Respondents with missing information on any variable described above are excluded.

Logistic regression in Stata 12 SE is used, and coefficients are average marginal effects (AME) predicted with the margins option. Contrary Temsirolimus manufacturer to what is often believed, log-odds ratios or odds ratios are not comparable across studies or models ( Mood, 2010 and Wooldridge, 2002). Therefore, AME are reported, which are easily interpretable as the average impact on the probability (0–1) of good health. For categorical variables, AME give the discrete difference in the probability of good health between the relevant category and the reference group. As the outcome is restricted to be 0 or 1 the estimated effects are not additive: If a person has many risk factors, the measured outcome can still not be worse than “not good.” Trametinib cell line The predicted probabilities of

good health in 2000 at different combinations of risk factors will therefore also be shown, using a type case, and varying the statistically significant lifestyle factors one by one and in combination for this case. The type case is a woman of average age, income and education, who usually drinks less than two glasses, eats vegetables daily, is not overweight, and does not see friends and family often (smoking, exercise and social support are set to vary). Because of sample size restrictions, response categories for some variables have been collapsed. In these cases, different categorizations have been tested, and those reported give the most robust results. Descriptives for all variables are given in Table 1. Recall that all respondents had good health in 1991, so the 20% reporting less than good self-rated health in 2000 or 2010 have seen deterioration. There are equal shares of men and women, and the average age in 1991 is 38 for respondents observed in 2000 and 36 for those observed in 2010 (this decline is explained by panel ageing, as those who remained in 2010 were younger in 1991 than those who remained in 2000). Around 30% are single households, and 28% are overweight in 1991. A majority, 74%, exercise each week, and around 60%

eat vegetables every day. 49% have never smoked, and around 30% currently smoke. Less than 10% never of drink alcohol, and of those who drink, around half usually drink more than a couple of glasses. Around half the sample see friends often and an equal share see family often. Only 4% lack social support. Table 2 gives regression results for self-rated health in 2000 (models 1A–1B) and in 2010 (models 2A–2B). In both cases, model A includes lifestyle variables, and model B additionally includes control variables. Model 1A shows that weekly exercise, usually drinking more than two drinks, and seeing friends often in 1991 are positively related to health in 2000 (statistically significant, P < 0.05), while smoking and lack of social support are negatively related to health (P < 0.05).

From these

results it was conclude that to sustain highly water soluble drug higher molecular weight intermediate ethoxyl content (48–49.5%) ethylcellulose polymer was more suitable. All authors have none to declare. Authors gratefully acknowledge the support of Department of Science and Technology, Nanomission (SR/NM/NS-101/2008), New Delhi for providing financial assistance. We also thankful to Aarti Drugs Pvt. Ltd. and Colorcorn Asia Pvt. Ltd. for providing Metformin hydrochloride and ethylcellulose respectively as gift samples. “
“Type 2 diabetes mellitus is a complex metabolic disorder that involves a huge number of pathophysiologic mechanism, including insulin resistance, decreased insulin secretion, and excess glucose production by liver among others.1 An oral hypoglycemic agent Repaglinide (REPA) is the first member of meglitinide class used in type 2 diabetes mellitus acts by binding to specific site on pancreatic β-cell ZD1839 and block ATP-dependent potassium channels to stimulate insulin release.2 Due to its short half-life (<1 h) required frequent dosing before meal and this may cause side effects

like headache, skeletal muscle pain and gastrointestinal effects.3 To enhance the bioavailability and decrease the side effects of REPA, a sustained release new drug delivery system is necessitate. Solvent evaporation, solvent diffusion, solvent extraction or any modification in the basic principle of emulsification technique produces the drug loaded controlled release nanoparticles of desired properties.4 Ethylcellulose Quisinostat cost (EC) is a non-biodegradable and biocompatible polymer which is extensively studied as encapsulating material for the controlled release of pharmaceuticals.5 and 6 A comparative study by Ubrich et al concludes that EC was efficiently sustained drug for maximum time than other polymers like PLGA and polycaprolactone.7 Therefore we selected EC as polymeric material for the preparation of repaglinide loaded ethylcellulose nanoparticles (REPA-EC

NPs). The aim of present study was to formulate REPA-EC NPs by solvent diffusion technique and characterize it. The characterization includes particle size and zeta potential determination, encapsulation efficiency, drug content, surface ADP ribosylation factor morphology, drug–polymer interaction study by FTIR, comparative XRD, in vitro dissolution study and drug release kinetics determination by different models. Repaglinide (REPA) was kind gift from Wockhardt Research Centre (Aurangabad, India). Ethylcellulose (300 cps viscosity grade) procured from Sigma–Aldrich USA. Ethyl acetate was purchased from Merck (Mumbai, India). Polyvinyl alcohol (PVA, MW Approx. 1,25,000) from SD Fine Chem Ltd. (Mumbai, India). The experimental work was performed by using triple distilled water filtered with 0.22 μ membrane filter. REPA-EC NPs were prepared by emulsion solvent diffusion technique.

Additionally, FomA has been recognized as a major immunogen of F. nucleatum [16] and [17]. Intriguingly, it has been reported that FomA is involved in binding between fusobacteria and Streptococcus sanguis on the tooth-surface and to Porphyromonas gingivalis (P. gingivalis)

in the periodontal pockets [18], supporting the view that FomA acts as a receptor protein in co-aggregation with other oral pathogenic bacteria. Thus, FomA is a potential target for the prevention of bacterial co-aggregation. selleckchem Classical treatments for periodontal diseases involve not only mechanical and antibiotic therapies but also surveillances on dynamic processes including the periodontopathogenic bacteria and the host responses. Chemical antiseptics are also used for treatments of periodontitis and halitosis. However, most of the chemical antiseptics fail to cure chronic, severe periodontitis and halitosis. Treatments using multiple doses of antibiotics to cure infection-induced periodontitis and halitosis have risks of generating resistant BIBF 1120 manufacturer strains and misbalancing the resident

body flora [19]. In addition, even though bacteria in the dental biofilm can invade the periodontal tissues, most of bacteria located in the dental biofilm and outside the host tissues are inaccessible to antibiotics. The treatments of periodontitis and halitosis have not been significantly improved during the past 40 years due to the lack of focus on the awareness that these diseases are polymicrobial diseases as opposed to mono-infections. Vaccines targeting oral bacteria [such as Streptococcus mutans (S. mutans) for dental caries; P. gingivalis else for periodontitis] are currently being evaluated [20] and [21]. However, these vaccines cannot combat the enhanced pathogenesis (e.g. co-aggregation/biofilms) by F. nucleatum. Since the plaque biofilm is a common feature for almost all oral

bacteria, blocking the bacterial co-aggregation at an early stage in biofilm formation will broadly prevent various biofilm-associated oral diseases including periodontitis and halitosis [22]. In the study, we demonstrate that F. nucleatum FomA is immunogenic, and that mice immunized with FomA produce neutralizing antibodies which prevent bacterial co-aggregation and, also gum abscesses and halitosis associated with co-aggregation. Moreover, immunization with FomA conferred a protective effect on bacteria-induced gum swelling and decreased the production of macrophage-inflammatory protein-2 (MIP-2) cytokine. These findings envision a novel infectious mechanism by which F. nucleatum interacts with P. gingivalis to aggravate oral infections. Moreover, this work has identified FomA as a potential molecular target for the development of drugs and vaccines against biofilm-associated oral diseases. F. nucleatum (ATCC® 10953) and P. gingivalis (ATCC® 33277) were cultured in 4% (w/v) trypticase soy broth (TSB, Sigma–Aldrich, St. Louis, MO) supplemented with 0.

An illustration of practical application of the method to the ErbB2/3 network model is given in Section 3. To create local sensitivity spectrum of our model parameters, each nominal parameter Pi was incremented and decremented by 1% of its value (dpi) and the normalised sensitivity coefficient for the area under the pAkt time course profile was calculated as follows ( Zi et al., 2008): CipAkt=SpAkt(Pi+dPi)-SpAkt(Pi-dPi)SpAkt(Pi)2dPiPi The construction and calibration of the ErbB2/3 model was carried out with the use of the DBsolve package for kinetic INCB024360 clinical trial modelling (Gizzatkulov et al., 2010 and Goryanin

et al., 1999). All GSA-related computations were run on Edinburgh University ECDF cluster: 10 nodes were used to run simulations of ODE system for 120,000 Sobol’s points; 200 nodes were used to calculate PRCC indexes for sensitivity analysis. Thus an average analysis took 20 h for model simulation and two hours for sensitivity analysis. ODE system was solved using CVODE solver from SUNDIALS package (Hindmarsh et al., 2005), sensitivity analysis was performed with the package ‘sensitivity’ selleck chemicals (http://cran.r-project.org/web/packages/sensitivity/index.html) in R environment (http://www.r-project.org/). PE04 and OVCAR4 cells were

grown as monolayer cultures in RPMI supplemented with 10% heat-inactivated foetal calf serum (FCS) and penicillin/streptomycin (100 IU/mL) in a humidified atmosphere of 5% CO2 at 37 °C. Time course experiments were set up by plating cells into 10 cm diameter petri dishes and leaving for 24 h. Cells were then briefly washed in PBS before transferring to phenol red-free DMEM containing 5% double Fossariinae charcoal-stripped serum supplemented with penicillin/streptomycin (100 IU/mL) and glutamine (0.3 mg/mL) for a further 48 h prior to treatment. Cells were treated with UCN-01 (protein kinase inhibitor; Calbiochem #539644; final concentration of 1 μM), LY294002 (PI3 kinase

inhibitor; Calbiochem #440204; final concentration 20 μM), Pertuzumab (ErbB2 inhibitor; final concentration 100 nM) and stimulation by Heregulin (R&D Systems; 396-HB-CF) was at final concentration of 1 nM. Cells were treated for 15 min with the aforementioned drugs as appropriate immediately followed by the addition of heregulin-β (1 nM). The concentrations of drugs used in the experiments corresponded to the dose causing 50% inhibition of cell growth. Samples were collected at time points of 1, 5, 30, and 60 min after initiation of heregulin treatment, washed in PBS, and immediately lysed in ice-cold isotonic lysis buffer [50 mM Tris–HCl (pH 7.5), 5 mM EGTA (pH 8.5), 150 mM NaCl, 1% Triton X-100] supplemented with aprotinin (10 μg/mL), phosphatase inhibitor cocktail A (Sigma, P2850), phosphatase inhibitor cocktail B (Sigma, P5726) and a protease inhibitor cocktail (Roche, 11836153001). Lysates were centrifuged for 6 min at 13,000g and protein concentrations of supernatants subsequently determined using the BCA assay (Sigma, BCA-1).

From 2000 through 2006, meningococcal serogroup was identified for isolates from 127 (45%) of 281 confirmed cases (Fig. 1); 105 (83%) were serogroup B, 20 (16%) were serogroup C and 2 selleck chemical (1%) were other serogroups (A [n = 1] and W135 [n = 1]). From 2007 through 2011, serogroup was determined for 335 (77%) of 437 meningococcal cases, and serogroup C replaced B as the most prevalent serogroup identified among confirmed

cases of meningococcal disease ( Fig. 1). Based on cases with known serogroup, cumulative incidence of serogroup C meningococcal disease in the city of Salvador was 0.1 cases per 100,000 population per year from 2000 through 2006 (Fig. 2) with 1 death (case-fatality, 5%). In 2007, 13 cases (0.45 cases/100,000 population) of serogroup C meningococcal disease were

identified with 2 deaths (case-fatality, 15%); in 2008, 53 cases (1.8 cases/100,000 population) were identified with 4 deaths (8%) and in 2009, 69 cases (2.3 cases/100,000 population) with 10 deaths (14.5%). From ABT-263 mouse 2007 to 2009, children younger than five years old accounted for 34 (25%) of 135 cases (incidence, 4.8 cases/100,000 children <5 per year; Fig. 3) and 4 (25%) of 16 deaths. Among 10–24 year olds, there were 43 (32%) cases (5.2 cases/100,000 population/year) and 3 deaths. MenC vaccine was introduced into the routine infant immunization schedule in the city of Salvador in February 2010,

with a catch-up vaccination campaign for all children younger than 5 years. In the first month, 87,111 doses of MenC were administered to children <5 years, reaching an estimated 44% coverage of the target population with at least one dose. By December 2010, an estimated 92% of children younger than 5 years had received at least one dose of MenC vaccine (Table 1). In the first six months of 2010, cases of meningococcal disease continued to increase, with 93% of 63 cases among persons 10–24 years of age. The state health department purchased an additional MenC vaccine and conducted mass vaccination in three phases of persons 10–24 years of age. The first phase, targeting 10–14 year olds, all began May 30; 160,554 (93%) of 172,624 MenC doses administered in this age group were applied in the first weekend of the campaign, reaching 75% of the target population. The second phase, targeting those 15–19 years began June 12; 145,249 (96%) of 151,884 MenC doses administered in this age group were applied in the first weekend. The third phase, targeting 20–24 year olds, was delayed until August 14; only 68,362 (67%) of 102,565 MenC doses administered in this age group were applied in the first weekend. At the end of the third phase, coverage with at least one dose of MenC had reached 80% among 10–14 year olds, 67% among 15–19 year olds, and 40% among 20–24 year olds (Table 1).

Setting: Hospital ward of a tertiary referral centre in Auckland, New Zealand. Participants: Adults scheduled for pulmonary resection via open thoracotomy. Exclusion criteria: (i) unable to understand written and spoken English, (ii) tumour invasion of the chest wall or brachial plexus, (iii) physiotherapy for a respiratory or shoulder problem within 2 weeks prior to admission, (iv) development of a postoperative pulmonary complication prior to randomisation on Day 1 postoperatively, or (v) intubation and mechanical ventilation ≥ 24 hours following surgery. Randomisation

of 76 patients allocated 42 to the intervention group and 34 to the control group. Interventions: Both groups received usual medical and nursing care via a standardised clinical pathway, which included early and frequent position changes, sitting out of bed on the first postoperative day, early ambulation and frequent pain assessment. In addition, the intervention Raf inhibitor this website group received daily targeted respiratory physiotherapy, which

comprised deep breathing and coughing exercises, assistance with ambulation, and progressive shoulder and thoracic cage exercises. Outcome measures: The primary outcome was incidence of postoperative pulmonary complications, defined using a standardised diagnostic tool. The secondary outcome was the length of hospital stay. Results: The primary and secondary outcomes were available for all enrolled patients. Neither the incidence of postoperative pulmonary complications [mean difference intervention-control 1.8% (95% CI –10.6 to 13.1%)] nor the hospital length of stay [intervention group median 6.0 days, control group median 6.0 days; p = 0.87) differed significantly between groups. The overall incidence of postoperative pulmonary complications (3.9%) was lower than expected. Conclusion: In adults following open thoracotomy, the addition of targeted respiratory physiotherapy to a standardised clinical pathway that included early mobilisation did not reduce the incidence of postoperative pulmonary

complications or change length of hospital stay. This study is a high-quality randomised controlled trial, and novel in comparing the efficacy of a postoperative physiotherapy program with a no-physiotherapy control group in patients undergoing open lung resection. Findings accord with the conclusion of a systematic all review of physiotherapy after cardiac surgery (Pasquina et al 2003) that there is no evidence of benefit of routine, prophylactic respiratory physiotherapy over standard medical/nursing care. In response, one would anticipate that physiotherapists working in this field, particularly those in Australia and New Zealand (Reeve et al. 2007), would re-examine their current practices. Notably, primary and secondary outcomes exhibited ‘floor’ effects, testament to the quality of care in such a first world, tertiary referral hospital setting.

No adverse events were associated with injections of either adjuvant or vaccine, based on clinical observations and hematological/biochemical analyses ( Tables S3–S7 in Supplemental Data). In agreement with Trial #1, dogs in the Saline group did not spontaneously cure (Fig. 2A). CS of five dogs in the Saline group increased by 1.4 (range: −1 to +5, where a positive difference equates with worsening disease symptoms and a negative difference indicates an improvement in clinical symptoms) between Day

0 and the endpoint (either Day 180 or at the time of death or rescue treatment) indicating increased disease severity in those dogs. Only one dog out of five (20%) in this group completed the 180-day study. In contrast to the Saline group, dogs in the Adjuvant and Vaccine groups showed clinical improvement (Fig. 2). Changes in CS for the Adjuvant group and the Vaccine group were −2 (range: selleck chemicals −4 to +3) and −1.6 (range: −6 to +4), respectively. Three out of five dogs (60%) in the Adjuvant group and 5 out of 10 dogs (50%) in the Vaccine group completed JNJ-26481585 purchase the study alive and without drug treatment (Table 3). Of the three Adjuvant-group dogs completing the study, two dogs (Day 0 CS = 6 and 7) received four injections; the third dog (Day 0 CS = 4) received six injections of MPL-SE. The five dogs in the Vaccine group

that finished the study alive and without rescue treatment all had a Day 0 CS <8; these dogs received six injections. In contrast, of the four dogs in the Vaccine group that were given

rescue treatment (Glucantime and/or amphotericin B), three had a Day 0 CS ≥8 (and two of the three received only four vaccinations). Clinical improvement, including lower CS, brought by the vaccine or adjuvant was often associated with clearance of parasites. This was observed for many of the improved dogs in the vaccine and adjuvant groups that were parasitologically negative for most, if not all, of the post-enrollment time points examined (Table Oxymatrine 4). In contrast, the saline placebo dogs and most of the other dogs that were eventually removed from the study, either because they showed no clinical improvement or because they died during the study period, remained parasitologically positive (Table 4). The observations recorded in Table 3 and Table 4 and the graphs in Fig. 2B and 2C suggest that the vaccine worked better in moderately sick dogs than in severely sick dogs. No clinical improvement was observed for dogs in the Vaccine group that were severely sick at the time of inclusion (CS ≥8 at Day 0, n = 4). The kinetics of CS for dogs scoring ≥8 was very similar for the Saline group and Vaccine group ( Fig. 2B). In contrast, moderately sick dogs (CS <8 at Day 0, n = 6) responded better to the vaccine; the CS for these dogs decreased by a mean 2.8 points, and 83% of them completed the 180-day study.

By RT-qPCR, mRNA of IL-8 showed an immediate down-regulation followed by a slow up-regulation which was statistically significant (P = 0.02) in a regression model against time ( Fig. 1). There was no discernible effect of vaccination on IL-1β ( Fig. 2) or IFNγ ( Fig. 3). TNFα expression was undetectable in a considerable number of samples: in 6 cases there was no detectable expression before or after vaccination; in 5 cases mRNA was detected only before vaccination, and in 5 cases only after vaccination. In the remaining 5 cases, click here there

was a modest down-regulation, but this was not statistically significant in view of the small number of data pairs. HIV-infected participants did not differ from HIV-uninfected this website participants with

respect to changes in cytokine expression following vaccination, and those biopsies in which TNFα expression was not detectable were not more likely to come from HIV-infected participants (data not shown). The safety of live, attenuated vaccines in HIV infected people is of paramount importance if vaccines are to play any role in reducing the burden of common diseases in tropical populations. In this study we found that in 34 HIV seropositive adults given a total of 58 courses of three live, attenuated oral vaccines there was no evidence of serious adverse events: no hospitalisations, no episodes of diarrhoea requiring treatment, no significant febrile illnesses, and no increase in symptoms such as abdominal pain, nausea or loss of appetite. There was no evidence of haematological toxicity. If we accept that oral vaccines do not either cause diarrhoea after 7 days have elapsed beyond the final dose of vaccine, there was no increase in diarrhoea. The interpretation of diarrhoea data in this setting is difficult if we use HIV seronegative adults as the comparison group, as at any given point

in time HIV infected adults have a higher incidence rate of diarrhoeal disease [19]. We believe that this explains the higher diarrhoea incidence after 7 days following vaccination. Our data are compatible with the hypothesis that these vaccines lead to a modest increase in mild, transient episodes of diarrhoea beyond 1 week in HIV infected adults. They are also explicable with there being a consistently increased risk of diarrhoea in HIV throughout the period of observation. We found no evidence that vaccines induce intestinal inflammation. IL-8 is a chemokine expressed by epithelial cells on contact with potentially invasive bacteria. The other, pro-inflammatory, cytokines showed no change in expression over the week following vaccination. While these data do not rule out a pathogenic effect of these vaccines, they offer considerable reassurance that rotavirus vaccine does not induce inflammation.

Nasal wash, BAL, nose GSK1120212 and lung tissues were collected on Day 46. RSV F-specific antibodies in cotton rat sera were measured in an enzyme linked immunosorbent assay (ELISA) as previously described [25]. Competitive inhibition by cotton rat sera of the binding of palivizumab monoclonal antibody

(ASD Specialty Heath Care Inc., Chicago IL) was measured by an ELISA method as previously described [25]. Serum RSV virus neutralization titers were determined as described previously [25]. Five days after intranasal RSV challenge, cotton rats were sacrificed and the lungs harvested. Lung tissues were homogenized and clarified by centrifugation at 12,000 × g for 10 min. Virus titer in the supernatant was determined by plaque assay as described previously [25]. Lung tissue slides were stained with hematoxylin, eosin (H&E) and observed under a Nikon Eclipse microscope. Slides were evaluated in a blinded fashion using a score of 0–4 (0 = none; 1 = minimal; 2 = mild; 3 = moderate;

4 = maximum inflammation) in order of increasing severity for each of the following 5 parameters: (a) peribronchiolitis; (b) perivasculitis; (c) bronchoiolitis; (d) alveolitis and (e) interstitial pneumonitis as described by Prince et al. [31]. Summary scores for animals in each group were used to generate an overall score/group expressed as the arithmetic mean + SEM of the individual animals. Comparisons between mean scores of each group and non-immune animal challenge scores were analyzed using Student’s t-test. The sum of the scores of five SCH772984 parameters

per animal was used for analysis of histopathology data. Pair wise t-test was analyzed in EXCEL while the GMT and 95% CI were calculated using Graph Pad Prizm. Immune responses to RSV F nanoparticle vaccine (30 μg) administered IM in the presence or absence of adjuvant were compared to animals that received passively transferred palivizumab at the recommended human dose of 15 mg/kg. As controls, animals were infected with 105 pfu of RSV-A Long and allowed to recover, or vaccinated with FI-RSV (Lot 100 at 1:25 dilution), or treated with placebo. Three weeks after the second vaccine dose the immunization with unadjuvanted PDK4 RSV F nanoparticle vaccine had induced titers of anti-RSV F serum IgG (Fig. 1A) that were significantly higher (p < 0.001, t-test) than cotton rats immunized with FI-RSV antigen or infected with RSV-A virus (p < 0.001, t-test). Adjuvant enhanced RSV F vaccine antibody titers by about 10-fold after the boost ( Fig. 1A). Cotton rats that received palivizumab (IM injection) exhibited lower anti-RSV F IgG serum titers compared to the polyclonal responses obtained following immunization with adjuvanted RSV F (GMT = 1926 vs 1469,084 E.U., respectively Fig. 1A). Antigenic site II on the RSV F polypeptide is the target of palivizumab [32].

1). Despite the convergence and interaction of these hormonal and

neurobiological variables that may render the adolescent particularly vulnerable to stressors, not all adolescents are adversely affected by stress and experiencing stressors during adolescence does not inevitability result in negative outcomes. However, it is unclear what may account for the different reactions that adolescents show in response to stress exposure. Some differences in the neurobehavioral responses to adolescent stress across studies are undoubtedly mediated by subtle or significant differences in the specific experimental paradigms and/or assays used. For instance, studies that exposed adolescent rats to social defeat stress found either increased or decreased anxiety-like behaviors in adulthood (Watt Ibrutinib chemical structure et al., 2009 and Weathington et al., 2012), but these diametrically opposed results can likely be explained by experimental

differences, such as the length and frequency of the social defeat and the animal housing conditions (i.e., single vs. group) used in these two studies. More intriguing, however, Vandetanib is the difference in how individual animals respond to a stressor within an experiment. A greater understanding and appreciation of this variation may potentially shed light on what makes some animals more or less resistant to stressful experiences. To

illustrate this stress-induced variability, I present a specific example from a pilot study we recently conducted. Briefly, in this study we exposed Vasopressin Receptor adolescent male rats to 1 h of restraint stress every other day from postnatal day (PND) 28–49. This age span was used as this 3 week period in rodents is associated with the most significant changes in physiological, neurobiological, and behavioral parameters as animals transition into adulthood (Spear, 2000). We then tested these animals in the forced swim test in young adulthood to measure depressive-like behaviors (Porsolt et al., 1977). We found that the rats exposed to restraint stress during adolescence showed a shorter latency to immobility than age-matched non-stressed controls (Fig. 2; unpublished observation). Though these results suggest that adolescent stress exposure leads to depressive-like behaviors in adulthood, these data are presented here to provide an example of the relatively high degree of variability in the experimental group. Specifically, the mean and standard deviation of the control group are 176.0 and 33.6, respectively, while the stress group is 72.2 and 79.3, respectively. This high standard deviation in the experimental group indicates a rather large spread around the mean.