All animal procedures were approved by local Animal Care Committe

All animal procedures were approved by local Animal Care Committee and are in accordance with the NIH Guide for the care and use of laboratory animals. Organotypic hippocampal slice cultures were prepared according to the method of Stoppini et al. (1991), with modifications (Valentim et al., 2003, Cimarosti et al., 2005, Horn et al., 2005 and Frozza et al., 2009). Briefly, 400-μm-thick hippocampal slices were prepared from 6 to 8-day-old male Wistar rats using a McIlwain tissue chopper and separated in ice-cold Hank’s balanced salt solution (HBSS) BYL719 chemical structure composed of (mM): glucose

36, CaCl2 1.26, KCl 5.36, NaCl 136.89, KH2PO4 0.44, Na2HPO4 0.34, MgCl2 0.49, MgSO4 0.44, HEPES 25; fungizone 1% and gentamicin 0.1 mg/mL, pH 7.2. The slices were placed on Millicell culture insert and the inserts were transferred to a 6-well culture plate. Each well contained 1 mL of tissue culture medium consisting of 50% minimum essential medium, 25% HBSS, 25% heat inactivated horse serum supplemented

with (mM, final concentration): glucose 36, HEPES 25 and NaHCO3 4; fungizone 1% and gentamicin 0.1 mg/mL, pH 7.3. Organotypic cultures were maintained in a humidified incubator gasified with 5% CO2 atmosphere at 37 °C for 30 days. Culture medium was changed three times a week. Aβ25–35 and Aβ35–25 (reverse peptide) stock solutions (675 μM) were prepared in sterile distilled water and stored at −20 °C. To obtain the fibrillar form of Aβ25−35 peptide, an aliquot of the stock solution was incubated under 37 °C during the 4 days preceding its use in culture (Casal et al., 2004). The so-called non-fibrillar Aβ corresponds to the peptide that was not subjected to the Vandetanib aforementioned activation process and was therefore added to the culture directly from stock solution. On the 28th in vitro day, the medium was replaced by a serum reduced medium (2.5%) into which 25 μM of fibrillar/non-fibrillar Aβ25–35 or Aβ35–25 was added or not (control slices). Previous experiments showed that this concentration (25 μM) of Aβ25–35 had the most toxic effect (data not shown), at least for the fibrillar peptide form. Cellular damage was assessed by fluorescent image analysis of propidium iodide (PI)

uptake (Noraberg et al., 1999). One hour before the end of the treatments, which means after 47 h of Aβ25–35 or Aβ35–25 exposure, 7.5 μM of PI was because added to the medium and incubated for 1 h. PI uptake is indicative of significant membrane injury (Macklis and Madison, 1990). Cultures were observed with an inverted microscope (Nikon Eclipse TE 300) using a standard rhodamine filter set. Images were captured and then analyzed using Scion Image software ( After capture of images, the area where PI fluorescence (transformed in pixels) was detectable above the background was analyzed using the “density slice” option of Scioncorp Software through the division of PI fluorescence by the total area of the slice (Valentim et al.

In conclusion, GS-4774 was safe and well-tolerated in healthy sub

In conclusion, GS-4774 was safe and well-tolerated in healthy subjects with injection-site reactions being the most frequently reported adverse events. GS-4774 was immunogenic and both weekly and monthly regimens led to rigorous immune responses at all doses evaluated. Further evaluation of GS-4774 is ongoing in patients with chronic HBV infection. Claire Coeshott, David Apelian, and Timothy Rodell were involved in the conception and design of the study and on data acquisition, analysis, and interpretation. Anuj Gaggar, Gong Shen, G. Mani Subramanian, and John G. McHutchison participated in the analysis and interpretation of data. All authors critically reviewed draft versions of the manuscript

and approved the final version. The authors would like to thank the buy Ibrutinib subjects and staff who participated in the study as well as Dr. Mrinalini

Kala at the University of Arizona who performed PBMC isolation. The work was previously presented, in part, at The Liver Meeting® 2013: 64th Annual Meeting of the American Association for the Study of Liver Diseases, November 01–05, Washington, DC. Severina Moreira, PhD, from Niche Science and Technology (Richmond-Upon-Thames, London, United Kingdom) provided writing and editorial support during development of this manuscript; these services were paid for by Gilead Sciences, Inc. This study was funded by Gilead Sciences, Inc. Conflict of interest statement: Anuj Gaggar, ZD6474 purchase Gong Shen, Mani Subramanian and John McHutchison are Gilead Sciences, Inc. employees. Claire Coeshott, David Apelian and Timothy Rodell are employees of GlobeImmune, Inc., the company that developed GS-4774 before it was licensed by Gilead Sciences, Inc. “
“African horse sickness virus (AHSV) is the causative agent of African horse sickness (AHS) which is lethal for up to 90% of

infected domestic horses [1]. AHSV infections CYTH4 of zebras and donkeys are less severe and mostly cause mild clinical symptoms or an asymptomatic infection. These equids are carriers of AHSV, which is transmitted by Culicoides midges, in particular by C. imicola in endemic areas [1] and [2]. It is believed that the distribution of AHSV is associated with the presence of these competent vectors. Currently, AHSV is endemic in tropical and sub-Saharan Africa, but sporadic cases and short-term epidemics in North Africa and Middle-East have been reported in the mid-20th century. In 1987, an outbreak of AHSV-4 on the Iberian Peninsula, which was extended for a few years in Spain and spread to Portugal and Morocco indicating that AHSV had overwintered and spread by European Culicoides midges [1] and [3]. The serogroup AHSV within the genus Orbivirus of the Reoviridae family consists of nine serotypes (AHSV-1 – AHSV-9). The virus particle contains ten genome segments of double-stranded RNA (dsRNA) encoding seven structural proteins (VP1-VP7). Additionally, at least three non-structural proteins (NS1-NS3) are synthesized in virus infected cells.

The results are shown in Fig 2 The analysis of serum cross-reac

The results are shown in Fig. 2. The analysis of serum cross-reactivity among PspAs from clades 1 and 2 revealed a significant variation in the level of recognition of different isolates. Of all antisera tested, four presented high levels of cross-reactivity with PspAs of both clades, being two from clade 1 – PspA M12 and 245/00 – and two from clade 2 – PspA 94/01 and P339. These sera were selected and tested for their ability to increase complement deposition on the surface of a panel of pneumococcal stains. We also determined the ability of the four selected

anti-PspA sera to increase complement deposition on the surface of various pneumococci. Eight pneumococcal strains Proteasome inhibitor expressing family 1 PspAs were incubated with the heat-inactivated pooled sera from: PspA 245/00, PspA M12, PspA 94/01, PspA P339, PspA P 278 or serum from mice injected with only Al(OH)3 followed by the addition of 10% fresh-frozen Selleckchem Gefitinib normal mouse serum. The samples were washed and labeled with FITC-conjugated goat anti-mouse C3. The percentage of bacteria coated with C3 >10 fluorescence intensity units was determined by flow cytometry. Antibodies generated against PspA 245/00, when incubated with pneumococcal strains expressing clade

1 PspAs, efficiently increased C3 deposition, in all serotypes tested. Interestingly, the same was observed with strains bearing clade 2 PspAs, even strain A66.1, which is a heavily encapsulated serotype 3 strain (Fig. 3 and Fig. 4). Fig. 4 summarizes the complement deposition results, Cell press after discounting the non-specific interaction, revealing a percentage of fluorescent bacteria not lower than 30% for all strains tested. On the other hand, antibodies generated against PspA M12 induced lower C3 deposition in both PspA clade 1 and clade 2 containing strains (Fig. 3 and Fig. 4). As for antibodies produced against PspA clade 2, anti-PspA 94/01 enhanced

the amount of C3 deposited on all bacteria tested, regardless of the PspA clade expressed on their surface. Anti-PspA P339, on the other hand, showed the poorest results, leading to an increase in the amount of C3 deposited on only half of the pneumococcal strains tested. Corroborating with the immunoblot results, a poorly cross-reactive serum in that assay, P278, also showed a reduced ability to induce complement deposition in most of the strains (Fig. 3 and Fig. 4). In summary, antibodies generated against PspA 245/00 and 94/01 were able to increase complement deposition on the widest range of pneumococci tested, being selected for further investigation of their potential to mediate opsonophagocytic killing by peritoneal cells.

Then ratio of water and methanol was changed

Then ratio of water and methanol was changed LY294002 in vivo to 40:60, peaks of both drugs were observed with good resolution without peak broadening, tailing, fronting and with

good sensitivity as well, at 35 °C temperature and flow rate of 0.7 ml/min. The effect of flow rate on the separation of peaks was studied by varying the flow rate from 0.5 to 1.0 ml/min; a flow rate of 0.7 ml/min was optimal for good separation and resolution of peaks in a reasonable time as shown in Fig. 2. The effect of flow rate on the formation and separation of peaks was studied by varying the flow rate from 0.5 to 1.0 ml/min; a flow rate of 0.7 ml/min was optional for good separation and resolution of peaks in a reasonable time. System suitability parameters with peak purity data are given in Table 1 and Fig. 2 shows the chromatogram for working standard mixture of DKP and TCS, respectively. The method was validated according to ICH guidelines. The following validation characteristics were addressed: linearity, range, accuracy, precision, specificity,

sensitivity (LOQ and LOD) and robustness. Specificity of the method was determined by analyzing samples containing a mixture of the drug product and excipients. All chromatograms were examined to determine if DKP & TCS. Linearity was determined for DKP in the range of 3.125–125 μg/ml and for TCS 0.5–20 μg/ml. The correlation coefficient (‘r2’) values were >0.998 (n = 6) indicating an excellent correlation between peak areas and analyte concentrations. Low values of LOD and LOQ indicate sensitivity of method. The LOD and LOQ values were found to be 2.5 and 0.4 μg/ml, Decitabine mouse 7.5 and 1.2 μg/ml for dexketoprofen and thiocolchicoside,

respectively. The assay for the marketed tablets was established tuclazepam with present chromatographic condition developed and it was found to be more accurate and reliable. The average drug content was found to be 99.92 %for DKP, 99.58 %for TCS for batch A and 99.71% for DKP, 99.65% for TCS for batch B of the labelled claim. With % RSD for DKP, 0.23–1.23 batch A, 0.43–1.2 batch B and 0.49–1.43 batch A, 0.69–1.33 batch B for TCS respectively. All the above values were found to be within specification as recommended by ICH guidelines and results of formulation analysis are given in Table 2. The mean percentage recoveries obtained were 99.54%, 98.50% for DKP and TCS and % RSD for DKP, TCS were 0.32–0.84 and 0.49–0.81, respectively. The developed method was found to be accurate as the mean percentage recoveries obtained for DKP and TCS were found to be within limit of 100 ± 1.5 %and % RSD values for DKP and TCS were <2%, as recommended by ICH guidelines. The intra-day and inter-day variation was calculated in terms of percentage relative standard deviation and the results are given in Tables 3 and 4 for DKP and TCS, respectively. The % RSD was found to be in the range of 0.53–1.47 for intra-day, 0.38–1.

Heparin or

Heparin or EX 527 in vivo bivalirudin was given to maintain an ACT > 250 seconds or an ACT of > 200 seconds with concomitant use of glycoprotein IIb/IIIa (GpIIb/IIIa) as per protocol. The OAS procedure was initiated by crossing the coronary lesion with the ViperWire Advance® coronary guide wire (Cardiovascular Systems, Inc., St. Paul, MN). Predilation with balloon angioplasty could be performed at the investigators’ discretion to allow introduction

of the IVUS imaging catheter for pre-procedural scan completion. The OAS procedure was initiated with the smallest crown size (choice of 1.25, 1.5, 1.75 or 2.0 mm) that was necessary to modify the calcified plaque and facilitate the delivery of the stent. OAS rotational crown speed ranged from 80,000 to 120,000 rotations per minute (rpm). After OAS treatment, dilatation with balloon angioplasty before and after stenting was allowed. Post-procedure residual stenosis was reported as a percentage of the vessel diameter, which was measured angiographically and evaluated by the treating physician. Device success was defined as a final achievement of ≤ 50% residual stenosis of the target lesion after OAS use only (before stent placement or any other adjunctive treatment), without a device malfunction. Procedural success was defined as ≤ 20% residual stenosis after stent placement. Debulking was based on pre- and post-diameter

stenosis of lesions treated

with OAS. Post-stent placement, antiplatelet therapy was given at the discretion of the investigator find more and consisted of ≥ 75 mg of aspirin given indefinitely and clopidogrel 75 mg daily given according to the stent manufacturer’s recommendation (typically, for 1 year if a DES stent was implanted). Patients were followed at 30 days, 3 months, 6 months, 2 years and 3 years post-index PDK4 treatment. The safety of the OAS was evaluated by procedural success, device success, TLR and overall major adverse cardiovascular events (MACE) rates at 6 months, 2 years and 3 years. The MACE rate was defined as a composite endpoint of cardiac death, MI and need for TLR. Per the study protocol, a Q-wave MI was defined as the development of a new pathological Q-wave greater than 1 mV in two or more contiguous leads while a non-Q-wave MI was defined as post-procedure elevation of CK to 3 times the upper lab normal value with elevated CK-MB and without pathological Q-waves present on the electrocardiogram. TLR was defined as any repeat revascularization of the target lesion. Reporting of angiographic complications consisted of no flow or slow flow due to distal embolization, abrupt or threatened closure of the treated vessel, spasm requiring any surgical intervention (which could not be resolved via medications), dissection, perforation and other events seen angiographically.

This sub-committee was responsible for the National Immunisation

This sub-committee was responsible for the National Immunisation Handbook (the Handbook)—the Government-produced national clinical guidelines aimed at all health professionals. These clinical guidelines were not directly connected

to Government vaccine funding decisions. In 1997, the Government decided to bring this advisory function inside the Department of Health and Ageing (DoHA) and remove it from under NHMRC governance by creating the Australian Technical Advisory Group on Immunisation (ATAGI) under the Minister for Health, with essentially the same functions as the former NHMRC sub-committee. However, the provision of advice function was narrowed to provide confidential advice to the Minister. In 2005, the Government introduced legislation to bring vaccine funding applications into the same transparent and predictable mechanism that had been used successfully for drugs. The Australian Pharmaceutical JQ1 manufacturer Benefits Scheme (PBS) has a long history of acceptability to Government and to industry, with an effective methodology to minimise price and to standardise a decision framework using cost-effectiveness evaluation based on a price per disability- or quality-adjusted life

year saved. These new arrangements have produced a high quality policy framework that has supported the introduction and public funding of many new vaccines. Ultimately, however, as with all countries, the capacity to pay regardless of future health savings is an immediate issue for governments that is constrained by the availability of funds drawn from the public purse that must support the full range of government commitments, both within and beyond the health

sector. The terms of reference of ATAGI Liothyronine Sodium are to: • provide technical advice to the Minister for Health and Ageing on the medical administration of vaccines available in Australia, including those on the NIP; There are a number of collaborating agencies that interact with ATAGI in the provision of advice and the formulation of policy and funding decisions (Fig. 2). The National Centre for Immunisation Research and Surveillance (NCIRS) of vaccine-preventable diseases, funded by the Australian Government, plays a major role in supporting ATAGI and its working parties, described below. Formal responsibility for vaccine safety monitoring resides with the ADRAC of the Therapeutic Goods Administration. The PBAC plays a key role, described below, in making vaccine funding recommendations to Government, based on the manufacturer’s submission, ATAGI advice and other expert health economic inputs. The NIC chaired by the Australian Government, is comprised of State and Territory Government immunisation directors plus members from the medical and general practice community, NCIRS and consumers.

Salbach et al (2011)

Salbach et al (2011) buy GSI-IX identified online access to research summaries and systematic reviews as a potentially important facilitator because this can save time to search and critically evaluate research articles. Studies on barriers and facilitators for EBP are potentially useful for designing and implementing interventions to change these factors and increase

the extent to which EBP is implemented. However, this research has certain challenges and limitations. Surveys of EBP barriers and facilitators have assessed the individual importance of a number of factors. However, there might be synergistic effects such that two seemingly minor barriers constitute an important obstacle to EBP if they interact. It is learn more also plausible that changes in specific barriers affect other barriers, suggesting that there are no simple cause-and-effect relationships between individual factors and the extent to which EBP is implemented. Rather, it is reasonable to assume that many factors are associated and interrelated in various ways that are not always

predictable (or measurable by means of surveys). Studying various barriers and facilitators to EBP in isolation makes research more manageable, but it may hinder in-depth understanding of how evidence-based physiotherapy can be increased. Another issue is whether all relevant barriers are examined in the barrier studies. Most studies have used quantitative designs, being based on survey questionnaires. These questionnaires usually consist of a number of barriers (such as ‘the research is not reported clearly and readably’ and ‘the amount of research information is overwhelming’) which the respondents are requested to rank on a Likert scale (eg, Iles and Davidson 2006, Grimmer-Somers et al 2007) or in terms

of selecting ‘your 3 greatest barriers to the use of EBP in your clinical practice’ (eg, Jette these et al 2003). The studies also incorporate questions regarding attitudes to EBP (eg, ‘EBP is an essential component of physiotherapy practice’), skills/self-efficacy in practising EBP (eg, ‘I do not feel capable of evaluating the quality of the research’) and knowledge of EBP-related terms. Although these studies have covered many aspects of EBP, they probably do not encompass all potentially inhibiting factors. Surveying the perceived importance of a finite set of pre-determined barriers can yield insights into the relative importance of these particular barriers, but may fail to identify factors that independently affect EBP outcomes. Further, there is the issue of whether the barriers that have been identified by physiotherapists are the actual barriers.

Clinimetric: The SPHERE 12 has high internal consistency (PSYCH 0

Clinimetric: The SPHERE 12 has high internal consistency (PSYCH 0.90, SOMA 0.80) and test-retest reliability (PSYCH 0.81, SOMA 0.80) in general practice (Hickie et al

2001a, Hickie et al 2001b). When detecting lifetime occurrence of any mental disorder in a young adult community sample, trained psychologists found fair agreement (kappa = 0.39) between the broad screen (a positive score selleck inhibitor on PSYCH and/or SOMA) of the SPHERE 12 and the Composite International Diagnostic Interview (CIDI) (the gold standard for psychiatric diagnosis) (McFarlane et al 2008). The same study also reported an area under the Receiver Operator Curve (ROC) of 72.9 for the PSYCH subscale and 71.5 for the SOMA subscale. Substantial agreement was found between the PSYCH subscale and the HADS (Hospital Anxiety and Depression Scale) when the threshold score was 2 (kappa = 0.67) or 3 (kappa = 0.73) in a sample of cancer patients (Clover et al 2009). When the broad screen is used in general practice, it has high sensitivity (93%) and low specificity (20%), for detecting mental disorders. If the narrow screen (a positive score on PSYCH click here and SOMA subscales) is used, the SPHERE 12 shows a low sensitivity (47%) and

high specificity 72% ( Clarke and McKenzie 2002). Early identification of mental health disorders is essential for optimum patient care. The most appropriate setting for early detection is primary care. Physiotherapists in primary care

are commonly exposed to patients with diagnostic labels such as chronic fatigue syndrome or ongoing, unexplained pain. Epidemiological and genetic research has shown that there are strong links between non-specific somatic symptoms and anxiety and depression (Hansell et al 2011, Katon et al 2007) and this may lead to these disorders being missed (McFarlane et al 2008). Using a tool to screen for mental disorders is likely to help early identification and improved care. The SPHERE 12 is a potentially good candidate for this role because it is easy to apply and brief. The broad screen also has the advantage of high sensitivity, which means that ‘at risk cases’ Ketanserin are unlikely to be missed. However, it also has low specificity and only fair validity when compared with the CIDI, the gold standard of psychiatric diagnosis. This combination of features indicates a significant number of false positive ‘cases’ will be identified using the SPHERE 12 screen and this could lead to unnecessary and costly investigations (Phillips et al 2002). Consideration of a number of factors might make this tool more appealing to the primary care clinician. First, the suggested thresholds may not be the most appropriate to detect different mental health disorders in the primary care setting, (see Table in McFarlane et al 2008 p. 341).

0 and were classified into local (loco-regional) and systemic adv

0 and were classified into local (loco-regional) and systemic adverse events. The intensity of adverse events was graded as mild (grade 1/easily tolerated), moderate (grade 2/sufficient to interfere with daily activities) or severe (grade 3/preventing normal activity). The relatedness

of adverse events to the vaccination was graded as not related, possibly related, probably related or certainly related. Abnormal laboratory findings were scored for severity into severity grades 1–4 (based on “Toxicity grading scale for healthy adults and adolescent volunteers enrolled in preventive vaccine clinical trials” – FDA 2007 guidelines). QFT testing was done according to the manufacturer’s instructions and categorized as positive when the result was ≥0.35 IU/ml at baseline, and at 32 and 150 weeks after the primary vaccination. Blood samples for cellular buy Rigosertib immunity and antibody determinations were collected at baseline and at 1 and 6 weeks after both vaccinations, and at weeks 32, 52 and 150 post the primary vaccination. Briefly, 40 ml heparinized blood was centrifuged on Leucosep tubes (Greiner-bio-one, Austria) containing 15 ml Ficoll (LUMC pharmacy #902861) (20 min/800 g), after centrifugation plasma was removed for storage at −70 ̊C and PBMCs were

removed DAPT solubility dmso and washed three times with sterile PBS (LUMC pharmacy). PBMCs were aliquoted and stored in liquid nitrogen in RPMI (Invitrogen #22409-015) containing 20% fetal calf serum (PAA Laboratories #A15-043, Netherlands)/10% DMSO (Sigma #41650). After defrosting a minimum PBMC viability of 80% was considered acceptable for assay purposes. PBMCs were stimulated with pools from Ag85B or ESAT-6 peptides for 6 h or left unstimulated before staining for CD3, CD4, CD14, CD19, CD45RO, IFN-γ, IL-2, TNF-α, IL-22, IL-17A and CD154 (see online supplement) [18]. IFN-γ was determined using ELISpot from frozen samples to enable batch processing of longitudinally collected samples [19] and [20]. In this protocol, cells were thawed and pre-stimulated for 16–18 h, followed

by 24 h incubation in the ELISpot plate [10] (see online supplement). PBMCs were stimulated 6 days with H1 fusion protein and a panel comprising cytokines (IFN-γ, much IL-2, IL-4, IL-10, IL-13, IL-17A, IL-22, TNF-α), chemokines (IP-10, MIG, MCP-1, MIP-1b) and growth factors (VEGF and GM-CSF) were measured in undiluted cell culture supernatant samples using a Milliplex multiplex bead assay (see online supplement). Clinical data were collected in CRFs, subject diaries and laboratory records. The statistical analysis of the data was performed by JG Consult, an independent Contract Research Organization in accordance with a statistical analysis plan and GCP and ICH-guidelines and documented in the clinical trial report. Here we report safety results and safety analysis based on the statistical trial report which was performed using SAS software (SAS®, Cary, NC 27513, USA, version 9.

Microvessel counts were performed at ×400 (×40 objective lens and

Microvessel counts were performed at ×400 (×40 objective lens and ×10 ocular lens; 0.74 mm2 per field). Tumors with <200 microvessels/mm−2 were assigned a low microvessel density, whereas those with >200 microvessels/mm−2 were assigned a high microvessel density (Couvelard et al., 2005). One-way ANOVA followed by Dunnett’s and Tukey’s Multiple Comparison MI-773 solubility dmso Tests were performed to determine the significance of differences between control and all treatment groups and among groups

respectively using GraphPad PRISM version 5.0. Differences were considered significant in all experiments at p < 0.05 (*, significantly different from untreated controls; **, significantly different from C-DIM-5 and C-DIM-8 and doc single treatments unless otherwise stated). C-DIM-5 and C-DIM-8 were significantly cytotoxic (p < 0.05) to A549 cells with 24 h IC50 values of 14.29 ± 2.30 μM and 16.18 ± 1.59 μM respectively ( Fig. 1A and B). The broad spectrum of cytotoxic activities of the C-DIM compounds was also evident in LnCap, PC3, and H460 cell lines ( Fig. 1C and D). Interaction of C-DIM-5 and C-DIM-8 with doc inhibited A549 cell growth exponentially with

CI values of 0.46 ± 0.027 and 0.51 ± 0.031 (i.e. synergistic) respectively. Deposition on stages 3, 4, 5 and 6 were selected, representative of the respirable mass and used in the assessment of cytotoxicity ( Fig. 1E and F). Cell survival on stage 5 of the viable impactor significantly decreased to 17.75% and 17.10% (p < 0.05) after treatment with nebulized C-DIM-5 and C-DIM-8 respectively. Representative fluorescence micrographs 5-Fluoracil in vitro of acridine orange-ethidium bromide-stained cells revealed the percentages of cells undergoing apoptosis (Fig. 2A). This was after treatment with DMSO, doc (10 nM), C-DIM-5 (10 μM),

C-DIM-5 (10 μM) + doc (5 nM), C-DIM-8 (10 μM), C-DIM-8 (10 μM) + doc (5 nM), C-DIM-5 (20 μM), C-DIM-5 (20 μM) + doc (5 nM), C-DIM-8 (20 μM), and C-DIM-8 (20 μM) + doc (5 nM) ( Fig. 2A). There was evidence of induction of early and late apoptosis by doc (10 nM) [11.5 ± 1.00%], old C-DIM-5 (10 μM) [20.5 ± 1.85%], and C-DIM-8 (10 μM) [26 ± 1.05%] ( Fig. 2B). This was augmented when C-DIM-5 and C-DIM-8 where combined with doc [C-DIM-5 (10 μM) + doc (5 nM), 30 ± 2.90%; C-DIM-8 (10 μM) + doc (5 nM), 34 ± 3.60%] ( Fig. 2B). The number of apoptotic cells significantly increased (p < 0.05) at higher concentrations (20 μM) of C-DIM-5 [24 ± 1.80%] and C-DIM-8 [25.5 ± 2.40%]. This was further enhanced when 20 μM C-DIM-5 and C-DIM-8 were co-treated with 5 nM doc [40 ± 3.45%, and 41 ± 3.60% respectively] ( Fig. 2B). Treatment of A549 cells with DMSO resulted in accumulation of 72.34 ± 0.51% of cells in G1, 3.20 ± 0.13% in G2 and 24.58 ± 0.49% of cells in S-phase (Fig. 2C). However, after treatment with 10 μM C-DIM-5, 76.98 ± 0.51% of cells accumulated in G1, 1.20 ± 0.21% in G2 and 21.82 ± 0.52% in S-phase.