宠物抗病育种

宠物的抗病育种研究具有重要的意义,本文对开展抗病育种的必要性、宠物免疫抗病系统、疾病抗性遗传机制、免疫反应的遗传控制、宠物抗病常规育种、宠物抗病分子育种以及抗病育种方法的现状、存在的问题、展望进行了介绍。说明了对疾病抗性的选择有一个坚实基础。抗病育种是控制疾病的有效方法,应用前景美好。     

Tyrosinase family proteins are antigens specific to Vogt-Koyanagi-Harada disease

Vogt-Koyanagi-Harada (VKH) disease (and sympathetic ophthalmia) is an ocular inflammatory disease that is considered to be a cell-mediated autoimmune disease against melanocytes. The purpose of this study was to determine the Ags specific to VKH disease and to develop an animal model of VKH disease. We found that exposure of lymphocytes from patients with VKH disease to peptides (30-mer) derived from the tyrosinase family proteins led to significant proliferation of the lymphocytes. Immunization of these peptides into pigmented rats induced ocular and extraocular changes that highly resembled human VKH disease, and we suggest that an experimental VKH disease was induced in these rats. We conclude that VKH disease is an autoimmune disease against the tyrosinase family proteins.     

A stochastic compartment model representation of chronic disease dependence: Techniques for evaluating parameters of partially unobserved age inhomogeneous stochastic processes

Human disease states are commonly viewed in one of two ways. First, there is the clinical definition of disease as the presence or absence of a pathological condition. Second, there is the biologist's representation of disease as a point in a multivariate space of continuous physiological variables associated with suboptimal performance and survival. We present a model to represent dependency between multiple disease processes. The model is consistent with both concepts of disease and is designed to be estimated in the usual context of chronic disease information, i.e., a general lack of information about the time of disease incidence and progression. Consideration is made of the effects of individuals' differential susceptibility to disease and how these effects distinguish the disease incidence functions estimated at the individual level from those estimated for a population.     

Spatial correlated incidence modeling with zero inflation

Disease mapping models have been popularly used to model disease incidence with spatial correlation. In disease mapping models, zero inflation is an important issue, which often occurs in disease incidence datasets with high proportions of zero disease count. It is originated from limited survey coverage or unadvanced testing equipment, which makes some regions have no observed patients. Then excessive zeros recorded in the disease incidence dataset would mess up the true distributions of disease incidence and lead to inaccurate estimates. To address this issue, a zero-inflated disease mapping model is developed in this work. In this model, a zero-inflated process using Bernoulli indicators is assumed to characterize whether the zero inflation occurs for each region. For regions without zero inflation, a coherent and generative disease mapping model is applied for mapping the spatially correlated disease incidence. Independent spatial random effects are incorporated in both processes to account for the spatial patterns of zero inflation and disease incidence. External covariates are also considered in both processes to better explain the disease count data. To estimate the model, a Markov chain Monte Carlo algorithm is proposed. We evaluate model performance via a variety of simulation experiments. Finally, a Lyme disease dataset of Virginia is analyzed to illustrate the application of the proposed model.     

Measures of association between disease and genotype.

This paper is concerned with the statistical aspects of the phenomenon of disease occurring more frequently in individuals with some genotypes than in individuals with others. A correlation coefficient is defined to quantify association between disease and genotype. A distinction is made between the concepts of independence of allele and disease and independence of genotype and disease. This distinction is used to define two components of association which describe separate aspects of association of disease with genotype. One component is a measure of the association of disease with allele; the other a measure of the effect of allele interaction on association of disease and genotype. One aspect of the usefulness of the partition into components which is discussed is in expressing the recurrence risk of disease for a relative of an affected individual. A chi-squared analysis is provided to test hypotheses about the components of association and other hypotheses of genetic interest. This analysis is illustrated using a study done to determine the effect of the sex-linked dwarfing gene in male chickens on resistance to E. coli infection. This analysis shows a significant allele interaction effect on resistance to disease but no association of disease with alleles. In conclusion, some extensions and limitations of the proposed concepts and procedures are discussed.     

Spread of disease with transport-related infection and entry screening

An SIQS model is proposed to study the effect of transport-related infection and entry screening. If the basic reproduction number is below unity, the disease free equilibrium is locally asymptotically stable. There exists an endemic equilibrium which is locally asymptotically stable if the reproduction number is larger than unity. It is shown that the disease is endemic in the sense of permanence if and only if the endemic equilibrium exists. Entry screening is shown to be helpful for disease eradication since it can always have the possibility to eradicate the disease led by transport-related infection and furthermore have the possibility to eradicate disease even when the disease is endemic in both isolated cities.     

The affected sib method. III. Selection and recombination.

The affected sib-pair method has been used to investigate the mode of inheritance, and to estimate the "disease" allele frequency, for a number of HLA-associated diseases. One of the assumptions of the original sib-pair method is that the disease confers no selective disadvantage on affected individuals. This is obviously not the situation for most diseases. We have determined the expected HLA haplotype-sharing distribution among affected sib-pairs when selection against individuals with the disease is taken into account. We have shown that if the mode of inheritance of the selectively disadvantageous disease is recessive or additive, the original affected sib-pair analysis, ignoring selection, still estimates the true mode of inheritance, but usually yields an underestimate of the "disease" allele frequency. For intermediate and dominant models of disease predisposition, both the estimates of the degree of penetrance of the "disease" genotypes, and the "disease" allele frequency, are altered if selection is ignored in the analysis. Similarly, allowing for recombination between the "disease" locus and the HLA region does not affect the determination of the mode of inheritance of the disease if it is recessive or additive; in other cases, however, the estimate of the mode of inheritance is affected. The "disease" allele frequency is overestimated when nonzero recombination is ignored for all the modes of inheritance that have been studied.     

Gaucher disease and brucella: just a mere coincidence?

Gaucher disease type I and brucellosis are chronic diseases with similar symptoms and physical signs though the former is the most common lysosomal storage disease and the latter is an infectious disease. The similarities between these diseases make differential diagnosis difficult. Immunodeficiency is a feature of Gaucher disease type I and increases the susceptibility towards infections. A Gaucher disease type I patient with brucellosis is presented with improvement after treatment of brucellosis.     

Epidemiological models with prevalence dependent endogenous self-protection measure

A simple mathematical model for human disease epidemics that takes the human learning behaviour and self-protective measures into account is proposed and investigated. We have analysed the effect of endogenous self-protective measures with respect to the prevalence level of the disease and conversely. In the model it is assumed that people start reacting against contracting a disease with self-protective measures whenever they are informed about the disease and when the burden of the disease is in a recognizable stage. It is shown that increasing the average effectiveness of self-protective measures is more important in decreasing the prevalence of a disease than increasing the proportion of individuals in a population into which awareness is created.     

The Study of Golgi Apparatus in Alzheimer’s Disease

Alzheimer’s disease is an irreversible, progressive neurodegenerative disorder leading invariably to death, usually within 7–10 years after diagnosis and is the leading cause of dementia in the elderly. Not only is Alzheimer’s disease a tragic disease in which people suffer from neurodegeneration in the years to come, it also becomes an incredible burden on the public health system. However, there is currently no effective treatment to halt the progression or prevent the onset of Alzheimer’s disease. This is partly due to the fact that the complex pathophysiology of Alzheimer’s disease is not yet completely understood. Recently, Golgi apparatus is found to play an important role in Alzheimer’s disease. In this review, we discuss the changes of Golgi apparatus during clinical progression and pathological development of Alzheimer’s disease. First, changes of Golgi apparatus size in Alzheimer’s disease are summarized. We then address the role of Golgi apparatus in the neuropathology of Alzheimer’s disease. Finally, the role of Golgi apparatus in the pathogenesis of Alzheimer’s disease is discussed. Understanding the contribution of Golgi apparatus dysfunction to Alzheimer’s disease and its pathophysiological basis will significantly impact our ability to develop more effective therapies for Alzheimer’s disease.     

多囊肾病动物模型的研究进展

多囊肾病(Polycystic kidney disease,PKD)是以肾脏充满多个液性囊泡,细胞增殖异常,间质炎细胞浸润及细胞外基质重塑等病理特点为主的遗传性疾病。主要分为常染色体显性多囊肾病(Autosomal dominant polycystic kidney disease,ADPKD)及常染色体隐性多囊肾病(Autosomal recessive polycystic kidney disease,ARPKD)。ADPKD更为常见,发病率约为1:500-1000,约50%的患者到60岁会发展为终末期肾脏病。ARPKD较少见,发病率约为1:20000-1:40000,患者多在婴幼儿时期死亡。目前,一旦多囊肾发展为终末期肾脏病,除了肾脏移植和透析外没有更有效的治疗方法,因此,早期的诊治对延缓多囊肾进展及防止其发展为终末期肾脏病是至关重要的。多囊肾动物模型的建立在研究多囊肾疾病具体发病机制及新药研发中具有重要意义。本文介绍了PKD疾病动物模型的研究进展,包括经典PKD自发模型、化学诱导模型及基因修饰模型。     

An epidemiological model for the dynamics of Chagas' disease.

A model for the transmission dynamics of Chagas' disease is presented. The structure of the model is similar to that of the Ross-Macdonald model for malaria but includes an extra infectious compartment (chronically ill individuals) which is characteristic of Chagas' disease. In Chagas' disease there are two-main forms of transmission, by blood transfusion and by vector biting. The former is more common in urban environments and the latter is characteristic of rural settings. The characteristic long chronic (frequently asymptomatic) stage of Chagas' disease is potentially a risk factor that could enhance disease transmission by blood transfusion. The model evaluates the relative importance of both transmission modes in populations of constant size. The main results indicate that there is a strong tendency of the disease to reach an asymptotically stable endemic equilibrium point. Also, the magnitude of the basic reproductive number is very sensitive to the length of the chronic stage of the disease and hence it follows that early detection of cases (reducing the length of this stage) is important for the eventual eradication of the disease.     

我国蜜蜂主要病原检测技术

蜜蜂是重要的经济昆虫。蜜蜂病害威胁蜜蜂产业的发展。蜜蜂病害检测及病原鉴定是病害防治的基础。文章详细介绍我国蜜蜂常见6种主要病害(美洲幼虫腐臭病,欧洲幼虫腐臭病,囊状幼虫病,慢性麻痹病,微孢子虫病,白垩病)的病原快速准确的检测方法。     

Dynamics of an SIQS epidemic model with transport-related infection and exit-entry screenings

Population dispersal, as a common phenomenon in human society, may cause the spreading of many diseases such as influenza, SARS, etc. which are easily transmitted from one region to other regions. Exit and entry screenings at the border are considered as effective ways for controlling the spread of disease. In this paper, the dynamics of an SIQS model are analyzed and the combined effects of transport-related infection enhancing and exit-entry screenings suppressing on disease spread are discussed. The basic reproduction number is computed and proved to be a threshold for disease control. If it is not greater than the unity, the disease free equilibrium is globally asymptotically stable. And there exists an endemic equilibrium which is locally asymptotically stable if the reproduction number is greater than unity. It is shown that the disease is endemic in the sense of permanence if and only if the endemic equilibrium exists. Exit screening and entry screening are shown to be helpful for disease eradication since they can always have the possibility to eradicate the disease endemic led by transport-related infection and furthermore have the possibility to eradicate disease even when the isolated cites are disease endemic.     

Nonparametric methods for survival/sacrifice experiments

In many carcinogenicity studies, the time to disease occurrence is not clinically observable; a survival/sacrifice experiment is considered for nonparametric inference about the rate of disease occurrence. A multistate model for disease development and death is considered and an algorithm of the EM type for maximum likelihood estimation is obtained. Questions of identifiability and estimability are addressed. Under the model, interval hazards for disease occurrence are identifiable for intervals defined by the sacrifice times. A score test is developed appropriate for the comparison of two groups with respect to disease development without need of any assumption concerning lethality of the disease concerned.     

Pregnancy and inflammatory bowel disease.

Conclusions about the relationship between the pathophysiology and treatment of inflammatory bowel disease and the physiology and management of pregnancy are based on the results of several large physician surveys and retrospective chart reviews. Patients with active disease fare worse than those with inactive disease. There is little evidence that pregnancy affects the course of inflammatory bowel disease or that inactive inflammatory bowel disease affects the course of pregnancy. Judicious medical therapy is effective in controlling inflammatory bowel disease during pregnancy. Sulfasalazine or steroid therapy should not be withdrawn in a patient who needs it to achieve or maintain a quiescent state of inflammatory bowel disease during the course of pregnancy. Immunosuppressive therapy should be avoided. Aggressive medical therapy with total parenteral nutrition in a team approach with a gastroenterologist, surgeon, and perinatologist usually avoids the need for surgical intervention during pregnancy with a good fetal outcome in a patient whose disease is active. Contraception against pregnancy need only be considered in those patients whose disease is so severe that operative therapy is imminent.     

Immunology and immunotherapy of Alzheimer's disease

Although Alzheimer's disease is considered to be a degenerative brain disease, it is clear that the immune system has an important role in the disease process. As discussed in this Review, immune-based therapies that are designed to remove amyloid-beta peptide from the brain have produced positive results in animal models of the disease and are being tested in humans with Alzheimer's disease. Although immunotherapy holds great promise for the treatment of Alzheimer's disease, clinical trials of active amyloid-beta vaccination of patients with Alzheimer's disease were discontinued after some patients developed meningoencephalitis. New immunotherapies using humoral and cell-based approaches are currently being investigated for the treatment and prevention of Alzheimer's disease.     

The incidence and distribution of some diseases of the adult honeybee (Apis mellifera L.) in England and Wales

Although epidemics of bee disease have been repoited in Europe for hundreds of years it was not until recent times that detailed notes on the incidence and distribution of one of these epidemics, the so-called 'Isle of Wight disease' epidemic, were made.
Since 1918 four complaints of the adult honeybee, acarine disease, Nosema disease, Amoeba disease and bee paralysis, have been recognized in this country.
Surveys in England and Wales to determine the incidence and distribution of acarine disease, Nosema disease and Amoeba disease were carried out during the winters of 1941-2 and 1943-4. These surveys showed that none of these diseases is clearly confined to any definite areas of England and Wales. Acarine disease is, however, apparently more abundant in the west and south-west; and Nosema disease appears to be most prevalent in Buckinghamshire, Hertfordshire, Middlesex and Surrey, and also has other areas of heavy infection in Leicestershire and Cumberland, Lancashire and Yorkshire.
Sufficient cases of Amoeba disease have not yet been recorded for it to be possible to conclude that any one area is more heavily infected than another. It is estimated that approximately one out of every five or six of the colonies of bees in England and Wales is suffering from acarine disease. Less than 1% are likely to be suffering from Nosema or Amoeba disease. Bee paralysis is both common and widespread, but probably does little serious harm.