, 2007 and Carneiro et al , 2009) As B guianensis is a dioeciou

, 2007 and Carneiro et al., 2009). As B. guianensis is a dioecious species, outcrossing values were very high. However, differences between the multilocus outcrossing rate and single locus outcrossing rate were significantly different from zero (P < 0.05), suggesting the occurrence of bi-parental inbreeding within the population. Significant structure up to 300 m before logging was detected, with the coancestry coefficient

between individuals close to values expected between cousins (0.063). However, after logging the total population (reproductive trees and juveniles) did not show spatial genetic structure, suggesting that logging has Everolimus disrupted it ( Silva et al., 2008). The combination of wind and thrip pollinators of B. guianensis form ’thrip clouds’ that visit neighbouring trees, CX 5461 with three pollen donors per mother tree from a narrow geographic range. The non-random crossing of B. guianensis has important implications for conservation and seed collection programmes ( Silva et al., 2008). The Eco-gene simulation model was developed to study silvicultural impacts on temperate forests (Degen et al., 1996) and then adapted to be applied in tropical forest management (Degen et

al., 2003, Degen et al., 2004 and Kanashiro et al., 2002b). Considerable effort was taken to collect the information needed to run the model, and below we present some of the results. Sebben et al. (2008) provided results for the four species, B. guianensis, H. courbaril, M. huberi and S. globulifera, with the model parameterized using empirical

data from field studies in FLONA. Included data were genotypes at microsatellite loci, demography, ecology and growth for each species. Several scenarios, combining two different cutting diameters (45 and 60 cm dbh) and two different cutting cycles (30 and 65 years) as used in Brazil and French Guiana were tested. Logging scenarios were applied for six cutting cycles, and final genetic and demographic data PtdIns(3,4)P2 were compared to baseline data from corresponding control scenarios. At the end of the simulated period the basal area was strongly reduced under all conditions in B. guianensis, H. courbaril and M. huberi. Symphonia globulifera, however, was able to recover its basal area following logging in two scenarios. Based on these results, a Minimum Cutting Diameter (MCD) of 60 cm diameter at breast height was recommended. Simulations studies for D. odorata and J. copaia were undertaken by Vinson et al. (2013), which confirmed the importance in modelling of considering population density, growth patterns and breeding systems. Results in terms of basal area recovery were consistent with concerns stated by van Gardingen et al. (2006) who evaluated yield regulation options in the region. While the current Brazilian forest management regulations are sustainable for J. copaia, they are not for D. odorata in the long term.

4 ± 5 4%, n = 4), p < 0 01; ethanol + MRS + KRGE60 group vs etha

4 ± 5.4%, n = 4), p < 0.01; ethanol + MRS + KRGE60 group vs. ethanol + eticlopride + KRGE60

group (10.2 ± 2.5%, n = 4), p < 0.01; ethanol + MRS + KRGE60 group vs. ethanol + SCH23390 + KRGE60 group (27.4 ± 6.1%, n = 4), p > 0.05] ( Fig. 3B). Taken together, these results suggest that the anxiolytic effects of KRGE during EW were mediated by D2R in the CeA. Plasma CORT levels, a hormonal marker of anxiety in rats, were measured with an RIA to confirm the anxiolytic Raf targets effects of KRGE. Plasma CORT levels were significantly higher in ethanol-treated control rats (858.4 ± 181.3, n = 4) than in saline-treated controls [F (3, 13) = 18.2, p < 0.001; ethanol-treated control group (858.4 ± 181.3, n = 4) vs. saline-treated control group (318.6 ± 57.3, n = 5), p < 0.001]. Also in agreement with the behavioral data, the administration of both doses of KRGE significantly inhibited EW-related increases in plasma CORT levels [ethanol-treated control group vs. ethanol + KRGE 20 mg/kg group (473.2 ± 131.6, n = 4), p < 0.001; ethanol-treated control group vs. ethanol + KRGE 60 mg/kg

group (350.0 ± 80.7, n = 4), p < 0.001] ( Fig. 4). The HPLC analyses revealed significant decreases in the levels of DA and DOPAC in the CeA during EW. Treatment with KRGE dose-dependently reversed these deficiencies (Table 1) demonstrating that the anxiolytic effects of KRGE are mediated by the amygdaloid dopaminergic system. Western blot analyses revealed a reduction in the expression Leukotriene-A4 hydrolase of TH proteins in the CeA of ethanol-treated controls compared to saline-treated controls [F (2, 9) = 24.6, p < 0.001; saline-treated control

group (100%, n = 4) vs. ethanol-treated control group (36.2 ± 8.3%, Selleckchem ZVADFMK n = 4), p < 0.001]. However, the administration of KRGE (60 mg/kg) prevented these reductions [ethanol-treated control group vs. ethanol + KRGE60 (95.2 ± 23.4%, n = 4), p < 0.001] ( Fig. 5). The real-time PCR analyses revealed that EW significantly decreased the expression of TH mRNA in the VTA [F (2, 9) = 8.6, p < 0.01; saline-treated control group (100%, n = 4) vs. ethanol-treated control group (60.6 ± 10.0%, n = 4), p < 0.01]. However, the expression of TH mRNA in the CeA was spared (data not shown). Similar to protein expression in the CeA, KRGE (60 mg/kg) prevented the reduction of TH mRNA expression in the VTA during EW [ethanol-treated control group vs. ethanol + KRGE 60 mg/kg group (90.3 ± 22.2%, n = 4), p < 0.05] ( Fig. 6). Consistent with previous findings, the present study demonstrated that rats undergoing EW exhibit anxiety-like behavior as they spent less time in the open arms of the EPM [7] and [18]. The behavioral testing also revealed that both the 20 mg/kg and 60 mg/kg doses of KRGE significantly increased the time spent in the open arms, which reflects the anxiolytic effects of KRGE. The anxiety-reducing behavioral effects of KRGE were supported by biochemical evidence showing that KRGE inhibited plasma CORT secretion.

The histological findings of this experimental study were consist

The histological findings of this experimental study were consistent with

the lung pathology observed in biopsy specimens from fatal cases of severe malaria, which exhibit interstitial oedema and inflammatory cells in the lung tissue (Duarte et al., 1985 and Corbett et al., 1989). Even though interstitial oedema was observed at day 1, it was not enough to result in W/D Selleck CCI-779 ratio modifications. However, with the time course of lung injury, at day 5, W/D ratio increased probably due to the presence of consolidation resulting in an increase of lung weight. In the current study, IFN-γ, TNF-α, and CXCL1 production were measured in the lung tissue, since they are the main cytokines described in the pathogenesis of malaria (Angulo and Fresno, Selleck PD98059 2002). At day one, neutrophil infiltration may be associated with increased levels of CXCL1 as IFN-γ and TNF-α production was greater only by day 5. Since the alterations in lung histology were more exuberant than the changes in the current measured mediators, we cannot rule out the role of other cytokines, mechanisms such as oxidative stress (Sharma et al., 2012), or whether lung inflammation observed is triggered by changes in lung microcirculation. Indeed, in the lung microcirculation, low macrophage density and reduced blood velocity predispose infected erythrocytes to rosette formation and to cytoadherence to the endothelial lung microvasculature

rather than to larger blood vessels, 4��8C which leads to local endothelial activation in the lungs of P. berghei-infected mice ( Baer et al., 2007). Lung mechanics were measured by the end-inflation occlusion method, which allows for the identification of elastic, resistive, and viscoelastic/inhomogeneous components. It is well known that ALI increases elastic, resistive and viscoelastic/inhomogeneous pressures in the lungs during the early stages of acute lung injury (Rocco et al., 2004). Indeed, we observed

an increase in lung static elastance and resistive and viscoelastic/inhomogeneous pressures at days 1 and 5 in infected mice compared to SAL mice. These mechanical changes are consistent with the alveolar collapse and neutrophil infiltration observed at the same time points. It is interesting to note that in the cecal ligation and puncture (CLP) model of sepsis, which is widely compared to malarial infection (due to the development of systemic inflammation) (Garcia et al., 1995, Clark and Schofield, 2000, Clark and Cowden, 2003 and Mackintosh et al., 2004), ALI parameters such as neutrophil infiltration, respiratory mechanics, and cytokine production were observed very soon after the CLP procedure (Ornellas et al., 2011), whereas during malarial infection, cytokine-associated ALI was observed late in the course of the disease, suggesting the existence of a unique feature of P. berghei-induced lung injury early during infection.

, 2002) The patients were instructed to breathe deeply to overco

, 2002). The patients were instructed to breathe deeply to overcome the load. There were no requirements XL184 manufacturer for the breathing pattern or the breathing frequency to be adopted during the ILB. The chest wall volumes and breathing pattern were measured by optoelectronic plethysmography

(OEP-BTS, Milan, Italy) with a sampling frequency of 60 Hz. This non-invasive technique measures breath-by-breath changes in the volume of chest wall and its compartments (Aliverti and Pedotti, 2003 and Aliverti et al., 2009). Eighty-nine reflecting markers were placed over the front and back of the trunk along pre-defined horizontal and vertical lines. The landmark coordinates were measured with a system consisting of six infrared cameras, three of which were positioned in front of the participants and three of which were positioned behind the participants (Aliverti and Pedotti, 2003 and Aliverti

et al., 2009). The recorded images were transmitted to a computer, where a 3-D geometric model was formed (Cala et al., 1996). The chest wall was modeled from the compartments: pulmonary rib cage (RCP), abdominal rib cage (RCA) and abdomen (AB). For this study, we considered selleck compound the rib cage (RC) as the sum of the RCP and the RCA. The participants remained seated on a backless bench with their feet flat on the floor and their upper limps abducted, externally rotated and flexed (for the visualization of the lateral markers) and comfortably supported to minimize the activity of the accessory respiratory muscles both at rest and during ILB. The participants were instructed to look forward. To allow the cameras to capture the lateral chest wall markers, the examiner held the inspiratory threshold device at the participant’s right side. The chest wall volumes were determined

by analyzing the tidal volumes based on the difference (VT) between the end-inspiratory volume (Vei) and end-expiratory volume (Vee) of each compartment. The chest wall tidal volume (VTcw) was the sum of rib cage tidal volume (VTrc) and abdomen tidal volume (VTab). The breathing pattern was analyzed by the contribution of each compartment to the chest wall volume. The ratio of the inspiratory time to the learn more total time of the respiratory cycle, the respiratory frequency and the minute ventilation were also assessed. These ventilator parameters were obtained from chest wall volume variations measurements. Surface electromyography (EMG System do Brazil Ltd, São Paulo, Brazil) was used to record the muscle respiratory activity. Because a wireless device was not available, to avoid covering the OEP markers by EMG electrodes and cables we evaluated only the sternocleidomastoid (SMM) and abdominal (ABD) muscles. An EMG system with a biological signal acquisition module consisting of eight channels, an amplifier gain of 1000× and a common mode rejection ratio >120 db was used for data acquisition.

An f

An click here increase in islands and lateral sand bars in the reach is also shown in Fig. 5C. Analysis indicates that the reach gained 23,600 m2 of island area in 40 km of reach (the length of the reach is limited by the extent of the aerial photos). The areal extent of island area in 1999 was 150% greater

in 1950. Additionally, the island morphology has shifted from in-channel islands (indicative of the pre-dam river) to large islands attached to the outside of meander bends with distinctive distributary channels running through them. These are essentially former islands that have become attached to the banks as a result of excess sediment cutting off side channels. The Reservoir-Dominated selleck Interaction reach is located 140–190 km downstream from the Garrison Dam. Reservoir effects vary both annually and seasonally due

to changing reservoir levels creating a recognizable deltaic morphology. The Reservoir-Dominated Interaction reach is characterized by aggrading islands, sand bars, and the flooded meander bends (former meanders that have been flooded by the reservoir). 9 of 11 sites indicate deposition greater than the natural variability (269 m2). Fig. 4A is typical of cross sections in this area and shows al decrease in cross-sectional area of 411 m2. No suitable historic aerial imagery was available for this section of the river but current conditions indicate higher levels of low elevation sand bars than other sections of the river. The active extent of this reach can migrate drastically

from year to year depending on the reservoir level (as much as 160 km longitudinally, Fig. 6). Although the 50 km reach encompasses most of the delta in a typical discharge year, changes in releases from either dam can substantially change the active extent of the reach. Consequently, the depositional morphology and ultimately the Reservoir-Dominated Interaction reach can have a broader spatial distribution (Fig. 6A and B) than can be accounted for by a single year (insets A1 and A2, B1 and else B2). Although the lake level and backwater effects are highly spatially and temporally variable, the most recent set of aerial photos indicate the area of maximum deposition encompasses only this 50 km section of river. The morphology of this reach changes with varying lake levels. Islands, flooded meander scrolls, and deltaic splays are alternatively exposed and flooded. A large numbers of dead trees from flooding and those washed downstream litter the landscape and are present in channel. The Reservoir reach (Lake Oahe) is remarkably stable. This reach extends from approximately 190 km to just upstream of the Oahe Dam; 512 km downstream from Garrison Dam. Cross-sections in this section extend into the first 100 km into this reach. All 12 cross sections in the Oahe reach shows deposition greater than natural variability from 1963 to 1989 (269 m2).

e ,

changes to human–prey population dynamics, human popu


changes to human–prey population dynamics, human population densities, or other input parameters) do not support the overkill model (see Belovsky, 1998 and Choquenot selleck products and Bowman, 1998). Given that these models disagree in their outcomes and can only provide insights into the relative plausibility of the overkill model, the strongest evidence for overkill comes from the timing of megafaunal extinctions and human colonization. In the Americas, the major megafauna extinction interval coincides with the late Pleistocene arrival of humans about 15,000 years ago (Dillehay, 2000, Meltzer, 2009 and Meltzer et al., 1997). Most of the megafauna were lost by 10,500 years ago or earlier, generally coincident with the regionalization of Paleoindian projectile points, often interpreted as megafauna hunting technologies, in North America. Similarities are seen in Australia with first human colonization at about 50,000 years ago and the extinction of the continental megafauna within 4000 years on the mainland (Gillespie, 2008 and Roberts et al., 2001) and slightly later on Tasmania (Turney et al., 2008). The association of megafauna extinctions and

human arrival in Eurasia is more difficult to demonstrate. Hominins (e.g., Homo erectus, H. heidelbergensis, H. neandertalensis) were present in large parts of Eurasia for roughly two Selleck Protease Inhibitor Library isothipendyl million years, so Eurasian mammals should have co-evolved with hominins in a fashion similar to Martin’s African model. With the first AMH arriving in various parts of Eurasia between about 60,000 and 50,000 years ago, apparently with more sophisticated brains and technologies, AMH may have sparked the first wave of megafaunal extinctions at ∼48,000 years ago ( Barnosky et al., 2004). Overkill opponents argue that the small number of documented megafauna kill sites in the Americas and Australia provides no empirical evidence for the model (Field et al., 2008, Field

et al., 2013, Grayson, 1991, Grayson and Meltzer, 2002 and Mulvaney and Kamminga, 1999). For North America, Grayson and Meltzer (2003) argued that only four extinct genera of megafauna were targeted by humans at 14 archeological sites. In South America, even fewer megafauna kill sites have been found (see Fiedel and Haynes, 2004:123). Australia has produced no clear extinct megafauna kill sites, save one possible site at Cuddie Springs (Field et al., 2002, Field et al., 2008, Field et al., 2013 and Mulvaney and Kamminga, 1999). In both Australia and the Americas, these numbers are based on conservative interpretations of archeological associations, however, and other scholars argue for considerably larger numbers of kill sites.

The body mass index (BMI)/age and height/age indices were calcula

The body mass index (BMI)/age and height/age indices were calculated to characterize the population, using as reference the cutoffs (Z-scores), established by the WHO. 14

The body fat percentage (BF%) was measured by a DXA equipment (Lunar Prodigy Advance DXA System – analysis version: 13,31, GE Healthcare) and estimated by the following BIA equipment: tetrapolar horizontal Biodynamics®, model 450 (BIA 1), tetrapolar vertical Tanita®, model BC-558 (BIA 2), tetrapolar vertical Biospace®, equipped with eight tactile electrodes, InBody® 230 model (BIA 3), and bipolar vertical Tanita®, model INCB018424 cell line 2220 (BIA 4). BF% was analyzed according to the classification proposed by Lohman15, considering as excess body fat values ≥ 20% for males and ≥ 25% for females, and as low body fat percentage

CDK inhibitor drugs < 10% for males and < 15% for females. Assessment by BIA was performed in two stages, following the protocol proposed by Barbosa16 and later, within an average time period of 9±4 days, without the protocol. The protocol involved previous preparation aiming to standardize the hydration status to undergo the BIA assessment and consisted of the following: be at least seven days after the last menstrual period and seven days before the next; undergo complete fasting in the previous 12 hours; refrain from physical exercises in the previous 12 hours; no alcohol consumption in the previous 48 hours; no use of diuretics for at least seven days before the assessment; and urination 30 minutes before the assessment. Adolescents were also asked to

remove metal objects such as earrings, rings, watches, and others, which could interfere with the passage of electrical current. The Kolmogorov-Smirnov normality test was performed to determine variable distribution (parametric Idoxuridine or not) and thus choose the most appropriate statistical test to evaluate data. Parameters with normal distribution were expressed as mean and standard deviation; those with non-normal distribution were expressed as median and range. The chi-squared test was used to compare prevalence. In case of continuous variables, Student’s t or Mann-Whitney’s tests were performed to compare two, and Kruskal-Wallis’s test was used to compare three or more; Wilcoxon’s test was used when two evaluations were performed by the same individuals using the same equipment (with and without protocol). The kappa index was used to determine the agreement between the assessments by BIA and DXA, classifying it according to the criteria by Landis and Koch17, with the following concordances: from 0 to 0.19: poor; 0.2 to 0.39: weak; 0.4 – 0.59: moderate; 0.6 to 0.79: substantial; 0.8 to 1.0: almost perfect. ROC curves were constructed to verify the capacity of BIA in predicting excess body fat when compared to DXA. Areas under the curve (AUC) were calculated with their respective 95% confidence intervals. The null hypothesis would be accepted with an AUC value ≤ 0.50.

85 This association may depend on the protective effect of breast

85 This association may depend on the protective effect of breastfeeding on maternal depression, as depression is the best predictor of child maltreatment and neglect. The impact of breastfeeding on the maternal attention sensitivity towards infant distress was also recently shown.86 Literature consistently shows that breastfeeding provides a wide amount of benefits for

both the child and the mother. The psychological benefits for the mother are still in need of further research. Despite the high rate of breastfeeding initiation, a large decrease in the number of mothers who breastfeed from the first few weeks postpartum is observed. Public TSA HDAC cost health authorities’ efforts to promote breastfeeding initiation have been successful; however, the same has not been observed Obeticholic Acid supplier regarding its maintenance for a recommended period

of time, which is for two years or more, and exclusively during the first six months.16, 17 and 18 Identifying the possible underlying factors to this situation is a goal for research in this field. Maternal mental health may be one of the reasons behind this reality. A recent empirical study conducted in Portugal suggests that screening for depression symptoms during pregnancy can help identify women at risk for early cessation of exclusive breastfeeding.30 There is now empirical evidence that pregnancy

depression is one of the factors that may contribute to breastfeeding failure.29, 30, 32, 33, 45 and 56 Studies suggest an association between breastfeeding and postpartum depression, and the direction of this association is still unclear. While Glutamate dehydrogenase some suggest a negative association between breastfeeding and postpartum depression,40, 41, 42 and 43 others point to a negative association between postpartum depression and breastfeeding.27, 46, 49, 52, 53 and 54 Results from several studies provide empirical evidence that breastfeeding may act as a protective factor for depression during the postpartum, improving both maternal psychological well-being (namely through the regulation of sleep and awake patterns13 and 14 and increased self-efficacy)45 and 73 and adequate parenting, through the enhancement of the emotional involvement with the infant,75 and 77 mother-infant interaction,45 and 83 attention sensitivity towards infant stress,86 and protection against child neglect.85 Breastfeeding can also protect women from depressive symptoms, by aiding the regulation of the HPA axis (throughout the regulation of diurnal basal cortisol secretion),8, 9, 10, 11 and 12 which has been consistently shown to be deregulated in the presence of depressive symptoms.

Production of TNF-α was inhibited in the patient’s serum, whereas

Production of TNF-α was inhibited in the patient’s serum, whereas IL-10 production was not (Fig. 2C and D). Disseminated NTM disease usually occurs in patients who are severely immunocompromised, such as those with HIV disease or AIDS. However, some dNTM disease cases do not have HIV infection. There are two retrospective clinical analyses of dNTM disease without HIV infection.7 and 8 Chou et al. reported that

their 18 patients without HIV infection were usually febrile with elevated WBC counts.7 NTM was mainly isolated from not only the lung but also blood or bone marrow, and MAC was the most frequently detected pathogen in their study.7 Chetchotisakd et al. reported that NTM was selleck chemical most frequently detected in lymph nodes in their 129 dNTM patients without HIV infection.8 It is noteworthy that in both of these studies, dNTM patients had other opportunistic or severe infections in addition to the NTM. These included Salmonellosis, severe systemic intravascular PF-02341066 purchase infection, fungal infections including Aspergillus spp, Candida spp and Penicillium marneffei,

and viral infections including varicella zoster and cytomegalovirus. Furthermore, the cases with dNTM disease, confirmed by detection of NTM in multiple specimens, often did not have HIV. With adequate anti-AFB treatment, the survival rate was better than without such treatment. Female gender and co-infection with other bacterial pathogens were associated with poor outcomes. However, HIV infection had no significant prognostic impact. In 2005, two important studies detected autoantibodies against IFN-γ

in plasma from dNTM patients without HIV L-NAME HCl infection.4 and 5 IFN-γ has a crucial role in the control and regulation of NTM disease because some mutations in the genes for Th1 cytokines and their receptors are associated with severe conditions.9 Watanabe et al. reported that anti-IFN-γ autoantibody is detected even in sera from healthy individuals.10 However, the reason for the existence of an autoantibody against IFN-γ remains unclear. Evaluating anti-IFN-γ autoantibody in healthy individuals is important for elucidating the autoantibody differences between dNTM patients and healthy individuals. There must be an underlying factor triggering the onset of dNTM disease in the absence of HIV-infection. Regarding these previous reports, we considered it to be important for understanding the present patient’s pathophysiology to assay his serum. We wanted to know whether his serum contained specific immunoglobulins which bound and neutralized IFN-γ. To assay anti-IFN-γ autoantibody, we applied a protocol allowing comparison with bioassay results obtained using normal PBMNCs, as described in previous reports.5 In our view, mediastinal lymphadenopathy with elevated WBC counts and leukocytosis, of unknown origin, should prompt assay of the patient’s serum to detect anti-IFN-γ autoantibody. In addition, we suggest that infectious organisms such as P.

PGA-coated lipoplexes of 50 µg of ApoB siRNA-Chol were intravenou

PGA-coated lipoplexes of 50 µg of ApoB siRNA-Chol were intravenously administered via lateral tail veins into mice. At 24 h post-injection, mice were fasted for 24 h. At 48 h post-injection, blood was collected from the carotid arteries of mice under anesthesia, and allowed to stand for 1 h at 37 °C. Serum low-density-lipoprotein (LDL) cholesterol level Buparlisib was measured using a commercial

LDL cholesterol detection kit according to the manufacturer’s instructions (HDL and LDL/VLDL Cholesterol Quantification Kit, Bio Vision Incorporated, Milpitas, CA, USA). Serum was prepared by separation of the coagulated whole blood of female C57BL/6Cr mice (7 weeks of age; Sankyo Lab. Service Corp., Tokyo, Japan) 24 h after intravenous injection of cationic and anionic polymer-coated lipoplexes of 50 µg of Cont siRNA-Chol. Aspartate aminotransferase (AST/GOT) and alanine aminotransferase (ALT/GPT) BMS754807 activities in the plasma were determined using commercially available test reagents (GPT-UV test Wako and GPT-UV test Wako, respectively; Wako, Osaka, Japan). Normal values were determined using blood obtained from age-matched, untreated mice. The statistical significance

of differences between mean values was determined by using Student’s t-test. A p value of 0.05 or less was considered significant. The cationic lipid, 1,2-dioleoyl-3-trimethylammonium propane (DOTAP), has frequently cAMP inhibitor been used as a cationic lipid for a liposomal delivery system of siRNA

by several research groups [[14], [15], [16] and [17]]. Among cationic liposomes, DOTAP/Chol liposome is commercially supplied as an in vivo transfection reagent (e.g., in vivo MegaFectin™ from Qbiogene Molecular Biology, in vivo Liposome Transfection Reagent from Sigma-Aldrich), which was demonstrated to have high transfection efficiency in the lungs by intravenous injection. Here, we selected chondroitin sulfate C (CS), poly-l-glutamic acid (PGA) and poly-aspartic acid (PAA) as materials for coating cationic DOTAP/Chol lipoplexes of siRNA and evaluated their potential for use as an siRNA delivery vector. First, we prepared DOTAP/Chol liposome and measured the particle size and ζ-potential. The liposome size was about 80 nm and the ζ-potential was +50 mV. When the liposomes were mixed with siRNA, the lipoplex size was about 280 nm and the ζ-potential was +40 mV. Next, we coated the lipoplexes with anionic polymers, CS, PGA and PAA, at various charge ratios (−/+), and prepared CS-, PGA- and PAA-coated lipoplexes. With increasing amounts of CS, PGA and PAA being added to the lipoplex, their sizes decreased to 150–200 nm and ζ-potential to a negative value (Fig. 1A–C). Although the sizes of CS-, PGA- and PAA-coated lipoplexes were smaller than that of cationic lipoplex, the anionic polymers may be able to strongly compact the cationic lipoplex by the electrostatic interaction.