Establishment of a Rat Model of Portal Vein Ligation Combined with In Situ Splitting

Background

Portal vein ligation (PVL) combined with in situ splitting (ISS) has been shown to induce remarkable liver regeneration in patients. The purpose of this study was to establish a model of PVL+ISS in rats for exploring the possible mechanisms of liver regeneration using these techniques.

Materials and Methods

Rats were randomly assigned to three experimental groups: selective PVL, selective PVL+ISS and sham operation. The hepatic regeneration rate (HRR), Ki-67, liver biochemical determinations and histopathology were assessed at 24, 48, and 72 h and 7 days after the operation. The microcirculation of the median lobes before and after ISS was examined by laser speckle contrast imaging. Meanwhile, cytokines such as TNF-α, IL-6, HGF and HSP70 in regenerating liver lobes at 24 h was investigated by RT-PCR and ELISA.

Results

The HRR of PVL+ISS was much higher than that of the PVL at 72 h and 7 days after surgery (p<0.01). The expression of Ki-67 in hepatocytes in the regenerating liver lobe was stronger in the PVL+ISS group than in the PVL group at 48 and 72 h (p<0.01). There was a significant reduction in microcirculation blood perfusion of the left median lobe before and after ISS. Liver biochemical determinations and histopathology demonstrated more severe hepatocyte injury in the PVL+ISS group. Both the mRNA levels of TNF-α and IL-6 and the protein levels of TNF-α, IL-6 and HGF in regenerating liver lobes were higher in the PVL+ISS than the PVL alone.

Conclusions

The higher HRR in the PVL+ISS compared with the PVL confirmed that we had successfully established a PVL+ISS model in rats. The possible mechanisms included the reduced microcirculation blood perfusion of the left median lobe and up-regulation of cytokines in the regenerating lobes after ISS.     

狂犬病小鼠模型的制作

目的建立狂犬病病毒感染动物疾病模型。方法狂犬病病毒CVS-B2C毒株以10LD50剂量腿部肌肉注射接种4~6周龄的BALB/c小鼠,0.2 mL/只,于BSL2实验室负压IVC设备内饲养观察,并对其模型进行评价。结果小鼠接种狂犬病病毒后一周左右就出现临床症状,表现为饮食量下降,毛皮慢慢失去原先的光泽,体重下降,并出现麻痹等症状,进而死亡,部分小鼠出现躁狂的症状或抽搐性和强直性痉挛,而对照组小鼠则表现正常。DFA法检测结果：感染上狂犬病毒的小鼠脑组织涂片中出现特异性荧光抗体染色反应,而对照组动物的小鼠脑组织涂片未出现荧光抗体染色反应。RT-PCR法检测结果：从感染小鼠脑组织标本中提取病毒RNA,引物扩增出的目的基因片段,大小约为1kb,为N蛋白。免疫组化法检测结果：感染狂犬病毒的小鼠脑切片显示出棕色阳性颗粒,对照组小鼠脑切片染色阴性。病理检测结果：HE染色可见感染小鼠脑组织炎性细胞浸润,神经细胞胞质内出现内基体以及神经细胞退行性病变。结论成功的复制出小鼠狂犬病病毒感染模型,为研究和控制狂犬病奠定了基础。     

大鼠实验性牙周炎模型简便方法的建立

目的探讨建立大鼠实验性牙周炎模型简便方法。方法麻醉后,用大镊子固定暴露牙龈,再用眼科弯剪对两侧牙齿周围牙龈划割剥离,每天喂10%的白砂糖水和白砂糖水浸泡的软饲料。结果两周后出现牙周袋,三周后动物蜷曲少动,牙周袋加深,牙周袋有食物残渣,触之易出血,牙槽骨呈弹坑状吸收至根尖,并且出现明显的临床症状改变。白细胞数量增加,其中以中性粒细胞增加为主。结论此方法简便易行,便于普及,实验周期短,2～3周即可形成典型牙周炎,并可见牙周袋形成,模型稳定,个体差异小,值得推广。     

兔在体心脏缺血再灌注模型的制作方法的改进

目的建立兔在体心脏缺血再灌注模型的新方法。方法40只新西兰大白兔随机分为缺血再灌注组（25只）,假手术组（15只）。缺血再灌注组采用＂二线二结＂法结扎心脏左前降支30 min,然后恢复心肌灌注3h;假手术组仅将线从左前降支周围心肌中穿过,但并不结扎。实验中连续描记心电图。两组分别于结扎（穿线）前和再灌注（穿线）后1 h从股静脉取血1 mL测定血清肌钙蛋白。实验结束时取心肌行2,3,5-氯化三苯基四氮唑和苏木精-伊红染色。结果缺血再灌注组心电图存在ST-T的动态演变,再灌注1 h后血清肌钙蛋白浓度明显高于术前（0.47±0.35 vs.0.33±0.31,P=0.002）。两种染色方法均证明存在心肌坏死。结论＂二线二结＂法能够既方便又成功地建立兔在体心脏缺血再灌注模型。     

豚鼠高脂血症模型的建立及机制探讨

目的建立豚鼠高脂血症模型,探讨模型形成机制并与大鼠模型进行比较。方法豚鼠模型和大鼠模型1组用低胆固醇（0.1%）饲料诱导,大鼠模型2组用高胆固醇（1%）饲料诱导,连续诱导4周。第3、4周分别取血测定血清脂质水平及CETP表达,4周末剖取肝脏检测肝脏FC、TG、ACAT、CYP7A1等指标。动态观察两种动物形成高脂血症状况。结果与对照组比较,豚鼠模型组于第3周血清TC、LDL-C、TG分别升高3.92倍、3.75倍和1.24倍,4周末血清CETP表达、肝脏ACAT活性明显增加,但肝CYP7A1水平变化不大。大鼠模型1组经低胆固醇饲料诱导4周,血脂水平变化不明显,模型2组经高胆固醇饲料诱导于第3周血清TC、LDL-C分别升高1.24倍和1.54倍,明显低于同期豚鼠模型组,4周末大鼠两个模型组肝CYP7A1活性显著增强,血清TG、CETP水平、肝ACAT活性均未见明显变化。结论豚鼠对高脂饲料较大鼠敏感,是一种比大鼠更理想的高血脂模型动物,模型形成机制与血清CETP表达、肝ACAT及CYP7A1活性变化密切相关。     

Using Trust to Establish a Secure Routing Model in Cognitive Radio Network

Specific to the selective forwarding attack on routing in cognitive radio network, this paper proposes a trust-based secure routing model. Through monitoring nodes’ forwarding behaviors, trusts of nodes are constructed to identify malicious nodes. In consideration of that routing selection-based model must be closely collaborative with spectrum allocation, a route request piggybacking available spectrum opportunities is sent to non-malicious nodes. In the routing decision phase, nodes’ trusts are used to construct available path trusts and delay measurement is combined for making routing decisions. At the same time, according to the trust classification, different responses are made specific to their service requests. By adopting stricter punishment on malicious behaviors from non-trusted nodes, the cooperation of nodes in routing can be stimulated. Simulation results and analysis indicate that this model has good performance in network throughput and end-to-end delay under the selective forwarding attack.     

支气管哮喘伴发抑郁大鼠模型的建立

目的探讨建立支气管哮喘伴发抑郁动物模型的方法。方法选择Wistar大鼠,随机分为对照组与模型组,模型组采用卵蛋白(ovalbumin,OVA)激发法建立哮喘模型,在此基础上给予慢性轻度不可预见性应激(chronic unpredictable mild stress,CUMS)28d,观察大鼠体质量、体征、肺组织结构、支气管肺泡灌洗液白细胞计数等变化,并用Open-field实验评价大鼠活动度和好奇心,通过糖水消耗实验评价大鼠快感缺乏与否。结果与对照组相比,模型组大鼠体质量增长明显缓慢(P0.05);肺组织呈哮喘样病理改变;支气管肺泡灌洗液白细胞总数、嗜酸粒细胞及淋巴细胞增多;Open-field实验,大鼠垂直活动得分、水平活动得分显著降低(P0.05);糖水消耗量明显减少(P0.05)。结论OVA激发复合CUMS可成功制备支气管哮喘伴发抑郁大鼠模型。     

A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium

Despite the well-known close association, direct evidence linking disturbed flow to atherogenesis has been lacking. We have recently used a modified version of carotid partial ligation methods [1,2] to show that it acutely induces low and oscillatory flow conditions, two key characteristics of disturbed flow, in the mouse common carotid artery. Using this model, we have provided direct evidence that disturbed flow indeed leads to rapid and robust atherosclerosis development in Apolipoprotein E knockout mouse [3]. We also developed a method of endothelial RNA preparation with high purity from the mouse carotid intima [3]. Using this mouse model and method, we found that partial ligation causes endothelial dysfunction in a week, followed by robust and rapid atheroma formation in two weeks in a hyperlipidemic mouse model along with features of complex lesion formation such as intraplaque neovascularization by four weeks. This rapid in vivo model and the endothelial RNA preparation method could be used to determine molecular mechanisms underlying flow-dependent regulation of vascular biology and diseases. Also, it could be used to test various therapeutic interventions targeting endothelial dysfunction and atherosclerosis in considerably reduced study duration.Download video file.^{(125M, mp4)}     

A Novel,Open Access Method to Assess Sleep Duration Using a Wrist-Worn Accelerometer

Wrist-worn accelerometers are increasingly being used for the assessment of physical activity in population studies, but little is known about their value for sleep assessment. We developed a novel method of assessing sleep duration using data from 4,094 Whitehall II Study (United Kingdom, 2012–2013) participants aged 60–83 who wore the accelerometer for 9 consecutive days, filled in a sleep log and reported sleep duration via questionnaire. Our sleep detection algorithm defined (nocturnal) sleep as a period of sustained inactivity, itself detected as the absence of change in arm angle greater than 5 degrees for 5 minutes or more, during a period recorded as sleep by the participant in their sleep log. The resulting estimate of sleep duration had a moderate (but similar to previous findings) agreement with questionnaire based measures for time in bed, defined as the difference between sleep onset and waking time (kappa = 0.32, 95%CI:0.29,0.34) and total sleep duration (kappa = 0.39, 0.36,0.42). This estimate was lower for time in bed for women, depressed participants, those reporting more insomnia symptoms, and on weekend days. No such group differences were found for total sleep duration. Our algorithm was validated against data from a polysomnography study on 28 persons which found a longer time window and lower angle threshold to have better sensitivity to wakefulness, while the reverse was true for sensitivity to sleep. The novelty of our method is the use of a generic algorithm that will allow comparison between studies rather than a “count” based, device specific method.     

A Novel MMP12 Locus Is Associated with Large Artery Atherosclerotic Stroke Using a Genome-Wide Age-at-Onset Informed Approach

Genome-wide association studies (GWAS) have begun to identify the common genetic component to ischaemic stroke (IS). However, IS has considerable phenotypic heterogeneity. Where clinical covariates explain a large fraction of disease risk, covariate informed designs can increase power to detect associations. As prevalence rates in IS are markedly affected by age, and younger onset cases may have higher genetic predisposition, we investigated whether an age-at-onset informed approach could detect novel associations with IS and its subtypes; cardioembolic (CE), large artery atherosclerosis (LAA) and small vessel disease (SVD) in 6,778 cases of European ancestry and 12,095 ancestry-matched controls. Regression analysis to identify SNP associations was performed on posterior liabilities after conditioning on age-at-onset and affection status. We sought further evidence of an association with LAA in 1,881 cases and 50,817 controls, and examined mRNA expression levels of the nearby genes in atherosclerotic carotid artery plaques. Secondly, we performed permutation analyses to evaluate the extent to which age-at-onset informed analysis improves significance for novel loci. We identified a novel association with an MMP12 locus in LAA (rs660599; p = 2.5×10⁻⁷), with independent replication in a second population (p = 0.0048, OR(95% CI) = 1.18(1.05–1.32); meta-analysis p = 2.6×10⁻⁸). The nearby gene, MMP12, was significantly overexpressed in carotid plaques compared to atherosclerosis-free control arteries (p = 1.2×10⁻¹⁵; fold change = 335.6). Permutation analyses demonstrated improved significance for associations when accounting for age-at-onset in all four stroke phenotypes (p<0.001). Our results show that a covariate-informed design, by adjusting for age-at-onset of stroke, can detect variants not identified by conventional GWAS.     

N-Methyl-d-Aspartate Releases γ-Aminobutyric Acid from Rat Striatum In Vivo: A Microdialysis Study Using a Novel Preloading Method

Abstract: In vivo microdialysis was used in conjunction with a novel dual-label preloading method to monitor changes in extracellular levels of γ-aminobutyric acid (GABA) and glutamate due to N -methyl- d -aspartate (NMDA) infusion in the striatum of conscious, unrestrained rats. [¹⁴C]GABA and [³H]glutamate were applied in the dialysis stream for a preloading period of 30 min, after which dialysis perfusion was continued for up to 6 h and dialysate samples were collected for analysis by liquid scintillation spectrometry. NMDA (300 μ M in the dialysate) caused significant rises in both ¹⁴C and ³H content measured in the dialysates, the majority of which remained associated with the preloaded GABA and glutamate, respectively. The NMDA-evoked release of both GABA and glutamate was blocked by the specific NMDA receptor antagonist 3-[(±)-2-carboxypiperazin-4-yl]propyl-1-phosphonic acid (CPP), indicating that the response was receptor mediated. The NMDA-stimulated release of glutamate was also totally abolished by concomitant application of the adenosine agonist 2-chloroadenosine or by prior frontal decortication. However, these two treatments caused little change in NMDA-evoked GABA release. These results show that NMDA causes release of GABA from the striatum in vivo by an NMDA receptor-mediated mechanism and that the majority of this release is not secondary to glutamate release from terminals of the corticostriate pathway. In addition, they confirm the results of previous studies investigating the effect of NMDA on endogenous glutamate release.     

A Novel Rat Model to Study the Role of Intracranial Pressure Modulation on Optic Neuropathies

Reduced intracranial pressure is considered a risk factor for glaucomatous optic neuropathies. All current data supporting intracranial pressure as a glaucoma risk factor comes from retrospective and prospective studies. Unfortunately, there are no relevant animal models for investigating this link experimentally. Here we report a novel rat model that can be used to study the role of intracranial pressure modulation on optic neuropathies. Stainless steel cannulae were inserted into the cisterna magna or the lateral ventricle of Sprague-Dawley and Brown Norway rats. The cannula was attached to a pressure transducer connected to a computer that recorded intracranial pressure in real-time. Intracranial pressure was modulated manually by adjusting the height of a column filled with artificial cerebrospinal fluid in relation to the animal’s head. After data collection the morphological appearance of the brain tissue was analyzed. Based on ease of surgery and ability to retain the cannula, Brown Norway rats with the cannula implanted in the lateral ventricle were selected for further studies. Baseline intracranial pressure for rats was 5.5±1.5 cm water (n=5). Lowering of the artificial cerebrospinal fluid column by 2 cm and 4 cm below head level reduced ICP to 3.7±1.0 cm water (n=5) and 1.5±0.6 cm water (n=4), a reduction of 33.0% and 72.7% below baseline. Raising the cerebrospinal fluid column by 4 cm increased ICP to 7.5±1.4 cm water (n=2) corresponding to a 38.3% increase in intracranial pressure. Histological studies confirmed correct cannula placement and indicated minimal invasive damage to brain tissues. Our data suggests that the intraventricular cannula model is a unique and viable model that can be used to study the effect of altered intracranial pressure on glaucomatous optic neuropathies.     

Preventing Olanzapine-Induced Weight Gain Using Betahistine: A Study in a Rat Model with Chronic Olanzapine Treatment

Olanzapine is the one of first line antipsychotic drug for schizophrenia and other serious mental illness. However, it is associated with troublesome metabolic side-effects, particularly body weight gain and obesity. The antagonistic affinity to histamine H₁ receptors (H₁R) of antipsychotic drugs has been identified as one of the main contributors to weight gain/obesity side-effects. Our previous study showed that a short term (2 weeks) combination treatment of betahistine (an H₁R agonist and H₃R antagonist) and olanzapine (O+B) reduced (−45%) body weight gain induced by olanzapine in drug-naïve rats. A key issue is that clinical patients suffering with schizophrenia, bipolar disease and other mental disorders often face chronic, even life-time, antipsychotic treatment, in which they have often had previous antipsychotic exposure. Therefore, we investigated the effects of chronic O+B co-treatment in controlling body weight in female rats with chronic and repeated exposure of olanzapine. The results showed that co-administration of olanzapine (3 mg/kg, t.i.d.) and betahistine (9.6 mg/kg, t.i.d.) significantly reduced (−51.4%) weight gain induced by olanzapine. Co-treatment of O+B also led to a decrease in feeding efficiency, liver and fat mass. Consistently, the olanzapine-only treatment increased hypothalamic H₁R protein levels, as well as hypothalamic pAMPKα, AMPKα and NPY protein levels, while reducing the hypothalamic POMC, and UCP₁ and PGC-1α protein levels in brown adipose tissue (BAT). The olanzapine induced changes in hypothalamic H₁R, pAMPKα, BAT UCP₁ and PGC-1α could be reversed by co-treatment of O+B. These results supported further clinical trials to test the effectiveness of co-treatment of O+B for controlling weight gain/obesity side-effects in schizophrenia with chronic antipsychotic treatment.     

A Novel Regioselective Desulfation Method Specific to Carbohydrate 6-Sulfate Using Silylating Reagents

Sulfated primary alcohols and methyl α-D-galactopyranoside 6-sulfate were converted into desulfated and trimethylsilylated alcohols and galactoside, respectively, by treating their pyridinium salts with N,O-bis(trimethylsilyl)acetamide (BTSA) or N,O-bis(trimethylsilyl)triftuoroacetamide (BTSTFA) in pyridine. Sulfated secondary alcohols and methyl galactoside 2-, 3-, and 4-sulfates did not have their sulfates eliminated under similar conditions, indicating that the reaction was specific to the primary hydroxyl groups. Methyl α-galactoside 2-sulfate was preparatively obtained by the BTSA treatment of methyl α-galactoside 2,6-disulfate, indicating that the method is applicable to regioselective desulfation on a preparative scale.     

一种利用STO饲养层细胞制备拟胚体的新方法

建立了一种利用STO饲养层细胞制备拟胚体的新方法。该方法选用生长至80%饱和密度的STO细胞,经丝裂霉素C(10 mg/ml)处理4 h后以8×104 cm-2的密度接种培养12 h,制备饲养层,再将ES-D3细胞以1×104 cm-2的密度接种其上,首先用含mLIF的DMEM培养液培养24 h,再更换拟胚体诱导培养液,5～9天后获得了各成熟阶段的拟胚体。形态结构和分化潜能等研究表明,该方法制备的拟胚体结构典型,具有产生3个胚层谱系来源的功能细胞的潜能。与传统拟胚体制作方法如悬滴培养法相比,具有操作简便,拟胚体形成率高,重复性好等优点,是开展哺乳动物早期胚胎发育和干细胞分化研究的理想工具。     

A Novel Brain Neurovascular Unit Model with Neurons,Astrocytes and Microvascular Endothelial Cells of Rat

A novel triple cell neurovascular unit (NVU) model co-culturing with neurons, brain microvascular endothelial cells (BMECs) and astrocytes was established in this study for investigating the cerebral diseases and screening the candidates of therapeutic drug. We have first performed the cell identification and morphological characterization, analyzed the specific protein expression and determined the blood-brain barrier (BBB) function of the co-culture model under normal condition. Then, we further determined the BBB function, inflammation, cell injury and the variation of neuroprotective factor in this model after anoxia-reoxygenation. The results suggest that this model exhibited a better BBB function and significantly increased expression of P-glycoprotein (Pg-P) and ZO-1 compared with BMECs only or co-culture with astrocytes or neurons. After anoxia-reoxygenation, the pathological changes of this model were basically resemblance to the pathological changes of brain cells and BBB in vivo. And nimodipine, an antagonist of calcium, could reverse those changes as well. According to our observations, we deduce that this triple cell co-culture model exhibits the basic structure, function and cell-cell interaction of NVU, which may offer a more proper in vitro system of NVU for the further investigation of cerebral diseases and drug screening.     

Characterizing Movement of Ground-Dwelling Arthropods with a Novel Mark-Capture Method Using Fluorescent Powder

A major knowledge gap exists in understanding dispersal potential of ground-dwelling arthropods, especially in forest ecosystems. Movement of the ground-dwelling arthropod community was quantified using a novel mark-capture technique in which three different colored fluorescent powders in two separate mixtures were applied to the floor of a deciduous forest in concentric bands 3, 8, and 15 m from the center of 30 × 30 m experimental plots. The majority (67.1%) of ground-dwelling arthropods did not cross a colored band when fluorescents were mixed with protein powder in 2014. However, when mixed with sand in 2015, 77.3% of captured arthropods were marked with fluorescent powder, with the majority of individuals crossing one band (41.2%), suggesting limited dispersal by most individuals in the community. Only 2.8% and 15.0% of arthropods crossed all three bands in 2014 and 2015, respectively, which further indicates that individuals have limited dispersal. Responses were taxon-specific, and a high proportion of some arthropods such as millipedes and harvestmen crossed two or three bands. Limited dispersal by most individuals may have important implications for the structure and distribution of ground-dwelling arthropod communities, as well as their responses to natural or anthropogenic disturbances. Our results demonstrate the feasibility of this novel technique for self-marking and capturing individuals in the field to investigate dispersal of ground-dwelling arthropods.     

Rat Brain Free Glucose and Lactate Measurement by a Novel Method Using Bisecting Decapitation-Extrusion and Enzyme Denaturation at Five Seconds

This study investigates a novel method as a means for animal decapitation with rapid brain removal and enzyme denaturation. Briefly, the rat head is simultaneously decapitated and bisected. Either half of the in situ brain is aspirated under -250 mm Hg pressure into a modified small plastic syringe and then extruded through a needle as a fine strand into a relatively large volume of 2 M urea at 95 degrees C. After cooling, sonication, and centrifugation of the brain homogenate, the supernatant is measured enzymatically for brain free glucose and lactate concentration. Enzyme denaturation is effected within 4-6 s. The results are in good agreement with published values for glucose and lactate using other rapid enzyme inactivation techniques.     

A Novel Model to Predict Esophageal Varices in Patients with Compensated Cirrhosis Using Acoustic Radiation Force Impulse Elastography

Background & Aims

Few noninvasive methods can accurately identify esophageal varices (EVs) in patients with compensated cirrhosis. We developed and validated a novel, acoustic radiation force impulse (ARFI) elastography-based prediction model for high-risk EVs (HEVs) in patients with compensated cirrhosis.

Methods

A total of 143 patients with compensated cirrhosis between February, 2010 and February, 2013 (training set) and 148 between June, 2010 and May, 2013 (validation set) who underwent ARFI elastography and endoscopy were prospectively recruited. Independent predictors of HEVs were used to construct a prediction model.

Results

Based on multivariate analysis, we developed two new statistical models, a varices risk score and ARFI-spleen diameter-to-platelet ratio score (ASPS), the latter of which was calculated as ARFI velocity × spleen diameter/platelet count. The area under receiver operating characteristic curve (AUROC) of the varices risk score and ASPS to predict HEVs were 0.935 (95% confidence interval [CI] 0.882–0.970) and 0.946 (95% CI 0.895–0.977), respectively. When ASPS, a simpler model with a higher AUROC, was applied in the validation set, acceptable diagnostic accuracy for HEVs was observed (AUROC = 0.814 [95% CI 0.743–0.885]). To detect HEVs, a negative predictive value of 98.3% was achieved at ASPS <2.83, whereas a positive predictive value of 100% was achieved at ASPS >5.28.

Conclusions

ASPS, a novel noninvasive ARFI-based prediction model, can accurately identify HEVs in patients with compensated cirrhosis. ASPS <2.83 may safely rule out the presence of HEVs, whereas patients with ASPS >5.28 should be considered for endoscopic examinations or appropriate prophylactic treatment.     

A Prostate Cancer Model Build by a Novel SVM-ID3 Hybrid Feature Selection Method Using Both Genotyping and Phenotype Data from dbGaP

Through Genome Wide Association Studies (GWAS) many Single Nucleotide Polymorphism (SNP)-complex disease relations can be investigated. The output of GWAS can be high in amount and high dimensional, also relations between SNPs, phenotypes and diseases are most likely to be nonlinear. In order to handle high volume-high dimensional data and to be able to find the nonlinear relations we have utilized data mining approaches and a hybrid feature selection model of support vector machine and decision tree has been designed. The designed model is tested on prostate cancer data and for the first time combined genotype and phenotype information is used to increase the diagnostic performance. We were able to select phenotypic features such as ethnicity and body mass index, and SNPs those map to specific genes such as CRR9, TERT. The performance results of the proposed hybrid model, on prostate cancer dataset, with 90.92% of sensitivity and 0.91 of area under ROC curve, shows the potential of the approach for prediction and early detection of the prostate cancer.