Here we report the ability of

Here we report the ability of this website EEA to inhibit alpha glucosidase. HPLC analysis revealed that the major constituents of the extracts are vinblastine an alkaloid compound which showed a sharp peak at 2.850 mV respectively (Fig. 1). EEA was able to inhibit alpha glucosidase inhibitory activities in vitro in dose dependent manner. It has been recently reported that tea polyphenols inhibited glucose transporter of small intestine epithelial cells. Ethyl acetate extracts showed better activity than acarbose

with smallest IC50 values was 73.64 μg/mL. The most active extract showed competitive inhibition. Chemical analysis indicated that the α-glucosidase inhibitor was flavonoid. 23 In addition, polyphenols controlled the rise in blood glucose level when humans fed with fixed amount of carbohydrates with food, because a negative correlation was indicated by the polyphenolic content and glycemic index. 24 The enzyme inhibitors impede digestion through their action of digestive enzymes which play ABT-199 cell line a key role in the digestion

of plant starch and portions. Our results showed strong inhibition of alpha glucosidase activity. Higher inhibitory activities of EEA against alpha glucosidase that our results confirmed suggest its potential in prevention and therapy of obesity and diabetes. In most of the cases the mechanism of inhibition occurs through the direct blockage of the active center at several sub sites of 17-DMAG (Alvespimycin) HCl the enzyme. EEA has a good free radical scavenging

activity against all the four radicals. Maximum percentage inhibition was found against hydroxyl radical (71.15%). Alpha glucosidase activity performed under in vitro conditions showed an interesting result of 83.33% inhibition further in vivo study of α-glucosidase inhibition was carried out in lowering maltose and sucrose levels in blood. EEA treated and Acarbose treated animals did not show any change in the plasma glucose level. Hence EEA has a potential ability to inhibit the alpha glucosidase enzyme thereby causing partial digestion and keeping the blood glucose level normal. All authors have none to declare. “
“miRNAs are short (16–21 nt) endogenous, non-coding RNA (ncRNAs) molecules that regulate pervasive in higher eukaryotic gene expression at the post translation level of protein-coding genes, by the binding to complementary sequences in the 3′ UTR of multiple target messenger RNA (mRNA) and promote their degradation and/or translational inhibition.1 There are evidences that miRNAs have been implicated in various biological processes including cell proliferation and apoptosis during development, cell–cell interactions during development of the peripheral nervous system,2 to stress resistance and fat metabolism,3 from cellularization and segmentation on embryos4 to cardiogenesis5 and muscle growth,6 signaling, cell fate identity, organ differentiation and development, stress responses and carcinogenesis.

All AWPs are chaired by an ATAGI member, and depending on the iss

All AWPs are chaired by an ATAGI member, and depending on the issue, may be co-chaired by the senior representative from another statutory group such as CDNA or NIC, depending on the issue. Membership is always expertise-based, and may involve other ATAGI members, NIC members, and experts in a specific area who are not members of ATAGI provided they are free of high-level conflicts of interest. In this last case, where unique I-BET-762 chemical structure outside expertise is required, an invitation to submit technical material or other advice may be sought, but they cannot be an active member of the AWP. AWPs are supported by one or more scientific officers from the NCIRS who are responsible for assembling

the written report, obtaining resource materials and conducting further analysis if required. Crucial to the quality and timely delivery of high quality

advice to Government and to providers is selleck inhibitor the policy branch of the NCIRS. ( Since 2005, the vaccine funding advisory framework in Australia was changed to bring vaccines into the overall policy framework that has been used for drugs for some years. The PBAC was established to consider submissions, usually from manufacturers, based on cost-effectiveness applications for pharmaceuticals or new vaccines. The Chair of the PBAC is appointed full-time, but the Committee’s membership is otherwise made up in a similar way to that of the ATAGI, with clinicians, academics and others with particular expertise. PBAC meets three times annually to consider submissions, and then provides a recommendation to Government on whether or not to fund and on what basis. In the case of vaccines, the sponsor may submit for either NIP listing (free to eligible people and listed on the NIP), or PBS listing (requires a co-payment, and is not listed on the NIP). In Australia, the general criteria for suitability for listing on the NIP are defined in the Vaccine Appendix of the PBAC submission framework (Table A.1). Medicines Australia is the umbrella group representing pharmaceutical Mephenoxalone manufacturers in Australia, and its sub-committee the Medicines Australia

Vaccine Industry Group (MAVIG), is a consortium of vaccine manufacturers. MAVIG has played an important role in coordinating the industry view of national policy matters in industry’s representation to Government. It played a key role in the consultation and development phase of the vaccine appendix to the PBAC guidelines (Table A.1). ATAGI conducts formal ‘in camera’ consultations with vaccine manufacturers annually (ATAGI Industry Days) at which companies separately present their latest developments and plans for vaccines. This has proved to be an important two-way communication process to permit ATAGI to plan its working party activities and to coordinate with PBAC for pre-submission advice for upcoming submissions.

It is noteworthy to mention that IFN-γ responses to both liver- a

It is noteworthy to mention that IFN-γ responses to both liver- and blood-stage antigens have been positively correlated with protection [34]. In the same line, we found that the heterologous prime-boost Ad35-CS/BCG-CS induced significantly

higher numbers of CSp-specific IFN-γ-producing cells, indicating the induction of a type 1 T-cell response. The heterologous prime-boost administration also elicited the highest levels of CSp-specific IgG and in particular IgG2a. This finding has great implication for CSp-specific antibody responses, which might confer protection because the IgG response in the current heterologous prime-boost administration was mainly induced against the C-terminal region of CSp domain. The fact that the antibody response was stronger against C-CSp implies that epitopes responsible CSp-specific antibody responses are located in the C-terminal domains of the protein. Prolonged survival of a subset of PCs in BM has been implicated as the key component of the long-term maintenance of antibody titers [35]. In this study, heterologous prime-boost administration

was also the most efficient combination in terms of generating long-lived antibody responses; as shown by the induction of higher numbers of CSp-specific LLPCs upon restimulation with C-CSp. The effect of Ad35-CS/BCG-CS combination is of particular importance as LLPCs are thought to be instrumental for the acquisition of immunity against clinical malaria in endemic areas [36]. Furthermore, a recent study has shown that a GMZ2 vaccine, a fusion too protein consisting of the N-terminal portion of the glutamate rich protein (GLURP) fused OTX015 in vivo to a C-terminal fragment of merozoite surface protein 3 (MSP3) plus the synthetic TLR4 agonist glucopyranosyl lipid A (GLA),

elicits the highest number of LLPCs secreting cells specific for both the GMZ2 fusion protein and its two components [14]. In our current study, we tried to achieve simultaneous B- and T-cell responses against P. falciparum CSp. Heterologous prime-boost immunization regimens including vaccination of Ad35-CS followed by BCG expressing the P. falciparum CSp, could be one of the best approaches. The sporozoite challenge experiments are underway to define the protective efficacy of this prime-boost protocol. We would like to acknowledge Dr Katarina Radošević from Crucell Company (The Netherlands) for the critical review of the manuscript. We kindly thank the personnel in the animal facility of the Wenner-Gren Institute for monitoring the welfare of animals. Funding sources: This work was supported by grants from the European Commission (FP6 PRIBOMAL Project Number: LSHP-CT-2007-037494) and European Virtual Institute for Malaria Research (EVIMalaR; 7th Framework Programme). Conflict of interest statement: The authors declare that no competing financial interest exists. AR is employed by Crucell, a vaccine development company.

While there may be alternative explanations, immune interference

While there may be alternative explanations, immune interference between TRAP and RTS,S must be considered

as a leading explanation for the failure to see protection in the RTS,S/TRAP group. We have no real understanding as to how the anti-TRAP antibodies that were induced impacted on the anti-CS responses. While a specific correlate Akt inhibitor of protection for RTS,S has not been identified, analyses of potential correlates of protection consistently emphasize the association between protection and high levels of CS antibodies at the time of sporozoite exposure [2], [3], [4] and [5]. In the Phase II study reported here, peak RO4929097 IgG responses to CS in the RTS,S/TRAP group were approximately 50% of what would

have been typically observed in individuals receiving RTS,S alone. In contrast to CS, TRAP appears to be inherently more immunogenic, and in both the Phase 1 and Phase 2 studies, similar anti-TRAP humoral responses were observed with the combination and the component vaccines. Immunological interference between antigens in combination vaccines is a well-known although highly unpredictable phenomenon that can occur even in the presence of a potent adjuvant. In the Phase 1 study, low levels of cross-reactive anti-TRAP antibody responses observed in the RTS,S/AS02 group may be due to antibodies directed against the thrombospondin-like type 1 sequence in the C terminus of CS [39], [40] and [25]. At this point, there is no way of knowing conclusively as to whether or not measured or unmeasured immune responses to TRAP impacted on other aspects of the immune response induced by RTS,S. In the Phase 1 study, the RTS,S- and TRAP-specific responses evaluated by proliferative responses, and IFN-γ and IL-5 secretion in the culture supernatant, were similar for vaccinees who received the combination

nearly RTS,S + TRAP/AS02 and for vaccinees who received either RTS,S/AS02 or TRAP/AS02. At the time of evaluation in 1999, assays were not in place to measure CS-specific cellular responses. Hence, the RTS,S-specific responses recorded were the combined responses specific to both the HBs and CS antigen components of the RTS,S vaccine. In the Phase 2 trial, the vaccination regimens elicited low RTS,S- and TRAP-specific T cell responses, measured by IFN-γ ELISPOT assay, and were notably lower when compared to other studies using the same methodology [5] and [38]. After challenge, all infectivity controls, 5 of 5 TRAP/AS02 vaccinees and 10 of 11 RTS,S + TRAP/AS02 vaccinees developed parasitemia. There was no evidence of any prevention or delay of parasitemia by TRAP/AS02.

Batch FM 18 and FM 19 showed 12 h floating but drug release was l

Batch FM 18 and FM 19 showed 12 h floating but drug release was less Trametinib research buy the FM 10. Matrix forming gums like Xanthan gum and Guar gum also tried from FM 20 and FM 21 for floating behavior, but they were failed to float because of high densities. The drug release profile of cefdinir floating layer is shown in Fig. 3 and Fig. 4. The release profile from FM 10 in a

controlled manner with no burst release was seen. The release profiles seemed dependent on the initial drug concentration. FM 1, FM 2, FM 15, FM 16, FM20 and FM 21 did not show adequate floating tendency. To analyze the cefdinir release mechanism as well as to select the matrix layer for CBT formulation, in vitro release data were fitted into various release equations and kinetic models like first order, zero order, Higuchi and Korsmeyer and Peppas. FM 10 (Matrix layer) was chosen as the optimized formulation because

it showed more linearity between the cumulative percentage cefdinir released versus time (zero order) and Korsmeyer and Peppas, as indicated by the highest value of the correlation coefficient R2 among all the matrix layer formulations, and best fitted both zero order (R2 = 0.9986) and Korsmeyer check details and Peppas (R2 = 0.9838) models. Thus, it may be concluded that drug release from cefdinir matrix layer is best explained by the Korsmeyer and Peppas model and zero order. The value of the slope (0.8891) indicates that the drug released by zero order type

as shown in Table 5. CBT showed biphasic release (as shown in Fig. 3 and Fig. 4), in the first phase of the drug release profile depended on the concentration of the drug in the upper layer as an immediate dose, was released in less than 60 min, because of fast releasing components of loading layer. Second phase of release, the data were fitted into various kinetic models. Based on the n (0.8891) value of Korsmeyer and Peppas model, the mechanism of cefdinir floating layer followed zero order. The FTIR of plain drug, CBT and Placebo tablet is depicted in Fig. 5. The characteristic peaks of pattern followed the same trajectory as that of the drug alone with minor difference due to dilution effect. Stability ADP ribosylation factor studies were carried out at 45 °C and 75% RH for three months (climatic zone IV condition for accelerated testing) to assess their long-term (2 years) stability of CBT formulation. The protocols of stability studies were in compliance with the guidelines in the WHO document14 for stability testing of products intended for the global market. After storage, the formulation was subjected to a drug assay, floating behavior and in vitro dissolution studies. The statistical analysis of the parameter of dissolution data (F 2 = 70.

All samples were processed and analyzed at Natera Inc’s Clinical

All samples were processed and analyzed at Natera Inc’s Clinical Laboratory Improvement Act (CLIA)-certified and College of American Pathologists (CAP)-accredited laboratory (San Carlos, CA). Laboratory testing

was performed as previously described using validated methodologies for cfDNA isolation, polymerase chain DNA Synthesis inhibitor reaction amplification targeting 19,488 SNPs, high-throughput sequencing, and analysis with the next-generation aneuploidy test using SNPs (NATUS) algorithm.2, 3, 4 and 5 Samples were subject to a stringent set of quality-control metrics. A second blood draw (redraw) was requested if total input cfDNA, fetal cfDNA fraction, or signal-to-noise ratio did not meet quality metrics, or for poor fit of the data to the model. In cases of large regions (>25%) of loss of heterozygosity or suspected maternal or fetal mosaicism, redraw was not requested. Reports included a risk score for the 4 aneuploidies; when requested, reports included fetal sex. Risk scores were calculated by combining the maximum likelihood estimate generated by the NATUS algorithm with maternal and gestational age prior risks. All samples with a risk score ≥1/100 were reported as high risk for fetal

Y-27632 price aneuploidy and samples with risk scores <1/100 were considered low risk. For the purposes of this study, the high-risk results were further divided into a maximum-risk score of 99/100 or an intermediate-risk score of ≥1/100 and <99/100. The presence of >2 fetal haplotypes (indicative of either triploidy or multiple gestation) was reported only when the confidence was >99.9%. Additional sex chromosome aneuploidies (XXX, XXY, and XYY) were reported from June 2013. The following patient characteristics were requested for each sample: maternal date of birth, maternal weight, gestational age, and whether a paternal sample was included. Patients with available International Classification of Diseases, Ninth

Revision (ICD-9) codes ( Appendix; Supplementary Table 1) were categorized into 3 subcohorts: (1) “low risk” if aged <35 years and no aneuploidy-related high-risk codes; (2) “at risk” for fetal aneuploidy based solely on maternal age ≥35 years; or (3) “high risk” for fetal aneuploidy by ICD-9 code, regardless all of maternal age. High-risk indications included positive screening tests, ultrasound anomalies, and relevant family history. Patients without reported ICD-9 codes were categorized by maternal age as low risk (<35 years) or high risk (≥35 years). Follow-up information on high-risk results was obtained by telephone and recorded in an internal database. Clinical follow-up was completed on June 14, 2014, at which time all pregnancies were completed. Two partner laboratories accounting for 38.1% of the total 31,030 cases were responsible for their own follow-up efforts and were excluded from outcome calculations. Providers were encouraged to share information about false-negative (FN) results.

The filtrate on concentration yielded a syrupy mass which on the

The filtrate on concentration yielded a syrupy mass which on the paper chromatographic examination of concentrated

hydrolyzate revealed the presence of d-glucose only. The quantitative estimation of the sugar(s) in the glycoside RS-2 was done by the procedure of Mishra and Rao, which indicated that the glycoside consisted of aglycone; RS-2(A) and d-glucose in equimolar ratio of 1:1. The sodium metaperiodate oxidation, of the glycoside RS-2 indicated that at consumed 2.04 molecule of periodate and liberated 1.07 molecules of formic acid confirming that one molecule of d-glucose was attached to one molecule of aglycone RS-2(A) and also confirmed that the glucose was present in the pyranose form in the glycoside RS-2. A comparison of the UV spectrum of the aglycone RS-2(A) and the glycoside, RS-2, the position of attachment of sugar moiety to the aglycone was fixed at position 7, on the basis of following facts BKM120 nmr as mentioned in discussion. Thus keeping together all the above facts, a tentative structure to the glycoside RS-2 was portrayed in Fig. 5. The glycoside RS-2 on permethylation by procedure of Kuhn’s of followed by the acid hydrolysis of permethylated glycoside, yielded the aglycone (confirmed by m.m.p., Co-PC) and 2,3,4,6-tetra-O-methyl-d-glucose selleck compound (confirmed by Co-PC and Co-TLC), which indicated the involvement of C-1 of glucose in the glycosylation.

On hydrolysis with enzyme emulsion solution the glycoside RS-2 yielded the aglycone RS-2(A) which was identified as; 5,7,4-trihydroxy 3-(3-methyl-but-2-enyl), 3,5,6-trimethoxy-flavone and d-glucose, confirming β-linkage between aglycone and d-glucose. Keeping all the above facts together it was concluded

old that the 7 –OH of aglycone was linked with C–I of the d-glucose via β-linkage. Thus the structure to the glycoside RS-2 was assigned in Fig. 6 and it was identified as; 5,4-dihydroxy–3-(3-methyl-but-2-enyl) 3,5,6-trimethoxy-flavone-7-O-β-d-glucopyranoside. The curative properties of medicinal plants are mainly due to the presence of various complex chemical substances of different composition which occur as secondary metabolites.11 and 12 They are grouped as alkaloids, glycosides, flavonoids, saponins, tannins; carbohydrates & essential oils. Any part of the plant may contain active components.13 The medicinal action of plants is unique to particular plant species or groups of plants and is consistent with this concept as the combination of secondary products in a particular plant is taxonomically distinct.14 Arid and semi-arid plants are good sources for the production of various types of secondary metabolites which include alkaloids, flavonoids, steroids, phenolics, terpenes, volatile oils, saponins, tannins, lignins and so many other metabolites. F. limonia L. (Family Rutaceae) commonly known as Wood Apple or Kaitha & is widely distributed in most tropical & subtropical countries.

Journal of Physiotherapy will continue to advocate for the adopti

Journal of Physiotherapy will continue to advocate for the adoption of GRADE and better reporting of comparative research in its efforts to help advance evidence-based physiotherapy. “
“This 59th volume marks the first occasion of publication of clinical trial protocols in Journal of Physiotherapy. A trial protocol is a document that is developed before a research study commences. It provides the background and justification for the trial, describes the trial method,

and documents how the data will be analysed. Protocols of clinical trials have been published in a number of health science journals for several years. It is recognised that this process helps to improve the standard and communication of health-related research in the following ways ( Chalmers and Altman 1999, Eysenbach 2004): • Allowing readers to compare the planned trial with how the E7080 in vitro trial was actually conducted In addition, trial protocols are likely to be of value to clinical physiotherapists because they: • Help physiotherapists easily stay abreast of the cutting edge of physiotherapy research It is the intention of the Journal of Physiotherapy Editorial Board that the protocols published in this journal will provide these benefits to the research and clinical

communities. In alignment with the Journal’s standards of publication, published protocols will describe flagship trials that have been funded by nationally or internationally competitive funding schemes. Selleckchem Enzalutamide The abstract of each protocol will be published in the printed issue, accompanied by a commentary from a distinguished expert in that field. The aim of the commentary is to help readers understand the these potential impact that the trial will have on physiotherapy practice or the way we understand therapeutic modalities and/or diseases managed by physiotherapists. The commentary

will also highlight important strengths and limitations of the trial that will aid readers with their interpretation of the trial. The full trial protocol will be available online, for those who wish to read further detail about the study. While the publication of trial protocols is one important step that can reduce misconduct in the publication of research findings, it is by no means a panacea for such wrongdoing, which may be the result of ineptitude or scientific fraud (Hush and Herbert 2009). For example, a review of protocols published in The Lancet found instances where the primary and secondary outcomes and subgroup analyses were different from those in the protocol ( Al-Marzouki et al 2008). These insights from a leading medical journal with experience of publishing trial protocols have been useful in the development of clear criteria for authors considering publication of a trial protocol in Journal of Physiotherapy.


and p = 0 0292), but not against H1N1 A/New Jersey/0


and p = 0.0292), but not against H1N1 A/New Jersey/08/76. Of note, the cross-reactive HI antibody profiles against the distant H1N1 viruses A/Swine/Italy/14432/76 selleck kinase inhibitor and A/New Jersey/08/76 after 2 immunizations (serum sample day 42) were generally in agreement with the calculated antigenic distances that were obtained using post-infection sera. Remarkably, only the cross-reactive HI antibody profile against the distant H1N1 virus A/Swine/Ned/25/80 induced in group 4 (15 μg HA split antigen) was in agreement with the calculated antigenic distance (p = 0.1269) whereas these cross-reactive HI responses in the other groups were significantly lower (p ≤ 0.0245). Parenteral, non-adjuvanted trivalent influenza vaccine (TIV) (group 2) displayed relatively limited immunogenicity inducing after two immunizations only in one out of the six ferrets a homologous HI antibody titer ≥40 (titer range 13–70; Fig. 1A) and no cross-reactive HI antibody titers (mean titer <40 (Fig. 1B–D). VN antibody responses closely paralleled those measured in the HI assays. Homologous VN antibody titers were induced after a single intranasal immunization with Endocine™ adjuvanted split, or whole virus antigen: In 4 out of 6 ferrets of group 3 (5 μg HA split antigen; titers ≤8–64), in 5 out of 6 ferrets ABT199 of group 4 (15 μg HA split

antigen; titers ≤8–724), in all ferrets of group 5 (30 μg HA split antigen; titers 11–627) and in 2 out of 6 ferrets of group 6 (15 μg HA whole virus antigen; titers ≤8–64). Terminal deoxynucleotidyl transferase A second immunization increased the VN antibody titers in all ferrets, irrespective of the antigen and antigen dose (groups 3–6, titers 64–859, 64–8192, 41–3435 and 32–304) (Fig. 2A). A third immunization was effective in 5 out of 6 animals in group 3 (titers, 362–2436), 2 out of 6 in group 4 (titers, 662–4871), 3 out of 6 in group 5 (titers, 724–4884) and in all animals of group 6 (titers, 113–747). The differences in VN antibody

titers between the 3 split antigen HA doses (groups 3, 4 and 6) were not significant (p > 0.05). However, mean VN antibody titers in group 4 (15 μg HA split antigen) were significantly higher than in group 6 (15 μg HA whole virus antigen); p = 0.03 and p = 0.01 after 2 and 3 immunizations, respectively. Measuring VN antibodies against the distant viruses H1N1 A/Swine/Ned/25/80 and H1N1 A/Swine/Italy/14432/76 showed the highest cross-reactive VN antibody titers in group 4 (15 μg HA split antigen) after 2 immunizations, but the differences were not significant (Fig. 2B and C, respectively). Parenteral, non-adjuvanted TIV (group 2) did not induce VN antibody titers (Fig. 2). Challenge with the homologous wt-pH1N1 was performed four weeks after the last immunization. All ferrets of groups 3–6 (i.n. Endocine™ adjuvanted pH1N1/09 vaccines) as well as control group 1 (i.n. saline) survived the follow-up of 4 days post inoculation (dpi), when they were euthanized.

5 kg) vs normal birth weight (as a binary variable), small

5 kg) vs. normal birth weight (as a binary variable), small AZD6244 for gestational age vs. appropriate for gestational age (as a binary variable), rate of infant growth from birth to three months of age, infant weight at 12 months of age and season of birth (harvest/wet season January–June; hungry/dry season July–December). Rate of change in weight from birth to three months was calculated as the difference between sex-specific birth weight standard deviation score and sex-specific weight at three months standard deviation score. We also looked at weight for age standard

deviation differences between three and six months of age and six and 12 months of age. Associations between these early-life exposures and antibody responses were tested by multiple linear regression analysis. Probability values <0.05 were considered to be statistically significant for all tests. All statistical

analyses were performed using DataDesk, version 6 for Windows, Data Description Inc., Ithaca, NY. A total of 858 individuals met the criteria for recruitment into the current study. Of these, 78 were known to have died prior to follow up, leaving a cohort of 781 to be traced. Of this number, 145 were excluded on the basis they were currently participating in another ongoing study and three because they were confirmed to be pregnant by an MRC midwife prior to the start of the study. Of the remaining 633 individuals who were eligible to participate, 241 were not available [dead (4), self-confirmed as pregnant (45), RGFP966 overseas (24), outside designated study area (58), not traceable (50), traceable but unavailable for study (60)] and 72 did not consent to participate. A total of 320 subjects Megestrol Acetate (41% of 781 followed up) consented and participated in the current study. Compared to non-participants, participants were younger (22.2 y vs. 23.0 y; p < 0.0001) and there were significantly more males than females (51.9% vs. 45.3%). No differences were observed between the participants and

non-participants in available early-life information (data not presented). Table 1 details the early-life characteristics of the subjects recruited. A total of 41 (12.8%) of subjects were born of a low birth weight (<2.5 kg), and a higher proportion of these were female. Of these, 13 were born pre-term (<37 weeks gestation), although 9 had a missing gestational age. A total of 267 (83%) of the cohort had gestational age assessments available. Using the William’s reference data [15], 51 (19%) of these infants would be considered small for gestational age (SGA). Male subjects were significantly heavier at three months and at 12 months of age, but the rate of early growth, expressed as the sex-specific change in z-score between birth and three months of age, three to six months, or six to twelve months did not differ between males and females. Characteristics of the study participants at follow up are detailed in Table 2.