The candidates for cold climate genes were reportedly evaluated from three areas: the uncoupling proteins, maternally-transmitted mitochondrial genes, and mitochondrial biogenesis. Given this, it is highly suggestive that in our own data mitochondrial proteins emerge as being differentially regulated in honey selleckchem bee populations originated in the colder Canadian climates as compared to populations from warmer climates. These findings suggest that honey bees have similar adaptive mechanisms to humans and therefore confirm the utility of using honey bees as models of human metabolic diseases, as well as to understand the epidemiology of these diseases. In conclusion, we have provided evidence for the molecular basis of honey bee adaptations to diverse environments.

Overall, energy-related mitochondrial pathways were up-regulated in bees adapted to colder climates while protein biosynthesis and degradation pathways were preferentially up-regulated in honey bees from warmer climates. The observations reported here increase our understanding of metabolic diversity in honey bee populations and lay a framework for biomarker use in selective breeding. Results may also be extrapolated to other species, confirming the need to consider the relationship of animal populations and their native biome in commercial agriculture and in natural environments. Furthermore, our findings underscore the value of honey bees as models of human diseases. Mass spectrometry- based proteomics has rarely been applied to ecology and population biology [17] but this study demonstrates that exploiting proteomics towards these goals can provide great insight into ecological issues and adaptive processes in nature.

Materials and Methods Reagents All chemicals used were of analytical grade or better and all solvents were of HPLC-grade or better; all were obtained from ThermoFisher-Scientific (St. Waltham, MA, USA). Other reagents used were purchased from the following commercial sources: Endopeptidase Lys-C, Wako Chemicals (Osaka, Japan); porcine modified trypsin, Promega (Nepean, Ontario, Canada); loose ReproSil-Pur 120 C18-AQ 3 ��m, Dr Maisch (Ammerbuch-Entringen, Germany); 96-well full skirt PCR plates, Axygen (Union City, CA, USA); fused silica capillary tubing, Polymicro (Phoenix, AZ, USA); protease inhibitor mixture, Roche Applied Science (Basel, Switzerland); NuPAGE Novex BisTris Gels, Invitrogen (Carlsbad, CA, USA).

Honey bee populations and sample collection Eight populations (Table 1) of bees were used in this study and all bees were imported AV-951 to and maintained at the Agriculture and Agri-Food Canada, Beaverlodge Research Farm, Beaverlodge, AB, Canada (55��18�� N; 119��17�� W) for one to two years. Multiple colonies (4�C10) from each population were sampled in triplicate and five bee midguts were pooled for each sample. Midguts were dissected from the abdomens of freshly decapitated bees by using forceps to grasp the terminal abdominal segments and pulling gently.

A constant value, which also corresponded to the molar occlusion, was added to the TPI score. For each student, recorded malocclusions find more were summed and a total TPI score was calculated. The severity of malocclusion was assessed according to the Malocclusion Severity Estimate (MSE) [9]. According to the scale modification proposed by Ghafari et al. [18], the constant value for neutrocclusion on the TPI form was scored as normal occlusion. Here, the normal occlusion level was assessed as 0.27 and a score of 0.27�C3.99 was regarded as a minor manifestation of malocclusion. In the current study, this modification was preferred. The periodontal status was recorded using the CPITN scores as described by WHO [17].

The CPITN scores were set so that 0 = healthy, 1 = bleeding on gentle probing, 2 = calculus or other plaque-retentive factors, 3 = shallow pocketing of 4-5mm, and 4 = deep pockets of 6mm or more. For the periodontal examination we used a dental mirror, an explorer, and the periodontal probe, as recommended by WHO [17]. During oral examination of each child, the number of decayed, missing, or filled teeth was recorded as the DMFT score.2.1. Statistical Analyses The data were analyzed using SPSS for Windows, version 13.0 (SPSS Inc., Chicago, IL, USA). TPI measurements for the different genders were compared using Student’s t tests and age groups were compared using analysis of variance (ANOVA). The effects of age, gender, mothers’ and fathers’ education levels, parents’ monthly income, and CPITN scores on TPI scores were examined using the chi-square test.

Spearman’s rank correlation coefficients were estimated to provide a measure of the association between TPI, CPITN, and DMFT scores. Levels of statistical significance were set at P < 0.05. 3. Results The children's parents' monthly income and educational status are shown in Tables Tables11 and and2.2. In the present study, the TPI scores showed that 36.4% of the students had normal occlusion, while 41.2% had slight, 15.7% had definite, 4% had severe, and 2.7% had very severe malocclusion (Table 3).Table 1Parental monthly income.Table 2Parental educational status.Table 3Orthodontic treatment need according to TPI scores.TPI values did not show any significant differences between pupils in different age, gender, and socioeconomic status groups, as calculated based on the children's mothers' and fathers' education and monthly income (Table 4).

Table 4Comparison of TPI scores with age, gender, parental education, and parental monthly income.According to the CPITN scores, 36.6% of students had a healthy periodontium, 35.3% showed bleeding on gentle probing, and 21.9% had signs calculus or other plaque-retentive factors. Only 13 students (1.5%) had shallow Batimastat pocketing of 4-5mm and 39 students (4.6%) had deep pockets of 6mm or more.

No significant differences in hormone levels were identified between patients and controls, but patients with hypogonadism presented the site a higher prevalence of MS.Diabetes mellitus, arterial hypertension, dyslipidaemia, obesity, and tobacco use are well known risk factors for cardiovascular disease because they are associated with endothelial dysfunction and the development of premature atherosclerosis. This endothelial dysfunction produces ED, due to reduced nitric oxide production and reduced vascular distensibility which inhibits an adequate erection during sexual intercourse [4, 12, 13]. ED has been linked in various studies with CD and MS [5, 6, 13].In our study, patients with ED have a much higher prevalence of MS than the control group.

These results are consistent with other results found in the literature which have shown that MS is strongly associated with ED [14�C16]. We have observed that the MS criteria most frequently recorded in patients with ED were abdominal obesity and systolic and diastolic hypertension. These results are similar to those published by Bal et al., who reported that higher blood pressure, fasting glucose, and abdominal perimeter were the risk factors that best predicted the onset of ED [15]. Patients with ED and MS have a reduced elasticity in large arteries, resulting in a higher flow pressure and more arterial hypertension. Patients with ED and MS show a higher risk of cardiovascular events [17]. Some biochemical mediators have been measured in patients with suspected endothelial dysfunction [6, 9, 18].

In our study, we have observed that patients with ED had higher levels of C-reactive protein but not higher levels of fibrinogen and D-dimer or a higher erythrocyte sedimentation rate. A statistically significant negative linear correlation between IIEF score and C-reactive protein levels was found, which means that high levels of this mediator are related to the severity of ED. Elevated C-reactive protein levels in patients with ED have been found in patients with endothelial dysfunction [8].In some patients with ED, the risk for CD and MS is associated with a deficit in testosterone levels [19, 20]. In our study, no significant differences were found in total, free, or bioavailable testosterone levels in patients with ED or Carfilzomib the controls. Patients were divided into two groups according to their levels of total testosterone (lower than 3.5ng/mL and higher to 3.5ng/mL), and the prevalence of MS and ED in these two groups was analysed. Patients with hypogonadism did not present with higher rates of ED, but they did demonstrate a higher prevalence of MS.

However, the signal to noise ratio is much superior at 690nm when compared to 840nm, hence all absorbance measurements have been carried out at 690nm in the present investigations.Figure 1Absorption spectra of arsenomolybdenum our site blue complex after cloud point extraction.3.1. Optimization StudyThe initial studies were carried out by extracting the formed arsenomolybdenum blue complex into nonionic surfactants like Triton X-100 and Triton X-114 as the TX series of nonionic surfactants have several advantages over other surfactants like commercial availability, low toxicity, low cloud point formation temperature and high density of the surfactant-rich micellar phase [13]. The quantitative extraction of the complex was obtained by both the surfactants, but, in case of Triton X-100, heating is required for cloud formation but in presence of Triton X-114, cloud formation takes place at room temperature.

Hence, Triton X-114 was used as a micellar phase to preconcentrate the analyte species before absorbance measurement. All the parameters influencing the complex formation and cloud point extraction have been optimized.3.1.1. Effect of Acidity The arsenomolybdenum blue complex forms in acidic medium; hence, the effect of sulfuric acid concentration on complex formation has been studied. The higher absorbance values corresponding to the sample versus reagent blank were obtained at an overall acidity value of 0.25M. The required acidity was achieved by the addition of 2mL of 1.25 molL?1 sulfuric acid and used in all further studies (Figure 2).Figure 2Effect of overall acidity.

3.1.2. Effect of Surfactant The effect of surfactant concentration on the quantitative phase separation of analyte through micelle is a crucial parameter in cloud-point-extraction based methods. Hence, we have examined two nonionic surfactants like GSK-3 Triton X-100 and Triton X-114 for the quantitative separation of the complex. Quantitative extraction of the complex from the aqueous phase was obtained by both surfactants, but the extraction of the complex at room temperature was achieved only with Triton X-114. The high density of Triton X-114 facilitates quick phase separation which can be easily achieved by simple centrifugation [16]. In case of Triton X-100, heating is required to attain cloud point temperature whereas Triton X-114 attains clouding at normal condition itself, that is, at room temperature [9]. Hence, Triton X-114 has been selected as a micellar phase for analyte separation. Quantitative extraction of the complex was achieved at 0.8% (v/v). The required surfactant concentration was achieved by the addition of 2mL of 4% surfactant solution (Figure 3).Figure 3Effect of Triton X-114 concentration.3.1.3.

For example, a single lactation cycle depleted a dam of 98% of her body burden of 2,4,5,2��,4��,5��-hexachlorobiphenyl [33].Presumably the principal driving forces selleck chemical Y-27632 behind the appearance of OCs in milk are the concentration of the OC in adipose tissue, the mobilization of adipose tissue to provide triacylglycerol fat in the milk, and the movement of OCs with the mobilized fat to the mammary gland cells. The interruption of enterohepatic circulation of OCs would be predicted to have an effect on their appearance in milk fat primarily through a reduction in their adipose stores. A schematic view of how dietary and enterohepatic lipid and OCs can enter milk is presented in Figure 2.Figure 2OC compounds (depicted by solid hexagons) are transported to mammary gland cells from adipose tissue carried by lipoproteins and albumin in blood (A).

Chylomicrons also carry OCs from both the diet and enterohepatic circulation (B). Aim 1 addresses transport …It is not clear, however, if a biologically significant amount of OCs in the lumen of the intestine enters milk directly without first passing through storage in the adipocytes. There is evidence in humans that a small fraction of dietary fatty acids from the diet enters milk within a period of time that is consistent with direct entry into milk [34]. It is not known if other lipophilic nutrients follow the pattern of the fatty acids and also appear in milk soon after ingestion. If dietary OCs or OCs secreted into the intestine accompany dietary fat into milk, then it may be possible to reduce their entry into milk lipids by dietary nonabsorbable lipid or lipase inhibitor.

At this time further study is needed to determine if this potential effect is clinically meaningful.8. Emerging Clinical ConsiderationsVarious medical bodies, such as the Pediatric Academic Societies, have recently concluded that ��low level exposure to environmental toxicity may be impacting the functioning of the current generation [35].�� With the recent emergence of abundant scientific literature correlating exposure to various toxicants with adverse clinical states and mounting awareness of the escalating chemical erosion of human health resulting from widespread bioaccumulation of chemical toxicants [36, 37], it is anticipated that intervention to diminish toxicant burdens in order to preclude and treat disease will eventually become a fundamental component of clinical medicine [38].

Numerous and varied disorders including congenital anomalies [39], neurodevelopmental conditions [40], autoimmune Cilengitide disorders [41], diabetes, [42], endocrine dysfunction [43], mental illness [44], cancer [45], neurodegenerative disease [46] and other assorted afflictions spanning the spectrum of medical specialties have now been directly linked, in some cases, to chemical toxicant exposures.

However, serum proangiogenetic markers are a simple method and have the considerable advantage selleck chemicals llc of not requiring an experienced pathologist to reliably assess. There have been only a few published studies on these serum proangiogenetic markers in clinical settings. However, confounding variables of known clinical prognostic factors were not considered in some of these reports. Therefore, we conducted this study to determine the independent association between these markers and clinical outcomes.In earlier studies, Salven et al. [12�C14] and Bertolini et al. [15] demonstrated a significant association between these markers and the outcomes of patients with NHL in concordance with our study. The correlation between high VEGF levels and poor CR rate also supported the hypothesis that high VEGF is responsible for an abnormal vessel structure of tumors leading to lowering drug delivery [4].

However, our more recent study found higher levels of pretreatment VEGF and bFGF, probably because the patients in our study had more advanced stages of disease. Ribatti et al. [16] and Crivellato et al. [17] also found that neovascularization was found frequently in high-grade lymphoma. The different serum VEGF and bFGF levels before treatment in patients with different degrees of disease, or due to other factors, may lead to difficulty in obtaining a single cut-off value for a predictor in all patients with NHL. In addition, the level of bFGF may be elevated due to other conditions associated with increased endothelial activity, infection, or inflammation [18, 19].

Importance roles of angiogenesis in lymphomas Cilengitide have been demonstrated in clinical studies. Tzankov and colleagues [20] performed immunohistochemical and morphometric studies in B-cell lymphomas and found higher microvessel density, and VEGF and COX2 in aggressive lymphomas. This result is in concordance with Ganjoo et al. [21] who reported that patients with negative stained VEGF-A or VEGF-R1 had a superior survival rate. These studies confirmed the potential importance of increased angiogenesis in prognosis and tracking of disease progression in non-Hodgkin lymphomas. In conclusion, our study suggests that serum VEGF and bFGF are associated with poor prognosis in patients with de novo non-Hodgkin lymphomas. Further studies are needed to determine more clearly whether monitoring of consecutive levels of these molecules during or after therapy could predict CR or relapse. In addition, these markers may play an important role in patient selection for antiangiogenetic treatment.AcknowledgementsThe authors are indebted to Ms. Somporn Sretrirutchai for her technical assistance.

Additionally in 2004, Jindadamrongwech and Smith identified the 78kDa band for DENV2 as the glucose-related protein, GRP78 (BiP) on membrane extracts of HepG2 [48]. Pretreatment with anti-GRP78 antibodies resulted in a partial inhibition of DENV2 infection suggesting that additional receptor elements were involved in the entry process of DENV. In 2007, Cabrera-Hernandez and coworkers again noted a modest but definite inhibition of DENV2 entry into HepG2 cells in the presence of specific antibody directed against GRP78 [49]. The reproducible inhibition about 40% of the viral wild-type entry clearly demonstrated that GRP78 acted as at least a minor receptor in DENV internalization [49]. Moreover, it was reported that liver/lymph node-specific ICAM-3-grabbing integrin (L-SIGN) [50], homolog of DC-SIGN, expressed on liver sinusoidal endothelial cells as well as a subset of endothelial cells in the paracortex zone of lymph nodes, had the ability to bind to DENVs [51, 52]. And its expression in THP-1 cells induced susceptibility to DENV infection [53]. Specific antibodies against L-SIGN could subsequently block the acquired susceptibility. The L-SIGN-dependent DENV infection of THP-1 cells offered an intriguing possibility for the participation of L-SIGN in DENV infection [49].6. Fc ReceptorsGenerally, DENV infection can induce subtype-specific humoral and cellular immune responses. If a secondary infection is caused by another serotype of DENV in the same individual, the preexisting antibodies will mediate virus infecting monocytes more efficiently. The outcome may be an increase in the viral replication and a high risk of severe dengue. This situation is referred to as antibody-dependent enhancement (ADE) of DENV infection. One possibility explaining this phenomenon is that in secondary infections, the virus may enter cells through the primary receptor(s) or it may also form immune complexes with preexisting nonneutralizing antibodies and interact with an alternative receptor, such as the immunoglobulin G (IgG) receptor (Fc gamma receptor, Fc��R), which exists in Fc��R-bearing cells including monocytes/ macrophages [54, 55]. By this process, the antibody-virus complexes may increase the ability of the virus to bind to and internalize into host cells, leading to maximum productive infection, that is, ADE of infection.7. DENV Receptors on Mosquito Cells Generally more is known about the detail of DENV replication cycle in mammalian cells as compared with that in mosquito cells. An Aedes albopictus mosquito cell line (C6/36) was frequently used for almost all studies associated with DENV receptors in host of mosquito during recent years.

..Figure 30Types and size of the sensilla of the Corixidae: Cymatiinae (Cymatia coleoptrata). selleck chem inhibitor (a) Several of the CH1 are placed on the lateral edge of the labium and below the apex; several PES and RBS2 are visible on AT. (b) RBS1, RBS2, and PES are spread unevenly …Finger-like sensillum (FRS) (Figure 2(b)). The base and tip of this type of sensillum are of the same width, but the shaft is slightly wider in the middle. This type of sensilla has been observed only in the Gelastocorinae (Gelastocoris oculatus Figure 16(f)).Freniale-like sensillum (HLS) (Figure 2(c)). This sensillum is designed as a long, thin hair with a tapered tip. It has been observed in the Gelastocorinae (Gelastocoris oculatus, Figures 16(b), 16(f), and 16(g)).Chaetic sensillum with a bisected tip (CHB) (Figure 2(d)).

The tip of the seta is divided into two short branches. This type of sensillum has been found only in the Nerthra nepaeformis (Figure 17(e)) (Gelastocoridae: Nerthrinae).Star-like sensillum (STS) (Figure 2(e)). It is a short cone divided into four or five narrow lobes. The base of the sensillum is sunken in a socket, and it is situated shallowly in a cavity. The lobes are prominent above the cuticular surface. This type of sensillum has been specific to the Aphelocheiridae (Aphelocheirus aestivalis, Figures 18(c), 18(d), and 18(e) and A. variegatus).Multilobed sensillum (MPS) (Figure 2(f)). This type of sensillum consists of a few narrow lobes, arising from a common stem. The base of the sensillum is sunken in a socket and the lobes evidently protrude above the cuticular surface.

This type of sensillum has been found in the Limnocorinae (Limnocoris lutzi, Figures 21(a) and 21(c)), Cryphocricinae (Cryphocricos hungerfordi, Figures 22(a), 22(b), 22(c), and 22(d); Ambrysus occidentalis, Figures 23(a), 23(c) and 23(e)) and the Naucorinae (Naucoris maculatus, Figure 24(a); Namtokocoris siamensis,Figure 24(d); Neomacrocoris handlirschi,Figure 24(g)) as well as in Ilyocoris cimicoides and Pelocoris femoratus, (Table 2).Figure 21Types and sizes of the sensilla of the Naucoridae: Limnocorinae (Limnocoris lutzi). (a) MPS are numerous and distributed in rows over the IV segment (dorsal view). (b) PAS (no. 1�C12) are located on the labial tip (SFL). (c) TRS1 (four) and TRS2 …Figure 22Types and sizes of the sensilla of the Naucoridae: Cryphocricinae (Cryphocricos hungerfordi).

(a) MPS are numerous and spread evenly on the IV segment (ventral view); TRS2 (four) are distributed over the ventral side (V) in one row near the apex of the …Figure 23Types and sizes of the sensilla of the Naucoridae: Cryphocricinae (Ambrysus occidentalis). (a) MPS are less numerous and spread Carfilzomib evenly over the III segment (dorsal view); several CH3 are present on the II segment (dorsal view). (b) CH2 and CH1 cover the …

05). In comparison with the normocholesterolemic diet group, serum levels available of TC, LDL-C, SGOT, and HDL-C were elevated in the sesame seed containing diet group (P > 0.05). Rabbits supplemented with sesame oil (5%) were found to have lower circulating concentrations of TC, LDL-C, HDL-C, SGOT, and SGPT (P < 0.05), whilst concentrations of TG, apo A, apo B, insulin, and glucose remained unaltered compared to the hypercholesterolemic diet group (P > 0.05). Comparison of sesame oil versus normocholesterolemic diet groups revealed an elevation of triglycerides and reduction in apo A concentrations in the sesame oil fed group (P < 0.05). None of the evaluated biochemical parameters did significantly differ between sesame seed and sesame oil supplemented groups (P > 0.05).4.

DiscussionFindings of the present study suggested that dietary supplementation with sesame oil significantly reduces TC and LDL-C concentrations in rabbits under a lipogenic diet. These findings are consistent with those of previous studies. Visavadiya and Narasimhacharya [30] examined the effects of supplementation with sesame seed powder at 5% and 10% doses along with either normal or hypercholesterolemic diet for a period of 4 weeks. Administration of sesame seed powder to hypercholesterolemic rats resulted in a significant decline in plasma and hepatic total lipid and cholesterol, and plasma LDL-C whilst increasing HDL-C concentrations. In another investigation to evaluate hypocholesterolemic and antioxidant activity of sesame protein isolate, Biswas et al.

[31] fed 18% sesame protein isolate with or without 2% cholesterol in comparison with casein to rats for 28 days. The results revealed that dietary sesame protein isolate reduces plasma total cholesterol, triacylglycerol, and LDL-C, increases HDL-C, and mitigates lipid peroxidation in both hypercholesterolemia and normocholesterolemic diet groups. Sirato-Yasumoto and associates demonstrated that supplementation with lignan-rich sesame Anacetrapib has a remarkable potentiating effect on hepatic fatty acid oxidation while downregulating the activity of lipogenic enzymes. These favorable metabolic effects of lignan-rich sesame were reported to be accompanied with a profound hypotriglyceridemic effect [32]. In a recent report, Asgari et al. [25] investigated the protective effects of sesame on postprandial lipemic and glycemic response as well as circulating concentrations of endothelial function biomarkers in hypercholesterolemic rabbits. Their results revealed that sesame supplementation is associated with significant declines in serum TC, LDL-C, SGPT, and fibrinogen. In the study by Kumar et al.

(15)Using??=��(t,��+E)?��(t,��)+K(��?��)??=��(t,��)+Ke?��(t,��)=��(t,��)?��(t,��)+Ke??as??d����dt��?d����dt�� the first-order Taylor expansion, the function ��(?) is rewritten =?��(t,��)?��E+h.o.t=G(t)E+h.o.t,(16)where h.o.t denotes the?as��(t,��+E)?��(t,��) things higher order terms of the series. We substitute (16) into (15) and yieldd��Edt��=G(t)E+h.o.t+KCTE=[G(t)+KCT]E+h.o.t.(17)We can transfer the (17) intod��Edt��=[G(t)+KCT]E(18)according to Lemma 1, we can know that the error system is asymptotically stable at zero if and only if the following condition is satisfied|arg(eig(G(t)+KCT))|�ݦ���2.(19)4. The Example Analysis and Numerical SimulationsExample 3 (dual synchronization of Van der Pol-Willis systems) ��In the first example, we can use the proposed method to achieve the dual synchronization of the Van der Pol system and the Willis system.

Master 1: Van der Pol systemd��x1dt��=x1?��x13?��x2+f1cost,d��x2dt��=l(x1?mx2+n).(20)Master 2: Willis systemd��y1dt��=y2,d��y2dt��=ay1+by12+cy13+dy2+f2cost.(21)So the corresponding slave systems are as follows:Slave 1:d��X1dt��=X1?��X13?��X2+f1cost+k1e,d��X2dt��=l(X1?mX2+n)+k2e,(22)Slave 2:d��Y1dt��=Y2+k3e,d��Y2dt��=aY1+bY12+cY13+dY2+f2cost+k4e,(23)where e = a1e1 + a2e2 + b1e3 + b2e4,e1 = X1 ? x1,e2 = X2 ? x2,e3 = Y1 ? y1, and e4 = Y2 ? y2.The G(t) matrix of the master systems is achieved asG(t)=?1?3��x12?��00llm00000100a+2by1+3cy12d?,(24)so the corresponding error ��(e1e2e3e4).

(25)We?matrix are as follows:(d��e1dt��d��e2dt��d��e3dt��d��e4dt��)=(1?3��x12+a1k1?��+a2k1b1k1b2k1l+a1k2lm+a2k2b1k2b2k2a1k3a2k3b1k31+b2k3a1k4a2k4a+2by1+3cy12+b1k4d+b2k4) should choose the appropriate parameters so that all the eigenvalues of the Jacobian matrix of (25) satisfy Matignon condition; that is, the eigenvalues evaluated at the equilibrium point are satisfied:|arg(eig(G(t)+KCT))|>����2.(26)The eigenvalue equation of the equilibrium point is locally asymptotically stable. From what we have discussed above, we can know that A and B are two known matrices; the parameter K can be appropriately selected for satisfying the Matignon condition. Dual synchronization of the Van der Pol system and the Willis system is simulated. The system parameters are set to be �� = 1/3, �� = 1, f1 = 0.74, l = 0.1, m = 0.8, n = 0.7, a = ?0.9, b = 3, c = ?2, d = ?0.1, f2 = 0.1, A = [1,1, 1], B = [1,1, 1], and �� = 1, soG(t)+KCT=(1?x12+k1?1+k1k1k10.

1+k2?0.08+k2k2k2k3k3k31+k3k4k4?0.9+6y1?6y12+k4?0.1+k4).(27)If ?295 < k1 < ?130, k2 = ?0.1, k3 = ?1, and k4 = ?400, which satisfy (18), the eigenvalue equation of the equilibrium point is locally asymptotically stable. We choosek1 = ?210, k2 = ?0.1, k3 = ?1, and k4 = ?400. The initial Brefeldin_A conditions of the master system 1 and the master system 2 are taken as x1(0) = 0.1, x2(0) = 0.2 and y1(0) = 0.2,y2(0) = 0.3; the initial conditions of the slave system 1 and the slave system 2 are taken as X1(0) = 0.