魏氏梭菌是芽孢杆菌科梭状芽孢杆菌,形态上两端钝圆,能形成芽孢,芽孢椭圆形,菌体呈梭状,有荚膜,无鞭毛.在自然界中分布极广,土壤、饲料、蔬菜、粪便,及人畜肠道中都有存在,属于典型的条件致病菌.魏氏梭菌能产生强烈的外毒素,外毒素与致病力有密切关系,有些外毒素可引起特异的肠毒血症,尤其魏氏梭菌A和C型合成分泌的毒素对犬危害性极大.犬魏氏梭菌感染发病速度快,病程短,致死率高,而且一年四季均可发生.
Cadmium (Cd) is a toxic environmental pollutant and induces toxic effects to organism. Nevertheless, the mechanism of Cd-induced toxicity in swine remains obscure. To explore this, 10 healthy 6-week-old weaned swine were placed into two groups stochastically, the Cd group was treated with a commercial diet containing 20 mg/kg Cd for 40 days. The results of histopathological and ultrastructural observations showed typical necrosis features and inflammatory cell infiltration in Cd group. Excessive Cd suppressed T-AOC and SOD activities, increased MDA content and ROS levels. Cd diet elevated the expression of RIPK1, RIPK3, and MLKL to activate the RIPK3-dependent necroptosis pathway. Results of Th1 and Th2 cytokines indicated that the levels of IL-4, IL6 and IL10 was increased, while the level of IFN-gamma was decreased, illustrating Th1/Th2 immune imbalance leads to aggravate inflammatory responses. Cd activated the TNF-alpha/NF-kappa B pathway and induced inflammatory responses via increasing the expression of HO-1, IL-1 beta, iNOS, COX2. Heat shock proteins were notably elevated in response to inflammatory reactions. And these effects were inhibited by necrostatin-1 (Nec-1) and N-acetylcysteine (NAC). Altogether, these data demonstrated that Cd induced necroptosis and inflammation to aggravate small intestine injury in swine by increasing the excessive accumulation of ROS and imbalanced Th1/Th2, respectively.
一、发病情况 某犬基地德国牧羊犬,7岁,公(未去势),常规免疫.主诉:8月份发现患犬下颌肿大,食欲减退,服用消炎药后症状好转.11月份,该犬开始精神不佳,喜卧,食欲明显下降.近日该犬拒绝进食,消瘦.
一、病例介绍 患犬法兰玖,母,5岁,马里努阿犬,完全免疫,定期驱虫.1个月前发情,未进行交配.几日前开始表现烦躁不安、食欲不振、口渴狂饮等症状.阴门处流出不定量暗红色脓性液体,气味恶臭.病犬肌肉注射3天头孢曲松钠,病情未见好转,遂入院治疗. 二、诊断 (一)临床检查 患犬体温39.8℃,心率128次/分,呼吸次数51次/分,眼结膜潮红,腹部增大,阴户肿大,阴道流出脓性血样分泌物、腥臭味.触诊可摸到充盈的子宫角,波动感明显并伴有疼痛反应,初步诊断为开放性子宫蓄脓.
2016年7月13日,本院诊断一病犬为“犬瘟热”,在治疗过程中,由于主人擅自给病犬饲喂川贝止咳药,导致该犬发生严重的过敏反应,经过近2周的治疗,康复出院,7d后跟踪调查,无不良反应.报告如下. 1病例情况 病犬为雌性、体重3.45 kg、年龄2月龄的金毛幼犬.主述:该犬未进行过任何免疫,2016年7月11日主人发现,其突然发生频繁咳嗽并伴有呕吐,大便正常但颜色较黑,到住地附近的动物医院就诊,诊断为犬瘟热(CDV),家中自行饲喂了半粒小儿感冒颗粒,由于外院无相关条件及设施开展治疗,故转来本校动物医院.
The aim of this study was to evaluate the influence of phosphorus (P) deficiency on the morphological and functional characteristics of erythrocytes in cows. Forty Holstein-Friesian dairy cows in mid-lactation were randomly divided into two groups of 20 each and were fed either a low-P diet (0.03% P/kg dry matter [DM]) or a control diet (0.36% P/kg DM). Red blood cell (RBC) indices results showed RBC and mean corpuscular hemoglobin decreased while mean corpuscular volume increased significantly (p < 0.05) in P-deficient cows. Erythrocyte morphology showed erythrocyte destruction in P-deficient cows. Erythrocytes' functional characteristics results showed total bilirubin and indirect bilirubin concentrations and aspartate transaminase and alanine transaminase activity levels in the serum of P-deficient cows were significantly higher than those in control diet-fed cows. Activities of superoxide dismutase and glutathione peroxidase in erythrocytes were lower, while the malondialdehyde content was greater, in P-deficient cows than in control diet-fed cows. Na+/K+-ATPase and Mg2+-ATPase activities were lower in P-deficient cows than in control diet-fed cows; however, Ca2+-ATPase activity was not significantly different. The phospholipid composition of the erythrocyte membrane changed and membrane fluidity rigidified in P-deficient cows. The results indicate that P deficiency might impair erythrocyte integrity and functional characteristics in cows.
犬蠕形螨病又称毛囊虫病或脂螨病,是由蠕形螨寄生于犬皮脂腺或毛囊大量繁殖而引起的一种顽固性寄生虫性皮炎。临床上常见、多发、较难治愈。目前犬的蠕形螨病发病率持续保持较高水平,一旦受训犬和工作犬患蠕形螨病往往会影响其训练和使用,甚至被淘汰,严重者如得不到及时治疗,会因脓毒血症、自体中毒或高度衰竭死亡。因此,对犬蠕形螨病的防治要采取综合措施,做到抓早、抓好。
伪狂犬病是由疱疹病毒科的伪狂犬病毒引起犬和多种动物共患的一种急性传染病,该病亦称奥耶斯基氏病,最早发现于美国,1902年匈牙利科学家在犬和牛身上首先分离出伪狂犬病病毒.伪狂犬病呈世界分布,许多哺乳动物对伪狂犬病毒易感,而且感染后常以死亡为结果,但猪例外,成年猪能耐过感染而生存下来,并成为病毒的储存宿主和传染源.犬是伪狂犬病毒最为敏感的动物,一旦感染发病,多在48小时之内死亡,特征性临床症状为突然瘙痒,剧烈地抓挠或啃咬某一部位,以下颌、头颈多见.携带伪狂犬病病毒的啮齿类动物是主要传染源,犬之间的水平传播尚未见报道.现介绍一例德国牧羊犬患伪狂犬病混合细菌感染的病例.
Hepatocellular carcinoma (HCC) is the most common cancer type. There is a correlation between selenium (Se) deficiency and the incidence of HCC. To clarify the effects of Se level on the risk of HCC patients, a meta-analysis was performed. A total of 9 articles published between 1994 and 2016 worldwide were selected through searching PubMed, EMBASE, web of science, Cochrane Library, Springer Link, Chinese National Knowledge Infrastructure (CNKI), and Chinese Biology Medicine (CBM), and the information were analyzed using a meta-analysis method. Heterogeneity was assessed by using the I2 index. Publication bias was evaluated by Begg's Test analysis. Pooled analysis indicated that patients with HCC had lower Se levels than the healthy controls [standardized mean difference (SMD)= -1.08, 95% confidence intercal (CI) = (-0.136, -0.08), P < 0.001]. Further subgroup analysis showed this effect to be independent of the study design, race or sample collection. In conclusion, this meta-analysis suggested an inverse correlation between Se level and the risk of HCC in humans patients.
Animals are exposed to various environmental stresses every day, including the stress associated with living in cold temperatures. The aim of this study was to investigate the possible mechanisms of interaction between lipid metabolism and inflammation induced by cold stress in the livers of chickens. Fifteen-day-old male chicks were randomly allocated into 12 groups (10 chickens per group). After exposure of the chickens to the cold stress, cholesterol fractionation was used to examine high-density lipoprotein (HDL) and low-density lipoprotein (LDL) concentrations. Aminotransferase activities were examined with the use of the aspartate transaminase (AST) and alanine transaminase (ALT) assay. The AMP-activated protein kinase α–proliferator-activated receptor α (AMPKα–PPARα) pathway genes (AMPKα1, AMPKα2, PPARα, carnitine palmitoyltransferaseI [CPTI], acetyl-CoA carboxylase [ACC]) and inflammatory cytokines (prostaglandin E synthase [PGEs], inducible nitric oxide synthase [iNOS], heme oxygenase-1 [HO-1], nuclear factor kappa-light-chain-enhancer of activated B cells [NF-κ;B], cyclooxygenase-2 [COX-2], and TNF-α-like factor [LITAF]) were also measured. The results showed that during the response to cold stress, serum LDL and HDL cholesterol concentrations increased. Histopathologic analyses provided evidence that liver tissues were seriously injured in the chickens exposed to the cold stress. Serum aminotransferase activities were also increased in the group of animals exposed to the cold stress. Additionally, the expressions of AMPKα–PPARα pathway genes and inflammatory cytokine genes were significantly increased in the animals exposed to cold temperatures. These results suggested that increased inflammation was a feature associated with a lipid-metabolism disorder in the livers of chickens exposed to cold stress.Efecto del estrés por frío en la expresión del mecanismo AMPKα-PPARα y de los genes pro-inflamatorios.Los animales están expuestos a varios tipos de estrés ambiental todos los días, incluyendo el estrés asociado con temperaturas frías. El objetivo de este estudio fue investigar los posibles mecanismos de interacción entre el metabolismo de los lípidos y la inflamación inducidos por el estrés por frío en el hígado del pollo. Se asignaron al azar quince pollitos machos de un día de edad en 12 grupos (10 pollos por grupo). Después de la exposición de los pollos al estrés por frío, se utilizó el método de fraccionamiento del colesterol para analizar las concentraciones de lipoproteínas de alta densidad (HDL) y de lipoproteínas de baja densidad (LDL). Las actividades de la aminotransferasa fueron examinadas mediante los ensayos de la aspartato transaminasa (AST) y de la transaminasa de alanina (ALT). También se determinaron los genes del mecanismo del receptor α activado por la proteína quinasa α proliferadora y activada por AMP (AMPKα1, AMPKα2, PPARα, palmitotransferasa de carnitina [CPTI], la carboxilasa de acetil-CoA [ACC]) y las citoquinas inflammatorias (protaglandina E sintetasa [PGEs], la sintetasa de óxido nítrico inducible [iNOS], la oxigenasa-1 del grupo heme [HO-1], el factor nuclear potenciador de las cadenas ligeras kappa de las células B activadas [NF-κ;B], ciclooxigenasa-2 [COX-2], factores similares al factor de necrosis tumoral alfa [LITAF]). Los resultados mostraron que durante la respuesta al estrés por frío, se incrementaron las concentraciones séricas de colesterol LDL y HDL. Los análisis histopatológicos proporcionaron evidencia que los tejidos hepáticos resultaron gravemente lesionados en los pollos expuestos al estrés por frío. La actividad de las aminotransferasas séricas también se incrementó en el grupo de animales expuestos al estrés por frío. Además, las expresiones de genes de la vía AMPKα- PPARα y de los genes de citoquinas inflamatorias fueron significativamente superiores en los animales expuestos a temperaturas frías. Estos resultados sugieren que el aumento de la inflamación era una caract
犬特应性皮炎(Canine atopic dermatitis,CAD)又称异位性皮炎,是一种区别于犬类过敏性皮炎(Canine atopic-like dermatitis,CALD)以皮炎和瘙痒为主要临床特征并具有遗传倾向的犬易患皮肤病。近年来,随着CAD发病机制研究的逐步深入,CAD的诊断和治疗方法也随之得到了发展。本文将针对近年来CAD上述方面的进展进行综述。
Animals are exposed to various environmental stresses every day, including the stress associated with living in cold temperatures. The aim of this study was to investigate the possible mechanisms of interaction between lipid metabolism and inflammation induced by cold stress in the livers of chickens. Fifteen-day-old male chicks were randomly allocated into 12 groups (10 chickens per group). After exposure of the chickens to the cold stress, cholesterol fractionation was used to examine high-density lipoprotein (HDL) and low-density lipoprotein (LDL) concentrations. Aminotransferase activities were examined with the use of the aspartate transaminase (AST) and alanine transaminase (ALT) assay. The AMP-activated protein kinase alpha-proliferator-activated receptor alpha (AMPKalpha-PPARalpha) pathway genes (AMPKalpha1, AMPKalpha2, PPARalpha, carnitine palmitoyltransferaseI [CPTI], acetyl-CoA carboxylase [ACC]) and inflammatory cytokines (prostaglandin E synthase [PGEs], inducible nitric oxide synthase [iNOS], heme oxygenase-1 [HO-1], nuclear factor kappa-light-chain-enhancer of activated B cells [NF-kappaB], cyclooxygenase-2 [COX-2], and TNF-alpha-like factor [LITAF]) were also measured. The results showed that during the response to cold stress, serum LDL and HDL cholesterol concentrations increased. Histopathologic analyses provided evidence that liver tissues were seriously injured in the chickens exposed to the cold stress. Serum aminotransferase activities were also increased in the group of animals exposed to the cold stress. Additionally, the expressions of AMPKalpha-PPARalpha pathway genes and inflammatory cytokine genes were significantly increased in the animals exposed to cold temperatures. These results suggested that increased inflammation was a feature associated with a lipid-metabolism disorder in the livers of chickens exposed to cold stress.
In this study,the effects of cold stress on the expression levels of HSP70 in duodenum,jejunum,ileum and cecum were studied.120 1-day-old male chickens were kept under the temperature of (30± 2) ℃ and were given commercial diet and water.When the chickens were 15 days old,they were randomly divided into 12 groups on average and were kept under the temperature of (12±1) ℃ for acute and chronic cold stress.The duration of acute cold stress were 0,1,3,6,12 and 24 h,and the duration of chronic cold stress were 5,10 and 20 d.0 h was the control group for the acute cold stress,and there were three control groups for chronic cold stress.After the cold stress treatment,the tissues were collected for real-time PCR assessment.The results showed that at the beginning of the acute cold stress and chronic cold strss,HSP70 expression levels were increased significantly(P0.01),but at the end of acute cold stress,the expression levels were decreased significantly(P0.01).The study suggested that HSP70 expressioin levels could be influenced by the cold stress and the expression levels be different by different tissues or different durations of the cold exposure.
The aim of this study was to investigate the effect of manganese on the hepatic cytochrome P450 enzyme system in cocks.400 fifty-day old Hy-line brown cocks were randomly divided into four groups.The cocks in four groups were respectively fed with the basal diet containing 0,600,900 and 1 800 mg·kg-1 MnCl2 to establish the sub-chronic manganism model.After 30,60 and 90-day treatment,the livers in every group were collected to detect the activity of microsomal cytochrome P450 enzyme system and the transcription level of CYP2H1 gene.The contents of cytochrome P450 and b5,the activities of aminopyrin-N-demethylase(AND) and aniline-4-hydroxylase(AH) were gradually declined with the increase of manganese in diet.The high dose group was significantly lower than the control group while there were no difference between the low and middle dose group and the control group.There were no markedly changes in the activities of NADPH-cytochrome C reductase(CR) and erythromycin-N-demethylase(ERND).The activity of CR declined at 30 and 60 d,but increased at 90 d.Besides,the CR activity of the high dose group was significantly higher than that in the control group(P0.01).The activity of ERND increased at 30 d but no markedly tendency appeared at 60 and 90 d.The ERND activity in the high dose group was significantly higher than that in the low dose group(P0.01).The transcription level of CYP2H1 mRNA in the low dose and high dose group at 30 d,the middle dose group at 60 d,and the low dose group at 90 d were higher than that in the control group.The transcription level of CYP2H1 mRNA in other treatment groups were lower than that in the control group.These results indicated that manganism could significantly changes the activities of microsomal-cytochrome P450s and the transcription level of CYP2H1 mRNA.
To determine the effect of MnCl2 exposure on apoptosis of cock sertoli-germ cell and on expression of Bak and Bcl-x mRNAs,cock sertoli-germ cells were cultivated in DMEM with the final concentrations of 0,2,3 and 4mmol/L MnCl2 respectively for 24h.The apoptosis was determined by TUNEL assay,and the expression amounts of Bak and Bcl-x mRNAs were examined by real-time fluorescence quantitative PCR.In result,compared with control group,the apoptosis index(AI) of cock sertoli-germ cell significantly increased(P0.01),the expression of Bak mRNA increased(P0.01) while the expression of Bcl-x mRNA decreased(P0.01) in 2,3 and 4mmol/L MnCl2 treatment groups.The result indicated that MnCl2 was able to induce apoptosis of cock sertoli-germ cell by up-regulating the expression of Bak mRNA and down-regulating the expression of Bcl-x mRNA.
The aim of this study was to discuss the role of mitochondria mediated apoptosis pathway in Sertoli-germ cell apoptosis induced by manganese in cocks.Cock Sertoli-germ cells were cultivated in the DMEM for 24 h added with MnCl2,whose final concentrations were 0,2,3,and 4 mmol·L-1 respectively.The apoptosis was detected by AO/EB double staining.Mitochondrial transmembrane potential was detected by flow cytometer.Expression of Cytochrome c(Cytc)in cytolymph was detected by western blotting.The activities of Caspase-9,3 were examined by spectrophotography.Compared with control group,the apoptosis index(AI)of cock Sertoli-germ cells was significantly increased(P0.01),mitochondrial transmembrane potential was significantly decreased(P0.01),expression of Cytc in cytolymph was increased,and the activity of Caspase-9,3 were increased(P0.01)in 2,3,and 4 mmol·L-1 MnCl2 group.The apoptosis mediated by mitochondria pathway was one of the reproductive toxic mechanisms caused by manganese.
To explore the roles of mitochondria complex and oxidative stress in the apoptosis of chicken embryonic neurons exposed to MnCl2,the content of ROS and GSH,the activity of mitochondria respiratory chain complex and apoptosis index in neurons cultivated in DMEM with the final concentration of MnCl2 (0,1.5,2.0,2.5mmol/L) for 24h were detected by using the kits.In result,with the increase of the concentration of MnCl2,the activities of mitochondria respiratory chain complexes Ⅰ,Ⅱ,Ⅲ and Ⅳ and the content of GSH decreased.But in 1.5mmol/L MnCl2 environment,the activity of mitochondria respiratory chain complexⅤ decreased,the content of ROS and the apoptosis index increased,and morphological changes of apoptosis were observed in the neurons.These results indicated that MnCl2 could induce the apoptosis of the chicken embryonic neurons which was performed through oxidative stress caused by decreasing the activities of mitochondria respiratory chain complexes.