Our findings support the need to confirm this differential rate in a larger cohort of children. Vaxtracker has been adopted for active surveillance of IIV in the find more community by the AusVaxSafety consortium and expanded for use in two Australian states, New South Wales and Victoria. Sites selected include paediatric hospitals

and general practice settings. To maintain the simplicity of Vaxtracker data for clinicians the collection of additional data to provide a richer analysis, such as medical conditions, will be collected from respondents when completing the online survey. The need to ensure high quality active surveillance for safety signals when introducing new vaccines at population level has been increasingly recognised. Early experience with the Vaxtracker on-line surveillance system suggests that it provides effective post-marketing surveillance, which is ideally suited to the introduction of vaccines for children. It allowed rapid analysis of reported adverse events by public health authorities. The authors declare no conflict of interest. We thank Stephen Clarke for his assistance with the online software and database development. We would like to acknowledge the general practice clinics and Vaxtracker participants for their contribution to vaccine safety surveillance. We would also like to acknowledge Dr. Bronwen Harvey

Sunitinib manufacturer at TGA for generous advice and proof isothipendyl reading. Whilst the Australian Department of Health provided financial assistance to Hunter New England Population Health, the material contained in the reports produced by the Centre should not be taken to represent the views of the Australian Department of Health. The content of the reports is the sole responsibility of the Hunter New England Population Health. “
“Rift Valley fever virus (RVFV) is a member of the family Bunyaviridae, genus Phlebovirus. This zoonotic arbovirus, endemic to Africa

and Arabian Peninsula, causes acute disease in newborn ruminants with up to 100% fatality rate, as well as acute disease in pregnant animals resulting in abortion storms. Naturally infected animals develop high viremia sufficient to infect the arthropod vector, even if the infection is inapparent. The economically important affected species include sheep, goat, cattle and camel, with the primary route of infection being mosquito bites. Humans can be infected by mosquito bites, and importantly also by exposure to blood and tissues of infected ruminants during slaughter, necropsy or while assisting aborting animals [1] and [2]. Although the disease and development of viremia in ruminants is preventable by vaccination, and ruminant vaccination is recommended to protect human population from RVFV infections, the number of RVFV vaccines in use is limited [3] and [4]. Availability of a reliable challenge model is a pre-requisite for future vaccine development, registration and licensing.

Anal. calcd. for C18H21Cl2N3O: C, 59.02; H, 5.78; Cl, 19.36; N, 11.47; O, 4.37. Found: C, 59.15; H, 5.88; N, 11.56. The synthesis of (SLN1–SLN10) successfully synthesised by using good literature. Majorly we selected related drug candidates, prepared skeleton. Simple convergent methodology worked for getting good yields overall. The final C–N coupling approached three techniques, where we concluded Sonication technique is see more good for getting good yield and time. We observed more spots in microwave reaction may be due to microwave other bonds also dislocated and afford low yield. The same conventional reaction yield shown less and taking long time. The explosive reactions, like azide and Mitsunobu reactions etc.,

are not useful for bulk scale. We recommend for small scale reactions in Ultra-Sonication SCR7 purchase reactions and microwave reactions based on our earlier experience. All authors have none to declare. The authors acknowledge the Osmania University for providing the research facility and the direct contributions for the staff of Department of Chemistry and Analytical team. “
“Vildagliptin chemically (S)-1-[N-(3-hydroxy-1-adamantyl) glycyl] pyrrolidine-2-carbonitrile, is a potent dipeptidyl peptidase IV (dip-IV) inhibitor, a drug for the treatment of diabetes. DPP IV

inhibitors represent a new class of oral antihyperglycemic agents to treat patients with type 2 diabetes. DPP IV inhibitors improve fasting and postprandial glycemic control without hypoglycemia or weight gain. Vildagliptin inhibits the inactivation below of GLP-1 and GIP by DPP IV, allowing GLP-1 and GIP to potentiate the secretion of insulin in the beta cells and suppress glucagon release by the alpha cells of the islets of Langerhans in the pancreas. 1, 2, 3 and 4 Literature survey reveals that vildagliptin can be estimated by UV spectroscopic method, 5 RP-HPLC method, which is a time consuming method

being the retention time is more than 10 min, 6 RP-LC/MS method, requires mass spectroscopy detection and the LOD and LOQ are more than the present method, and has a narrow linearity range, 7 HPLC method, which requires a solid-phase extraction and determination by high-performance liquid chromatography quadrupole time-of-flight mass spectrometry which requires a special attention throughout the study but the present work is a simple method. 8 So based on the above mentioned reasons the authors aim to develop a simple, sensitive and accurate RP-HPLC method for the estimation of vildagliptin in pure form and tablet dosage form. Waters 2695 HPLC system equipped with Agilent Eclipse XDB C18, 150 × 4.6 mm, 5 μ column, Rheodyne injector with 25 μL loop, 2996 PDA detector and Empower-2 software was used. Potassium dihydrogen orthophosphate of analytical grade, HPLC grade Milli-Q water and acetonitrile were used. Vildagliptin was a gift sample from Novartis, India. The tablets of vildagliptin were obtained from local pharmacy. 0.

Un certain nombre de gènes ont été identifiés : SOD1, FUS, TARDP43, OPT, VCP et C9ORF72, expliquant 70 % des formes familiales [58]. Elle peut être révélée, notamment dans RGFP966 mouse les formes bulbaires, à l’occasion d’une détresse respiratoire favorisée par un événement infectieux broncho-pulmonaire ou une fausse route ou dans les formes avec atteinte diaphragmatique

initiale [59]. Des signes extrapyramidaux, cérébelleux, une démence, l’atteinte du système nerveux végétatif, des anomalies sensitives objectives et une atteinte oculomotrice peuvent coexister avec un tableau classique de SLA. Il repose sur : • la mise en évidence de signes cliniques et électromyographiques d’atteinte du NMP et du NMC, au niveau encéphalique et médullaire (cervical, dorsal, lombo-sacré) ; Dans les formes difficiles ou atypiques, le diagnostic repose sur un faisceau d’arguments cliniques et paracliniques. Fait important, il n’existe pas de marqueur biologique spécifique de cette maladie. Des critères diagnostiques ont été proposés (critères d’El Escorial révisés ou critères d’Airlie House, 1998) [42] and [43]. Leur utilité est limitée du fait qu’ils ont été élaborés

pour la réalisation des essais cliniques et non pour aider au diagnostic. L’ENMG est l’examen de référence à condition qu’il soit réalisé learn more selon un protocole standardisé et effectué par un neurologue. Il confirme l’atteinte du NMP, montre l’extension à des zones cliniquement préservées et permet d’écarter certains diagnostics différentiels. Un protocole standardisé

est nécessaire au diagnostic positif. Il comporte : un électromyogramme de détection à l’électrode-aiguille, l’étude de la conduction motrice, l’étude des ondes F, la recherche des blocs de conduction moteurs, la stimulation répétitive et l’étude de la conduction sensitive périphérique. L’électromyogramme de détection Megestrol Acetate à l’électrode-aiguille objective au repos des signes de dénervation active (fibrillation et ondes lentes positives) associés à des fasciculations et parfois à des décharges complexes répétitives. Lors de la contraction volontaire, il objective la diminution du nombre de potentiels d’unités motrices recrutées traduisant la perte motoneuronale. Le caractère pathologique des potentiels reflète les phénomènes de dénervation-ré-innervation au sein des unités motrices. Les modifications du rythme de fréquence des potentiels d’unités motrices lors de la contraction volontaire sont inconstantes dans cette pathologie associant une atteinte périphérique et centrale. Ces anomalies sont à rechercher à différents niveaux médullaires (cervical, dorsal, lombo-sacré) et bulbaire. L’étude de la conduction motrice comporte 2 étapes. La mesure de l’amplitude du potentiel d’action musculaire global est le résultat combiné de la perte en axones moteurs et de la ré-innervation compensatrice : elle est normale au début de l’affection, puis la décroissance de l’amplitude est le témoin du degré de perte motoneuronale.

Two trials reported data about length of stay in ICU following preoperative exercise training, again with conflicting results. Arthur et al21 reported a statistically significant reduction in ICU length

of stay (median of two hours less) due to preoperative exercise, whereas Herdy et al16 reported no significant difference. The two-week program demonstrated no postoperative benefit to physical function MK0683 at six weeks (measured using the Short Form 36 Physical Component Summary score) and this trial was the only trial to examine physical function outcomes postoperatively.22 Outcome data for postoperative pulmonary complications and costs were not reported by any trials that examined exercise. There were no significant differences in hospital length of stay between groups in either trial examining counselling or goal setting as their primary intervention.23 and 24 Both of the trials above concluded that the programs were cost effective

when compared to usual care, although they used different metrics. Goodman et al23 reported that a preoperative support program lowered total costs by £2293, which was statistically significant (95% CI -3743 to -843). Furze et al24 reported that the incremental cost effectiveness ratio per quality-adjusted life year was £288.83, well below the thresholds for acceptability in the United Kingdom.25 selleck screening library None of the included trials reported data about postoperative pulmonary complications, physical function, time to extubation or length of stay in ICU. Meta-analysis of data from three trials showed that inspiratory muscle training caused a significant reduction in the

relative risk of developing postoperative pulmonary complications, as presented in Figure 9. No heterogeneity was present (I2 = 0%) and the pooled relative risk was 0.42 (95% 0.21 to 0.82). The relative risk reduction was 58% and the number needed to treat was 13 (95% CI 7 to 48). Only the large randomised controlled trial by Hulzebos et al26 investigated the effectiveness of preoperative inspiratory muscle training on time to extubation. They reported heptaminol a statistically significant reduction in the time to extubation with a median of 0.17 days (range 0.05 to 53.6) in the intervention group and 0.21 days (range 0.05 to 3.3) in the control group, p = 0.01. Meta-analysis of two trials by Hulzebos et al26 and 27 showed that inspiratory muscle training reduced length of stay in hospital significantly, with a mean difference of 2.1 days (95% CI -3.41 to -0.76) and no heterogeneity present in the analysis, as presented in Figure 10. Outcome data for length of stay in ICU, physical function and costs were not reported by any trials that examined preoperative inspiratory muscle training. Rajendran et al28 compared preoperative breathing exercises and multi-disciplinary education to a no-treatment control. The intervention group had a significantly lower incidence of postoperative pulmonary complications (RR 0.29, 95% CI 0.11 to 0.

The

epidemiology of rotavirus varies by setting [6]. Seasonality of infection is prominent in temperate climates while a low prevalence is maintained throughout the year in tropical countries [7]. The mode of transmission, though believed to be mainly feco-oral, is also possibly airborne and person-to-person because infection occurs in childhood irrespective of sanitary conditions [8]. Rotaviral gastroenteritis is usually accompanied by vomiting Smad3 signaling and fever and results in severe disease among infants [9]. Rotavirus is excreted in large numbers during diarrhea and the virus can remain infectious on inanimate surfaces, moist surfaces and hands. This report describes rotavirus infection detected by stool Raf inhibitor testing in children followed from birth to three years of age, with sampling during and in the absence of diarrhea. This study was conducted from 2002 through 2006 in three contiguous slums in Vellore, India after approval by the institutional review board of the Christian Medical College, Vellore. The study conduct, recruitment, and sample collection methods have been published previously [10]. Briefly, a birth cohort of 452 children was followed from birth till three years of

age, analysis was restricted to the 373 children who completed three years of follow-up. Surveillance of children for rotavirus infection was done by screening bimonthly stool samples and diarrheal stool samples, and clinical data were collected to record diarrheal severity 17-DMAG (Alvespimycin) HCl using the Vesikari score

with scores <5 considered mild, 6–10 moderate, 11–15 severe and 16–20 very severe [11]. In case of a surveillance sample, positive samples detected by ELISA (Dako Rota IDEIA, Ely, UK) were genotyped by reverse-transcription polymerase chain reaction (RT-PCR) for VP7 and VP4 amplification while for a diarrheal sample, irrespective of the ELISA result, one sample per episode was screened using RT-PCR for VP6 before genotyping [12]. The definitions for symptomatic and asymptomatic rotavirus infections used in this study are given in Table 1. Age-specific incidence and seasonality of symptomatic and asymptomatic infections were studied. The incidence rates were obtained by Poisson regression equations and frailty models adjusted for clustering of disease/infection within a child. For cumulative incidence of rotavirus infection, Kaplan–Meier estimates of median time to infection were calculated and compared between children infected with rotavirus overall and with specific genotypes. Factors influencing rotavirus infection as well as disease rates were studied using Poisson regression. To study the risk factors for rotavirus infection, children who experienced rotavirus infection in the first year were compared to children who did not experience rotavirus infection in the first year using multiple unconditional logistic regression.

Although more research is required to understand the effects of stress on avoidance strategies, avoidant behaviors are common among anxiety patients (Eifert and Forsyth, 2007, Craske and Barlow, 1988 and Sprang and LaJoie, 2009), suggesting that stress may enhance well-practiced avoidance strategies. It should be noted that although avoiding an aversive outcome may attenuate fear responses, the habitual avoidance of fearful situations may also prevent one from confronting aversive stimuli Z-VAD-FMK price and engaging in extinction processes, which can be detrimental to the treatment of anxiety symptoms. Therefore, while stress may hinder the initiation of avoidance behavior

during learning, overuse of avoidance

strategies may lead to habitual, potentially maladaptive avoidance behaviors that are facilitated by stress. Since the fear regulation techniques discussed above can be vulnerable see more to the effects of acute stress, as well as other contextual and temporal factors, emerging research in animals and humans has examined the interference or blockade of fear memory reconsolidation as a putative alternative to change fear. Normative models of memory suggest that immediately after learning, there is window of time in which newly encoded information is susceptible to interference. However, recent research suggests that memories must undergo an additional phase of consolidation each time they are reactivated, a restabilization process referred to as reconsolidation. Since it is often not feasible to interfere with the initial consolidation ADP ribosylation factor of traumatic experiences, interfering with reconsolidation offers the possibility of altering traumatic memories in a more permanent manner. In a typical reconsolidation paradigm, after an aversive association is acquired and consolidated, a time-dependent reconsolidation window is induced by a single presentation of the CS to reactivate the aversive memory. A variety of behavioral or pharmacological manipulations

can then be used during the presumed reconsolidation window to alter memory re-storage before later testing for the conditioned responses in the presence of the CS. Research in humans (Schiller et al., 2010, Schiller et al., 2014 and Steinfurth et al., 2014; see Schiller and Phelps, 2011 for review) and animals (Nader et al., 2000, Monfils et al., 2009, Einarsson and Nader, 2012 and Hong et al., 2013) has now demonstrated that disrupting or interfering with reconsolidation leads to the persistent modification of amygdala-dependent aversive associations. Recent research in rodents suggests that interfering with the reconsolidation of aversive association induces plasticity in the LA (Monfils et al., 2009 and Clem and Huganir, 2010) and in humans, reconsolidation of fear memory leads to diminished BOLD responses in the amygdala (Agren et al.

HIV envelope proteins are notoriously poorly immunogenic. Contrary to our previously conducted rabbit experiments check details [14] prior experiments in mice have indicated that i.vag as a sole route of administration for CN54gp140 alone does not elicit

detectable immune responses (unpublished data). As a result we selected a heterologous prime-boost regimen, increasingly prevalent in HIV vaccine research [21]. Remarkably, all topically administered i.vag formulations boosted sub-cutaneously primed mice, importantly in the absence of adjuvant. Of the responses detected locally within the vagina we cannot rule out, as has been reported in HIV infection [22], that serum transudation contributed. Nevertheless, the LSDF inserts have been shown to be a viable delivery modality for i.vag immunization. With respect to immunogenicity the study data indicated that in the case of the mouse model the LSDFs were not offering any additional benefits over i.vag administration of CN54gp140 formulated within PBS buffer alone. Perhaps with the exception

of lyophilized Carbopol® that may be prolonging or augmenting CN54gp140-specific systemic humoral effector immune 5-FU in vitro responses. The formulation (lyo-PC3HEC250HHX5PVP4) with the slowest release induces the lowest response, whereas the formulation (lyo-Carbopol®) with the fastest release closest to the PBS alone scenario marginally prolongs or augments the response. How translational this may be to other animal models, in particular NHPs and more importantly to humans is yet to be determined but this may be indicative that sustained release is not required rather an initial high burst release may suffice. The perceived benefits such as enhanced retention that drive such formulation development with respect to improving immune responses may not be wholly realised due to the size restrictions of the murine vaginal lumen. However although the LSDFs did not augment immune responses in comparison to those following administration of antigen in

PBS alone the problems associated with human i.vag the administration of vaccines in simple buffer solutions are not to be underestimated. As such the LSDFs that elicited comparable immune responses to those of the PBS group have the potential to provide additional attributes for vaginal mucosal vaccine delivery in humans. LSDFs can be self-administered with relative ease using conventional solid dosage vaginal applicators, compared to the instillation of buffers and to the administration of semi-solids, thus promoting higher acceptability and enhanced user compliance. The stability advantages have the potential to eliminate the requirement for cold-chain storage, and the reduction in weight associated with the removal of water could reduce constraints on distribution including expense.

placebo status (166.5 days vs. 430.5 days, respectively, p = 0.35), and the median time to death was not significantly different by vaccine or placebo status (137 days vs. 379 days, respectively, p = 0.17). No statistical differences were seen between the age at death or time to death among the HIV-exposed

infants Selumetinib cell line receiving vaccine vs. placebo (data not shown). In the Kenya site of the multi-country efficacy trial of PRV, the incidence of SAEs and mortality were not statistically different between the vaccine and placebo groups. We did not detect any case of intussusception despite study training to recognize and manage it, and comprehensive safety evaluation. Evaluation of the intensive safety surveillance cohort did not reveal significant differences between treatment groups with respect to all adverse events, in particular with respect to vomiting, diarrhea or elevated temperature, the

events of focus for the intensive safety surveillance cohort. Data from this trial should be reassuring for the many countries in Africa and Asia which are planning to introduce rotavirus vaccine, based on the 2009 WHO recommendation [20]. We observed significantly higher rates of vomiting, diarrhea or elevated temperature in both vaccine and placebo recipients in our trial compared to those BIBF 1120 solubility dmso observed during the earlier Rotavirus Efficacy and Safety Trial (REST) [10]; we did not, however, observe significant differences between the vaccine and placebo groups. It is likely our population was less healthy than the study population of the REST trial. These data represent the first systematic evaluation of PRV in HIV-infected and HIV-exposed infants and demonstrate no significant safety differences between those receiving the vaccine vs. placebo. Overall 5 (23.8%) HIV-infected vaccine recipients and 2 (12.5%) HIV-infected placebo recipients, and 4/88 (4.5%) HIV-exposed vaccine recipients and 4/89 Ketanserin (4.5%) HIV-exposed placebo recipients

reported a severe adverse event within 14 days of vaccination. There were proportionately more SAEs in the HIV-infected participants who received vaccine vs. placebo. Furthermore, we observed a tendency towards more HIV-infected vaccine recipients than HIV-infected placebo recipients having died, and having died at younger ages. This could not be explained by differences in levels of immunosuppression, nutritional status, or other clinical/demographic differences at the time of enrollment or throughout the trial between the two groups. This tendency was not observed among the HIV-exposed participants. Despite these differences among HIV-infected participants, the number of events was small and these differences could have been due to chance alone. Indeed, the excess of deaths observed in the HIV-infected vaccine recipients were not due to gastroenteritis, suggesting that these deaths were not vaccine-related.

A sequential IPV–OPV schedule or IPV-only schedule can be considered in order to minimize the risk of VAPP, but only after a thorough review of local epidemiology. Polio vaccine (IPV or OPV) may be administered safely to asymptomatic HIV-infected infants. HIV testing is not a prerequisite for vaccination. OPV is contraindicated selleck chemicals llc in severely immunocompromised patients with known underlying

conditions such as primary immunodeficiencies, thymus disorder, symptomatic HIV infection or low CD4 T-cell values [5], malignant neoplasm treated with chemotherapy, recent haematopoietic stem cell transplantation, drugs with known immunosuppressive or immunomodulatory properties (e.g. high dose systemic corticosteroids, alkylating drugs, antimetabolites, TNF-α inhibitors, SCR7 price IL-1 blocking agent, or other monoclonal antibodies targeting immune cells), and current or

recent radiation therapies targeting immune cells. IPV and OPV may be administered simultaneously and both can be given together with other vaccines used in national childhood immunization programmes. Before travelling abroad, persons residing in polio-infected countries (i.e. those with active transmission of a wild or vaccine-derived poliovirus) should have completed a full course of polio vaccination in compliance with the national schedule, and received one dose of IPV or OPV within 4 weeks to 12 months of travel, in order to boost intestinal mucosal immunity and reduce the risk of poliovirus shedding. Some polio-free countries may

require resident travellers from polio-infected countries to be vaccinated against polio in order to obtain an entry visa, or they may require that travellers receive an additional dose on arrival, or both. Travellers to infected areas should be vaccinated according to their national schedules. All health-care workers worldwide should have completed a full course of primary below vaccination against polio. “
“Aluminium (Al3+) is the third most abundant element in the Earth’s crust [1] and [2]. In 1825, it was isolated by the Danish physicist Hans Oersted [3]. Most aluminium is stably bound as an ore in clay, minerals, rocks and gemstones. Mobilisation of aluminium in the environment can result from natural processes (acidic precipitation) and through anthropogenic activities. This light-weight, non-magnetic, silvery white-coloured metal can be produced from the aluminium ore—bauxite—by a high energy-consuming mining process; it is this process which provides the world its main source of the metal. As a consequence of this technological progress, aluminium has become increasingly bioavailable for approximately the past 125 years [2]. Toxic mine tailings can leach and seep into aquifers, contaminating local water sources and soils. An increased solubility by anthropogenic pollutants such as acid rain is further contributing to this [5].

1). Liver weight of NDEA alone treated rats increased significantly (p ≤ 0.05) at the end of the 20th week of exposure when compared with normal rats. But treatment with MEWF prevented the increase in liver weight in rats exposed to NDEA. MEWF alone treated rats did not show any significant changes when compared to normal control ( Table 1). NDEA treated rats showed significantly (p ≤ 0.05) elevated serum levels of AFP, ALP, LDH and bilirubin when compared to normal control. A significant (p ≤ 0.05) reduction was observed in serum Duvelisib in vivo markers in the animals treated with Silymarin (100 mg/kg), MEWF (100 mg/kg and 200 mg/kg) compared

to NDEA treated group ( Fig. 2). In morphology and morphometry evaluation, NDEA treated rat liver become very large in size and a large number of hepatic nodules were observed (Fig. 3). Administration of Silymarin and MEWF (100 mg/kg b.w, 200 mg/kg) showed significant reduction in the nodule incidence in NDEA induced hepatocarcinogenesis (Table 2). Tissue biochemical analysis showed a significant (p ≤ 0.05) reduction in GSH, CAT and increased levels of MDA in NDEA treated group compared to normal control. A significant (p ≤ 0.05) elevation in GSH, CAT and MDA were observed in animals treated with Silymarin (100 mg/kg), MEWF (100 mg/kg and 200 mg/kg) compared to NDEA treated group ( Table 3). In NDEA intoxicated rat tissue enlarged nuclei, hyperchromatism, scattered masses of necrotic tissues,

proliferating hepatocytes and mild congestion of sinusoids with central vein dilation were detected VE-822 chemical structure in histopathological studies. However, treatment with MEWF at a dose of 200 mg/kg showed almost normal architecture with normal hepatocytes and uniform secondly sinusoids (Fig. 4). In immunohistochemical

analysis NDEA intoxicated rat tissue showed localization of VEGF around periportal area (arrow heads). A significant down regulation of VEGF was spotted in MEWF at a dose of 200 mg/kg treated group (Fig. 5) The dose-dependent cytotoxic effect of MEWF on PLC/PRF/5 cells was evaluated by MTT assay. The cells were treated with 50 and 100 μg/ml of MEWF and the inhibition of cell proliferation was assessed after 12 h, 24 h, 48 h and 72 h. MEWF exerted cytotoxic effect on PLC/PRF/5 cells in a dose-dependent manner with percentage of cell inhibition values 12.4 ± 0.8, 23.1 ± 0.9, 44.4 ± 1.7 and 55.8 ± 2.2 for 50 μg/ml and 24.2 ± 1.3, 33.8 ± 1.2, 56.8 ± 2.0 and 65.3 ± 2.5 for 100 μg/ml after 12 h, 24 h, 48 h and 72 h respectively. 5-flourouracil, used as positive control, showed an inhibition of 26.8 ± 1.0, 36.2 ± 1.5, 59.2 ± 2.3 and 70.2 ± 2.8 for 50 μg/ml and 14.7 ± 1.1, 25.2 ± 0.8, 47.9 ± 1.8 and 59.1 ± 2.3 for 25 μg/ml after 12 h, 24 h, 48 h and 72 h respectively. Treatment with MEWF exhibited significant cytotoxic effect on PLC/PRF/5 cells (p ≤ 0.05) when compared to the cells treated alone with DMSO. The results were graphically expressed in Fig. 6.