1 Although widely used in clinical practice by many physiotherapi

1 Although widely used in clinical practice by many physiotherapists worldwide, there is little evidence about the efficacy or effectiveness of this intervention.2, 4 and 5 Five systematic reviews have evaluated the effect of Kinesio Taping on selected

outcomes in different populations. Williams et al6 assessed Kinesio Taping only in the prevention and treatment of sports injuries. Bassett et al and Mostafavifar et al7 and 8 assessed the effects of Kinesio Taping in people with musculoskeletal conditions. Morris et al and Kalron et al9 and 10 widened the musculoskeletal focus to other clinical areas, such as neurological and lymphatic conditions. Currently, new trials of Kinesio Taping are Cobimetinib cost frequently being published. Although these five Vismodegib reviews were published recently, none of them included all of the following recent trials: 3, 11, 12, 13 and 14. Given this substantial amount of new data,

an updated systematic review was needed to inform clinicians and patients about the effects of this intervention in musculoskeletal conditions. The research questions of this systematic review were: Is Kinesio Taping more effective than no treatment or sham/placebo in people with musculoskeletal conditions for the outcomes of pain intensity, disability, quality of life, return to work and global impression of recovery? Is Kinesio Taping more effective than other interventions in people with musculoskeletal conditions for these outcomes? Is the addition of Kinesio Taping over other interventions more effective than other interventions alone in people with musculoskeletal conditions for these outcomes? Systematic searches were conducted of MEDLINE, Embase, CENTRAL, PEDro, SPORTDiscus, CINAHL, LILACS and SciELO. Papers were accepted in any language if a translation could be obtained.

Search strategies followed the recommendations of the Cochrane Back Review Group33. Detailed search strategies used in each database are described in Appendix 1 (see eAddenda for Appendix Calpain 1). The date of the last search was 10 June 2013. All clinical trial registers were also searched and manual searches were performed by checking the reference lists of each eligible article. Studies were considered for inclusion if they met the criteria presented in Box 1. Conference abstracts were excluded. Studies that were conducted on healthy participants or that only collected outcomes relating to physical performance (eg, muscle strength, vertical jumping) were also excluded. The primary outcomes were pain intensity and disability measured by any validated outcome measure.

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05 [20/400] and/or central VF <10 degrees), we defined the follow

05 [20/400] and/or central VF <10 degrees), we defined the following 4 categories of low vision and blindness with glaucoma as the main cause: (1) unilateral low vision: patients with low vision in 1 eye; (2) bilateral Selleckchem Z-VAD-FMK low vision: patients with low vision in the best eye; (3) unilateral blindness: patients blind in 1 eye; (4) bilateral blindness: patients with both eyes blind, mainly

caused by glaucoma in at least 1 eye. The cause of visual disability was determined by reviewing patient charts and analyzing the information in relation to the VF appearance. In most patients the main reason for visual disability was clear. In a few eyes it was impossible to determine a single cause of visual disability. Then we recorded a combination of causes. The date of the glaucoma diagnosis was set to the date of the first reliable VF showing a glaucomatous defect. The time for low vision or blindness was the first visit when the Humphrey field was centrally constricted to less than 20 degrees or 10 degrees, respectively, or when VA was permanently reduced to below 0.3 (20/60) or 0.05 (20/400), respectively.

Even in those few patients who had missed many consecutive visits during follow-up, all available data on visual function were analyzed as of the date from the next visit. Time with glaucoma blindness and the final outcomes in terms of low vision and blindness from glaucoma were determined in all included patients. Cell Cycle inhibitor Cumulative incidence of blindness and time with diagnosed SB-3CT glaucoma were calculated in the Data at Diagnosis group. We chose to calculate cumulative incidences with a competing risk method.13 Contrary to

the Kaplan-Meier method, the competing risk method does not “censor” individuals with competing risks. Thus, the probability of an event-free survival calculated with the competing risk method is a conditional probability, which takes both the event and the competing risks into account. In our analysis, blindness attributable to reasons other than glaucoma or death without blindness were modeled as competing risk events. Annual incidence rates were calculated setting all “study” events (blindness attributable to glaucoma) and all competing events to the time point just prior to the end of the annual period. In addition, cumulative incidences for blindness in at least 1 eye and bilateral blindness were calculated with the Kaplan-Meier method14 in order to be able to compare our results with previously published results. The Pearson χ2 test was used to compare the rates of low vision and blindness in the Data at Diagnosis and Follow-up Only groups. All statistical calculations were performed with SPSS version 19.0 (SPSS Inc, Chicago, Illinois, USA). Statistical significance was set to P < .05. Five hundred and ninety-two of 662 patients (89.4%) with manifest glaucoma with visual field loss met the inclusion criteria (Figure 2). Three hundred and sixty-seven (62.

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Eight-week-old female BALB/c mice (5 per group) were vaccinated w

Eight-week-old female BALB/c mice (5 per group) were vaccinated with either Qβ-Eot or Qβ-IL-5, or the combination of both without the addition of adjuvant. 50 μg of total protein of each vaccine was find more injected subcutaneously on days 0, 21 and 35. Mice were subjected to retro-orbital bleeding on days 0, 21, 35 and

45 and sera analyzed by the use of IL-5 and eotaxin-specific ELISA. ELISA plates were coated with mouse rIL-5 or r-eotaxin at a concentration of 5 μg/ml. Plates were blocked then incubated with serially diluted mouse sera. Bound antibodies were detected with enzymatically labeled anti-mouse IgG antibody. As a control, preimmune serum from the same mice was tested. Antibody titers were calculated as the serum dilution which led to a half-maximal of OD450 (OD50%). To induce allergic airway inflammation, female BALB/c mice (5 per group) were injected (i.p.) with 10 μg of OVA (Grade V, Sigma–Aldrich) mixed with 2 mg of alum (Aluminium Hydroxide

Gel Adjuvant, Brenntag Biosector, Denmark). 10 days later, mice were challenged daily with 100 μg of OVA by intranasal administration for 4 days. 24 hours after the last challenge, BAL and lungs were subjected to histology. Mice injected i.p. with OVA selleck chemicals llc and alum but not challenged intranasaly with OVA served as a negative control for disease induction in these experiments. To assay the activity of r-eotaxin, BALB/c mice (5 per group) were immunized i.p. on days 0 and 3 with 100 μg of OVA mixed with 2 mg

of alum. On day 14, mice were injected with either PBS or 0.5 μg of r-eotaxin i.v. Thirty min after injection, blood samples were collected from each mouse and blood smears were made. The slides were dried in air and stained with Kit RAL 555 (Réactifs RAL) according to manufacture’s protocol (a fast-acting variation of May-Grünwald Giemsa staining). The percentage of before eosinophils was evaluated with a light microscope. In the model of allergic airway inflammation, bronchoalveolar cells were collected in successive lavages (BAL) using 0.5 ml aliquots of PBS with 2% BSA at room temperature until the total volume reaches 1.2 ml. The total number of cells in the BAL was counted with a Coulter Counter (Beckman Coulter, Inc.). Cytospins were performed with Shandon Cytospin apparatus (Thermo Fisher Scientific, Inc.) and stained with Kit RAL 555 (Réactifs RAL) according to the manufacture’s protocol. Differential cell counts were performed with at least 200 leukocytes. Mouse lungs were removed and fixed in 10% PBS buffered formalin. Paraffin sections were stained with Chromotrope 2R to identify eosinophils [29]. For statistical analysis, Student’s t-test was used. p-Values <0.05 were considered significant. Recombinant murine IL-5 with an N-terminal hexa-histidine tag, an enterokinase cleavage site and a linker containing a cysteine residue was expressed and purified.

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Continued surveillance is required to monitor for strain changes

Continued surveillance is required to monitor for strain changes that may alter vaccine effectiveness or that may be a result of vaccination. However, data on strain changes need to be very carefully evaluated before attributing them to vaccination. Conflict of interest statement: The authors declare no conflicts of interest. “
“Diarrhea is the second-leading cause of childhood mortality worldwide, and is responsible for approximately 1.34 million deaths each year in children under 5 years of age [1]. Rotavirus is the primary cause of diarrheal disease in this population, accounting for 30–40% of diarrheal deaths [2]. Although the illness affects children in every

country, over 90% of the deaths occur in the developing world. The introduction of effective rotavirus vaccines creates the possibility of significantly reducing this website diarrheal mortality and hospitalizations. Growing evidence from middle and upper income countries where rotavirus vaccination has been introduced, suggests that the vaccine LDK378 molecular weight is associated with reduced hospitalizations and even death among children less than 5 years of age. According to recent reports from Europe, Australia and the United States, reductions of 70–95% of hospitalizations for rotavirus-specific diarrhea

and 35–48% for all-cause diarrhea have occurred after the vaccine was introduced into routine immunization programs [3], [4], [5], [6], [7] and [8]. These reductions in diarrheal hospitalizations have also been observed in lower-middle income countries in Latin America [9] and [10]. Sodium butyrate For the first time, real reductions in diarrheal deaths have also been recorded. In Mexico, researchers observed a 35% reduction in childhood diarrheal deaths after vaccine introduction, and in Brazil similar

trends were seen [11], [12] and [13]. In low-income countries that bear the vast majority of rotavirus mortality, there is less direct evidence of the effectiveness of vaccination at scale, in part because many of these countries are only now making decisions regarding national universal vaccination programs. Nicaragua introduced the vaccine into the routine immunization schedule in 2006 – the first GAVI-eligible country to do so. A 46% reduction against all rotavirus hospitalizations was noted, as well as a 58% reduction in the number of cases of severe rotavirus disease requiring intravenous (IV) fluids [14]. To make the decision to introduce new and relatively expensive vaccines, policy makers will benefit from reliable estimates of the costs and outcomes that might be attained through routine immunization. The best available estimates are typically based on a combination of regularly updated information on epidemiological burden, vaccine efficacy, immunization delivery, effectiveness, vaccine demand, price, and economic burden.

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Thus, we tested whether we could produce LVs containing a mutatio

Thus, we tested whether we could produce LVs containing a mutation in one of the packaging vectors that disabled the integrase protein in the lentivirus particle (and thus prevented integration of the provirus reverse-transcribed DNA) [14] and [15]. We demonstrated that ID-LVs could be produced at high titers and were effective at transducing human monocytes. Upon

terminal differentiation of the iDCs, expression of the transgenes (cytokines and antigen) persisted for 3 weeks. The constitutive and robust expression of cytokines (GM-CSF/IFN-α for SmyleDC and GM-CSF/IL-4 for SmartDC) enabled generation of stable and functional iDCs that could self-differentiate in vitro or in vivo. Since we noticed a modest (10–15%) gene marking of monocytes transduced with ID-LV-GFP, it is possible that ID-LVs expressing the cytokines needed for iDC differentiation and maintenance provide a selective this website mTOR inhibitor advantage for the transduced monocytes for about 3 weeks. A previous report demonstrated

that differentiated human APCs (DCs and macrophages maintained in culture for 4 and 8 days, respectively) could be transduced with ID-LVs [20], but the current work is the first demonstration that monocytes can also be effectively transduced with ID-LVs prior to their differentiation, which then maintain the DCs functional and alive. The capability of ID-LVs to infect monocytes seems to reflect what occurs during natural HIV-1 infection, as monocytes are one of the relevant HIV-1 reservoirs [32]. During initial infection (i.e., in non-activated

monocytes and CD4+ T cells), most of the viral cDNA exists as unintegrated linear DNA form (for which fewer copies eventually integrate), or nuclear circular forms, which can lead to “abortive” defective integrations or are ultimately degraded (for a review, see [33]). Nevertheless, prior to HIV-1 integration, transcription of and translation of viral genes present in the unintegrated DNA forms is observed which initiate a rapid sequence of events to shut-down the antigen-presentation machinery (such as down-regulation of MHC class I expression via Nef [34]). Ironically to the natural biology of HIV-1 hindering DC differentiation, HIV-1-derived ID-LVs co-expressing combinations of cytokines were actually able to potently induce DC differentiation. Other groups had previously reported the transduction of monocytes by LVs, but since these studies lacked of the 8 h GM-CSF/IL-4 pre-conditioning step to activate the monocytes prior to LV transduction [35] and [36], the gene transfer efficiency was usually low. Co-expression of GM-CSF/IFN-α or GM-CSF/IL-4 was readily observed in the monocytes preconditioned with cytokines and transduced with ID-LVs which induced their prompt differentiation into highly stable and immunologically competent APCs.

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Cervical cancer can arise from cells containing exclusively episo

Cervical cancer can arise from cells containing exclusively episomes, and for HPV16, around 30% (26–76% depending on study) of cervical cancers develop in this way [54], [180] and [181]. Around 70% of HPV16-associated cervical cancers contain integrated HPV16 sequences, while for HPV18, the viral genome is almost exclusively integrated [182], SKI-606 supplier [183], [184], [185] and [186]. In both cases, however, it is the long-term expression, and in particular, the over-expression of E6 and E7 and the accumulation of genetic errors, which are ultimately important in the progression from CIN3 to cervical cancer. Although most research on HPVs

has focused on the high-risk types from the Alpha genus, it is apparent that the low-risk types can very occasionally be linked with cancer progression, such as in persistent RRP [187]. Several reports have suggested that duplications within the HPV genome or occasional

integration may be important in these cases [188] and [189], but given the different functions of the low-risk E6 and E7 proteins, we would not expect the mechanisms of how these viruses predispose to cancer to be the same as for the high-risk types. Even so, it does appear that persistence is an important indicator of cancer risk in both cases, prompting the search for better methods of disease Selleck SP600125 treatment for low-risk PV types. Clearly, the genetic susceptibility of the host can play an important role in some cancers associated with low-risk HPV types, as evidenced from the study of WHIMS

and EV [35] and [38], the latter of which is associated with Beta HPV types that are usually only associated with asymptomatic infection in the general population. In EV patients, Beta HPVs are clearly associated with the development of non-melanoma skin cancer (NMSC; the most common cancer in adult light-skinned populations [190]), but in the general population and in immunosuppressed individuals, this has been the subject of much debate [191], [192] and [193]. These discussions have been stimulated, to a large extent, by the failure to detect Beta HPV DNA ubiquitously in skin cancers (in contrast to the situation seen Adenosine for the high-risk Alpha PVs in cervical cancer), and the finding that HPVs from the Beta genus are prevalent in normal skin even in the absence of disease. It appears however that these viruses may stimulate cancer progression in a manner that is mechanistically different to HPVs from the high-risk Alpha group. Indeed, our current thinking suggests that the E6 and E7 proteins from these HPV types may exert their effects at an early stage in the carcinogenesis process by inhibiting normal DNA damage repair or apoptosis in response to sunlight [194], [195], [196] and [197].

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FMDV is a single-stranded, positive-sense RNA virus (Genus Aphtho

FMDV is a single-stranded, positive-sense RNA virus (Genus Aphthovirus, family Picornaviridae). The viral genome is about 8.3 kb long, enclosed within a protein capsid. The capsid is composed of 60 copies each of four different structural proteins (VP1-4); VP1-3 are surface exposed while selleck VP4 is entirely internal. Crystallographic studies have identified the structure of the FMDV capsid [1] and [2]

and immunological epitopes have been mostly found on surface-oriented interconnecting loops between structural elements. Studies employing monoclonal antibodies (mAb) have identified antigenic sites by sequencing mAb neutralisation resistant (mar) mutants [3], [4], [5], [6], [7], [8] and [9]. Of the five antigenic sites reported so far for the most extensively studied serotype O, site-1 (G-H loop) is

linear and trypsin-sensitive whereas the others are conformational and trypsin-resistant. Equivalent HTS assay neutralising antigenic sites (except site 3) have also been identified for serotype A, with critical residues present in equivalent positions [3], [4], [5], [6] and [9]. Serotype A viruses are present on all continents where FMD is reported, and is antigenically diverse [10] often exhibiting poor cross-protection [11]. In the Middle East (ME), a new variant, A-Iran-05, was identified in samples collected from Iran in 2003 and subsequently spread to neighbouring countries [10] and North Africa [12]. This genotype replaced the A-Iran-96 and A-Iran-99 genotypes that were previously circulating in the region; did not cross-react with A/Iran/96 vaccine antisera and shared

a closer antigenic relationship with the older A22/Iraq vaccine strain (v/s) [10]. However, many samples isolated after 2006 did not even match with A22/Iraq v/s and so a new v/s, A/TUR/2006 was introduced. From sequence data, Jamal and colleagues indicated candidate amino acid (aa) substitutions in the capsid that might have contributed to these antigenic changes all [13]. More recently, there is evidence that viruses from the region now exhibit lower cross-reactivity with the A/TUR/2006 antisera. The aim of this study was to investigate the molecular basis of the antigenic variation in these viruses using capsid sequences and their corresponding antigenic relationship (r1) values. Fifty-seven serotype A viruses from the ME submitted to the Food and Agriculture Organisation’s World Reference Laboratory for FMD (WRLFMD) at the Pirbright Institute were used in this study (Supplementary table). Two are the v/s A22/IRQ/24/64 (A22/Iraq) and A/TUR/2006 that were originally isolated in Iraq and Turkey, in 1964 and 2006 respectively; the 55 other viruses were isolated over a fifteen year period (1996–2011).

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Another hypothesis is that the excitation of the cutaneous affere

Another hypothesis is that the excitation of the cutaneous afferents decreases the excitability of the propriospinal interneurons and motoneurons (Elbasiouny et al 2010), while others argue that ES applied to antagonistic muscles augments reciprocal inhibition of

agonistic spastic muscles (van der Salm et al 2006). However, similar to the beliefs about FES cycling on urine output and lower limb swelling, it is not yet clear whether FES cycling affects spasticity. There are some studies indicating an immediate dampening of spasticity from one-off episodes of ES but these studies are vulnerable to bias and do not provide convincing evidence of the effects of FES cycling on spasticity (Krause et al 2008, Skold et al 2002, van der Salm et al 2006). Therefore, the research question for this study was: Does

a learn more two-week FES cycling program increase urine output and decrease lower limb swelling and spasticity in people with recent spinal cord injury? A 5-week cross-over randomised trial was undertaken, where participants received both experimental and control phases. Each participant underwent the 2-week control phase and the 2-week experimental phase. During the experimental phase, participants selleck products received FES cycling for 2 weeks. During the control phase, participants did not receive any FES cycling. The order of the two phases was randomised with a 1-week washout period in between. Participants continued to receive other usual care throughout the trial. A blocked randomisation allocation schedule was computer-generated by an independent person to ensure equal numbers of participants commenced with the FES cycling phase and control phase (Schulz et al 2010). Each participant’s allocation was placed

in a sealed, opaque and sequentially numbered envelope and kept at an off-site location. Once a participant passed the initial screening process, an independent person was contacted, an envelope opened and allocation revealed. The participant was deemed to have entered the trial at this point. Fourteen participants with an upper motor neuron lesion following recent spinal cord injury were consecutively recruited from two Sydney spinal cord injury units found over an 18-month period commencing July 2011. Participants were included if they: had sustained a spinal cord injury (traumatic or non-traumatic) within the preceding six months; were currently receiving inpatient rehabilitation; were over 16 years of age; were diagnosed with an American Spinal Cord Injury Association Impairment Scale (AIS) of A, B or C with less than 5/50 lower limb strength according to the International Standards for Neurological Classification of Spinal Cord Injury; and could tolerate FES cycling for at least 20 minutes within a one-hour period. Participants were excluded if: they had participated in a FES cycling program in the preceding two weeks; ES was medically contraindicated; or they had a limited ability to comply.

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The observation

of these generalised ratings of exercise

The observation

of these generalised ratings of exercise intensity across modalities are in accordance with a previous review examining dosage and intensity of multi-modal exercise programs that concluded ‘few studies with robust interventions prescribing individually assessed intensities of each modality have been conducted’ (Baker et al 2007 p. 380). In particular, the Baker et al (2007) review of 15 trials found that balance training exercise intensity was reported using the rating of perceived exertion in one instance and otherwise was not reported (n = 9) or was reported as ‘progressive’ without use of any intensity-rating instrument (n = 5), which is consistent with the findings of this much larger review. The original AZD8055 cost rating of perceived

exertion scale described by Borg (1970) ranged from 6 to 20, with the intention JQ1 in vitro that the ratings could be multiplied by 10 to estimate heart rate between 60 and 200, respectively. This scale has been shown to have linear relationships with heart rate and work intensity (Borg 1973, Borg 1982, Skinner et al 1973). Initially, Borg designed the scale to measure exertion during physical activity (Borg 1973) but it has been more widely applied and numerous variants have been reported. The Borg scale has been reported as a reliable and valid means of rating the intensity of cardiovascular exercise such as treadmill running and cycling (Dunbar 1993), as well as strength training exercise through a linear relationship between proportion of repetition maximum and rating of perceived exertion (Gearhart et al 2001). Apart from the limitations

of an ordinal scale and being a rating of overall exertion, there would be difficulty applying this instrument in some populations due to cognitive impairment, language, and literacy. Therefore, a scale is yet to be found that could be applied in these circumstances. The searches for scales of balance exercise intensity did not identify an appropriate rating scale. The instruments that were found attempt Dichloromethane dehalogenase to quantify aspects of balance from a systems approach, using task performance criteria to assess balance performance rather than rating the intensity at which a task is completed. It is important to differentiate the concept of increasing task difficulty along a predictable trajectory from the measurement of the intensity, or difficulty, an individual experiences in trying to perform an activity or task anywhere along that spectrum of simple to complex tasks. The review has highlighted an important gap in the methods used to prescribe, implement and evaluate the effect of balance exercise programs. At this time, it is not clear if balance exercise intensity can be measured accurately.

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25 mm diameter and 0 25 μm film thickness The column oven temper

25 mm diameter and 0.25 μm film thickness. The column oven temperature was programmed from 50 °C to 300 °C for 2 °C min−1. Ionization of the sample components was performed in electron impact mode (EI, 70 eV). The temperature of the injector was fixed to 240 °C and one of the detectors to 200 °C. Helium (99.99% purity) was the carrier gas fixed with a flow rate of 1.51 mL min−1. The mass range from 40 to 1000 m/z was scanned at a rate of 3.0 scans/s. 1.0 μL of the methanol, chloroform and ethanol extracts of C. decandra was injected with a Hamilton syringe www.selleckchem.com/products/scr7.html to the GC–MS manually for total ion chromatographic analysis in split

injection technique. Total running time of GC–MS is 35 min. The relative percentage of the each extract constituents was expressed as percentage with peak area normalization. The spectrum of the unknown component was compared with

the spectrum of the known components stored in the NIST08s, WILEY8, and FAME libraries and was ascertained the name, molecular weight and structure of components of the test materials. The results obtained were interpreted. The mangrove plant C. decandra leaves were powdered using mechanical grinder and crude extracts were obtained by Soxhlet using chloroform, methanol Neratinib and ethanol. Specific concentrations of the crude compounds were obtained by dissolved in DMSO. The antifungal activity of crude extracts of C. decandra leaves was determined in vitro by Agar cup bioassay method against phytopathogenic fungi P. aphanidermatum, R. solani, P. oryzae and F. oxysporum by calculating the zone of Inhibition around the well. Among all leaf extracts, chloroform extracts of C. decandra leaves showed strong antifungal against P. aphanidermatum, R. solani, P. oryzae, C. oryzae and F. oxysporum

with zone of inhibition diameter (IZD) of 29 mm, 27 mm, 28 mm, found 28 mm and 28 mm, respectively at a concentration of 500 μg/mL. 25 mm, 24 mm, 22 mm, 25 mm and 23 mm of zone of inhibition diameter (IZD) showed respectively against P. aphanidermatum, R. solani, P. oryzae, C. oryzae and F. oxysporum at a concentration of 250 μg/mL. Methanolic extracts also showed highest antifungal activity next to chloroform extracts against P. aphanidermatum, R. solani, P. oryzae, C. oryzae and F. oxysporum with zone of inhibition diameter (IZD) of 27 mm, 28 mm, 25 mm, 26 mm and 27 mm respectively at 500 μg/mL concentration and 21 mm, 22 mm, 17 mm, 20 mm, 20 mm respectively at 250 μg/mL concentration. Ethanol extracts exhibited moderate activity showed against P. aphanidermatum, R. solani, P. oryzae, C. oryzae and F. oxysporum with zone of inhibition diameter (IZD) of 20 mm, 22 mm, 22 mm, 24 mm and 23 mm respectively at 500 μg/mL concentration. Clotrimazole exhibited higher degree of antifungal activity at a concentration of 50 μg/mL, when compared to higher concentrations of the test compounds. The antifungal activity of organic solvent extracts of C.

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