrhea and is associated with 453,000 childhood deaths globally [2]. India accounts for an estimated 457,000–884,000 hospitalizations, 2 million outpatient visits for diarrhea, resulting in huge medical and health care costs [1].

As such, the origin and physiologic functions of these vesicles are unknown, and, their roles in

the pathology of diseases have not been elucidated. Nevertheless, the strong association between their protein cargo load and disease manifestation implicates an active role in the pathophysiology, and therefore a sentinel for disease progression and resolution. The exclusiveness of the CTB and AV binding affinities for these vesicles indicate that the lipid compositions of these 2 vesicles are different and their membrane biogenesis originates from different microdomains in the plasma membranes. As different microdomains are functionally different, a difference in the origins and functions of these vesicles could be inferred. In addition, we noted that serum is a rich source of platelet microparticles but a relatively poor source

Compound Library of CTB- or AV-binding vesicles, suggesting that the most of CTB- or AV-binding vesicles in the plasma were not platelet microparticles. Based on our current understanding of membrane vesicles, we speculate that because the CTB-vesicles were rich in GM1 ganglioside, they could be derived from lipid rafts and therefore, were likely to be exosomes.8 On the other hand, it is difficult to speculate on the identity of AV-vesicles as exosomes, microvesicles, ectosomes and possibly Androgen Receptor animal study others have been reported to have exposed phosphatidylserines.8 In healthy cells, phosphatidylserines are mainly localized on the inner leaflet of the membrane and this asymmetry is actively maintained by ATP-dependent aminophospholipid translocase.14 In dying cells or membrane vesicles where ATP production is not sustainable, phosphotidylserines become exposed by spontaneous diffusion between the 2 membrane leaflets. ADAMTS5 We hypothesize that the absence of phosphatidylserines in CTB-vesicles could be due to the characteristic rigidity of the lipid rafts15 from which the CTB-affinity was supposedly derived. This

rigidity could restrict the diffusion of lipids and proteins in the plasma membrane and prevent spontaneous distribution of phosphatidylserines between the 2 lipid membranes. Analysis of CTB- and AV-vesicles in the plasma of preeclampsia patients and matched healthy controls revealed that they carry previously reported biomarker candidates for preeclampsia. However, the relative levels of each candidate biomarker in each of these 2 vesicles from plasma of patients and matched healthy controls were distributed into nearly all possible permutations. For example, CD105 was elevated in CTB- but AV-vesicles of PE patients, PAI-1 was elevated in both CTB- and AV-vesicles of PE patients, and CD9 was reduced in CTB-vesicles but not elevated in AV-vesicles of PE patients. This diverse permutation was further validated by a global proteomic profiling of the vesicles by mass spectrometry.

The means and standard deviation were calculated where appropriate. Statistical differences were determined by the ANOVA followed by Dunnett’s test and the level of significance set at p < 0.05. In many cases results were calculated as percentage of relevant control values (as the control values could vary between cell preparations and between experiments) to make understanding of the results easier. During the period of treatment with HOCS, there were no significant changes in the body weights of treated and untreated

animals; weight gain was normal in all the experimental groups. But there was a significant mTOR inhibitor decrease in the sex organ weights, namely testis, epididymis and seminal vesicle in all treated groups. Sex organ weights were highly decreased in the group III animals when compared to that of control animals (Table 1). The sperm of the control rats had normal counts, motility, and morphology (Table 2). In HOCS treated rats, the cauda epididymal sperm parameters showed evidence of dose dependent infertility. The sperm counts were significantly decreased in group II, group III and group IV animals compared to that of normal animals (Table 2). In group IV animals, the sperm counts were highly reduced selleck screening library when compared

to that of control rats. The sperm motility was highly inhibited in group II, group III and group IV animals (Table 2). More than 50% of the sperm had abnormal morphologies of various kinds, which included broken head, DNA damage sperm, coil in tail region of two or more sperm etc., were observed (Fig. 1). The plant extract intoxication exerted a significant decrease epididymal sperm concentration and sperm progress motility. The live/dead sperm count was increased in group II, group III and group IV animals. The reduction of sperm count and sperm motility were significantly (p < 0.05) higher in group IV treated animals when compared to that of control. Light photomicrography of the testicular tissue of vehicle treated rat showing intact lumen of seminiferous tubule, intact Bay 11-7085 basement membrane

and sertoli cells, intact interstitial tissue, cells of Leydig, and peritubular capillaries and venules. HOCS at 200 mg/kg, showing slight seminiferous tubular degeneration with scattered areas of interstitial edema (Fig. 2). There was also necrosis of the sertoli cell responsible for supporting developing spermatocytes. 300 and 400 mg/kg bw treated animals showing moderate to severe degeneration of the seminiferous tubules and shrinkage. Herbal drugs have been used since ancient times as medicine for the treatment of a wide range of diseases. Over the past decade, interests in drugs derived from higher plants, especially the phototherapeutic ones, have increased expressively. It is estimated that about 25% of all modern medicine are directly or indirectly derived from higher plants.7, 8, 9 and 10 The anti-fertility effect of HOCS confirmed by following measures.

Normally the balance is maintained between the oxidative attack

of the free radicals and the anti oxidative defense system prevailing in the cells and tissues.14Coleus edulis plant does not report pharmacological activities. It’s belonging plant species shows activates like antimicrobial, anti-oxidant and antiseptic. Therefore, it is worth conducting an investigation on the antioxidant potential of ACE, in cerebral infarction induced rats by BCA occlusion. In the present study, we attempted to study protective effect of ACE on acute ischemia reperfusion induced cerebral damage. Rucaparib ic50 In the brain, infarction size is an important determinant, to assessing the consequences of cerebral ischemia. Ischemia leads to neurological disability. The percentage of infarction was quantified by staining slices of brain with TTC. TTC was converted to red formazone pigment by Nicotinamide Adenine Dinucleotide (NAD) and dehydrogenase present in the living cells and unstained in dead cells. In I/R group of rats, noticeable cerebral infarction was developed. In our present study, pre-treatment with ACE produced dose dependent cerebroprotection by reducing the percent infarction

significantly; these reports were accordance with earlier reports. 10 In ischemia and reperfusion injury, this website brain cells are continuously exposed to free radicals by oxidative metabolism and inflammation. Furthermore, increased lipid peroxidation was marked Calpain as increased MDA levels in I/R and weaken the oxidative defense enzymes like SOD, CAT in I/R. In our study, we noticed increased MDA levels and decreased SOD, CAT levels in I/R grouped rats, significantly. As well as, in pre treated ACE groups, we observed that decreased levels of MDA and increased levels of CAT, SOD significantly. Thus, ACE may be strengthened the oxidative defense

mechanisms and reduced lipid peroxidation which is a marker of oxidative stress. There were several reports suggested that modulatory effects on lipid peroxidation and antioxidant enzymes following injuries such as cerebral ischemia. 15 and 16 According to these evidences ACE may be anti-oxidant. The present study results constitute evidence ACE had significant cerebroprotective activity and exhibited inhibitory effects against oxidative stress caused by cerebral ischemia and reperfusion injury. Suggesting that protective effect of ACE against cerebral infarction was mediated by antioxidant mechanism. This study further supports the possible use of ACE as a beneficial agent to ameliorate cerebral infarction. All authors have none to declare. “
“Staphylococcus aureus is the leading causative pathogen of hospital-acquired infections, which are increasingly resistant to antibiotics. 1, 2 and 3 Relapse episodes of S.

Two of these infants died, one in each study group, and are included in the mortality analysis below. For safety analyses, these infants were classified according to their enrolment status: 5/6 (3 vaccine and 2 placebo) and 1/6 (placebo) who converted at 9 months were exposed and negative at enrolment, respectively; at 12 months, 1 of those who seroconverted was exposed and 1 was negative (both were in the vaccine group) at enrolment. Including the extended follow-up of 300 participants through

September 30, 2009, 72 participants died at any time after receiving the first dose of PRV/placebo. These deaths occurred among 38/649 (5.9%) vaccine recipients and 34/643 (5.3%) placebo recipients (p = 0.66). For all participants, the two most frequent causes of death were gastroenteritis (13 among vaccine recipients and 11 among placebo recipients) and pneumonia (10 among vaccine recipients and 9 among buy NVP-BKM120 placebo recipients). FGFR inhibitor The overall mortality observed for the vaccine recipients was 60.7/1000 person-years and for the placebo recipients, 53.8/1000 person-years (p = 0.61). No significant differences were observed between the vaccine and placebo groups. Among the 38 infants HIV-infected at enrolment, 12 deaths occurred: 8 (38%) of those receiving vaccine and 4 (23.5%) of those receiving placebo (RR = 1.6; 95% CI = 0.59–4.5); p = 0.49) ( Table 5C).

Two deaths (10.5%) among the HIV-infected vaccine recipients

Rolziracetam and 1 death (10%) among the HIV-infected placebo recipients occurred before completing the 14-day response period following each dose. Overall, among the 21 HIV-infected infants in the vaccine group, 2 of 8 deaths were gastroenteritis-related, one of which was among a child classified as malnourished; 4 other HIV-infected vaccine recipients who died were classified as malnourished. Among the 17 HIV-infected infants in the placebo group, 3 of 4 deaths were gastroenteritis-related; 2 of these deaths were among children classified as malnourished ( Table 5C). Among the 177 infants HIV-exposed at enrolment, 12 deaths occurred: 6/88 (6.8%) of those receiving vaccine and 6/89 (6.7%) of those receiving placebo (Table 5D). Two of 6 deaths (33.3%) among the HIV-exposed vaccine recipients and 1 of 6 deaths (16.7%) among the HIV-exposed placebo recipients were gastroenteritis-related; one of the deaths in the vaccine group was in a child classified as malnourished. Among the 6 deaths in the HIV-exposed vaccine group, 1 participant seroconverted to HIV-infected prior to death (Table 5D). The median age at death for all vaccine recipients was 282 days (9.4 months), and for all placebo recipients, 223 days [7.4 months (p = 0.75)]. The median time to death after enrollment among vaccine recipients was 241 days; among placebo recipients it was 173.5 days (p = 0.47).

The DRCR.net25 reported 3 cases of endophthalmitis out of a total of 3973 injections (0.08%) in ranibizumab arms. The RISE and RIDE studies,13 taken together, reported a total of 4 endophthalmitis cases among a total of 10 584 injections administered. In the current study, all injections were performed in an ambulatory operating room, following recommended aseptic practices.17, 18, 19 and 20 The relatively high endophthalmitis rate in our study may be related to patient-related characteristics, such as poor socioeconomic status and hygiene habits.17

Finally, administering anti-VEGF to both eyes may increase the risk of systemic complications; GSK-3 inhibitor in fact, 1 of these patients had transient increase in creatinine levels during the study. In sum, in the current study, IV bevacizumab and IV ranibizumab were associated with improvement in mean BCVA and mean central subfield thickness in patients with center-involved DME at 48 weeks of follow-up when compared with baseline. Eyes in the IV bevacizumab group received a significantly higher number of injections than eyes in the IV ranibizumab group. During the study, eyes in the IV ranibizumab group experienced a faster recovery of BCVA compared with eyes in the IV bevacizumab group, which may be explained by the higher proportion of eyes in the IV ranibizumab group with a central subfield thickness <275 μm at intermediate-term study

follow-up visits. To our knowledge and based on a Medline search, this is the first report comparing IV bevacizumab and IV ranibizumab for the treatment of DME. The current see more study is limited by a small sample size; larger prospective studies are warranted to confirm our preliminary findings. All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Rodrigo Jorge

received travel support from Novartis to attend the 2012 American Society of Retina Specialists (ASRS) meeting. This study was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP), grant number 2010/013368; and Fundação Apoio ao Ensino, Pesquisa e Assistência (FAEPA) do Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo. Contributions of authors: conception and design of the study (I.U.S., Non-specific serine/threonine protein kinase A.M., R.C.S., R.J.); analysis and interpretation (A.B.N., E.T., F.P.P.A., R.P., R.C.S., J.A.C., A.M., I.U.S., R.J.); writing the article (A.B.N., E.T., F.P.P.A., R.P., J.A.C., A.M., I.U.S., R.J.); critical revision (A.B.N., J.A.C., R.C.S., I.U.S., A.M., R.J.); final approval of the article (A.B.N., E.T., F.P.P.A., R.P., R.C.S., J.A.C., A.M., I.U.S., R.J.); data collection (A.B.N., E.T., F.P.P.A., R.P., R.C.S.); provision of materials (A.B.N., E.T., F.P.P.A., R.P., R.C.S., J.A.C., R.J.); statistical analysis (A.M., R.J.); obtaining funding (A.B.N., E.T., A.M., R.J.); literature search (A.B.N., E.T., R.C.S., I.U.S., R.J.

As temporary freezing might have

reduced the potency of the vaccine, these subjects were excluded from participating in the malaria challenge. Of the 43 subjects enrolled, the mean age was 34.2 years (range: 20–45 years), 61% were males and the majority were Caucasian (49%) or African–American (40%). Transient pain at the injection site was the most frequently reported solicited local AE across vaccine groups in both studies, occurring with a similar incidence in each vaccine group (after 87–100% of doses) (Table 1). The frequency of Grade 3 pain was similar after vaccination across vaccine groups and studies (after 17–35% of doses). Grade 3 redness and swelling occurred after <7% of doses in any vaccine group. All Grade 3 AEs resolved within the initial 72-h Trametinib order follow-up period after each vaccination, with the majority of symptoms resolved within the first 24 h. The most frequently reported solicited general symptom in the Phase 1 study was myalgia (after 47–63% of doses across groups) and in the Phase 2 study fatigue (after 30–32% of doses across groups). Grade 3 general AEs occurred after <7% of doses in any vaccine group. In the Phase 1 study

all Grade 3 symptoms were considered to have a ‘probable’/‘suspected’ (PB/SU) relationship to vaccination and in the Phase 2 study, one report of Grade 3 malaise in a recipient of RTS,S + TRAP/AS02 was judged to have a PB/SU relationship to vaccination. Unsolicited AEs with a PB/SU relationship to vaccination

Roxadustat cell line were infrequent: influenza-like symptoms in 7 subjects (2 TRAP/AS02, 1 RTS,S/AS02, 4 RTS,S + TRAP/AS02), rigors in 1 subject (RTS,S + TRAP/AS02) and hypesthesia (numbness second of arm lasting 2 days) in 1 subject (RTS,S + TRAP/AS02) in the Phase 1 study; flu-like symptoms in 1 subject (RTS,S + TRAP/AS02) and upper respiratory tract infection in 1 subject (RTS,S + TRAP/AS02) in the Phase 2 study. No unsolicited AE with a PB/SU relationship to vaccination was of Grade 3 intensity. In both studies, no SAE was reported and no subject was withdrawn because of an AE. No clinically significant hematological, biochemical, or urine abnormalities were observed. In both studies, prior to vaccination, no volunteer had anti-CS antibodies (Table 2). In the Phase 1 study, the post immunization anti-CS GMTs at each timepoint were higher, but not statistically so, after administration of RTS,S/AS02 compared to RTS,S + TRAP/AS02. Post Dose 2, the anti-CS GMT in the RTS,S/AS02 group (85 μg/mL [95% CI: 53, 138]) tended to be higher than the RTS,S + TRAP/AS02 group (56 μg/mL [95% CI: 31, 100]) and higher than that of the corresponding Phase 2 post Dose 2 anti-CS GMT in the RTS,S + TRAP/AS02 group (35 μg/mL [95% CI: 20, 62]). In the Phase 1 study, an increase in anti-TRAP GMTs was observed after subsequent doses of TRAP/AS02 and RTS,S + TRAP/AS02 (Table 3); GMTs were similar in both groups.