The anemia of chronic renal failure revisited

The mechanisms of the anemia of chronic renal failure are reviewed. Ineffective erythropoiesis is undoubtedly the major cause of this anemia. The contributions of inadequate erythropoietin secretion by the diseased kidneys, suppressive effects of uremic "toxins" on erythropoiesis and red cell survival, excess blood loss, and plasma concentrations of parathyroid hormone, calcium and phosphate are discussed.     

Inherited erythrocyte pyruvate kinase deficiency in a beagle dog

A 1-year-old, female Beagle dog with minimal exercise intolerance was found to have a persistent, severe, and highly regenerative anemia, splenomegaly, and progressive osteosclerosis. Despite near-normal in vitro erythrocyte pyruvate kinase (PK) activity, the authors diagnosed PK deficiency by demonstrating a glycolytic block at the PK step, the lack of normal R-type PK isoenzyme, and the presence of M(2)-type PK in the animal's erythrocytes. The dam had half-normal erythrocyte PK activity, which supports an autosomal recessive mode of inheritance. We conclude from our studies that close similarities exist between erythrocyte PK deficiency in Beagle, Basenji, and West Highland White Terrier dogs and that this form of PK deficiency may be more widespread than previously thought.     

Idiopathic dyserythropoiesis in a dog

Idiopathic dyserythropoiesis in a dog was characterized by chronic nonregenerative normocytic normochromic anemia, cellular marrow and abnormal morphology of erythroid precursors. Serum concentrations of Vitamin B(12), folate and iron were inconsistent with secondary causes of dyserythropoiesis. The disorder appeared to be distinct from myelodysplastic syndromes described previously.     

In vitro Inhibition of Canine Complement‐Mediated Hemolysis

Background

Immune‐mediated hemolytic anemia (IMHA) is the most common hematologic immune‐mediated disease in dogs. Complement fixation on erythrocytes causes hemolysis. Complement inhibition decreases hemolysis in people with the hemolytic disease and also may prove effective in treating IMHA in dogs.

Hypothesis/Objectives

Evaluate the in vitro efficacy of 2 complement inhibitors used in humans against canine complement.

Methods

The inhibitory activity of the C3‐inhibitor compstatin and recombinant human C1‐esterase inhibitor (C1‐INH) was evaluated using an in vitro hemolytic assay and spectrophotometric measurement of released hemoglobin. Dose‐response curves for each inhibitor were generated.

Results

Compstatin decreased approximately 50% of canine complement‐mediated hemolysis in initial experiments. This inhibition largely was lost when a new lot of drug was purchased. C1‐INH showed a dose‐dependent inhibition. The highest concentration of C1‐INH tested (500 μg/mL) decreased >80% of canine complement‐mediated hemolysis, and the lowest concentration tested (31.25 μg/mL) decreased hemolysis >60%.

Conclusions and Clinical Importance

Human C1‐INH is a robust inhibitor of canine complement‐mediated hemolysis, whereas compstatin was minimally and variably effective. Human C1‐INH may substantially decrease complement‐mediated hemolysis in dogs with IMHA and warrants further investigation.     

绿色荧光示踪马传染性贫血病毒样颗粒在活细胞中的组装过程

马传染性贫血病毒(EIAV)gag基因编码的多聚Gag蛋白能够自动组装形成病毒样颗粒(VLPs)。为研究EIAV衣壳蛋白合成、组装及释放过程,本实验通过构建表达EIAV Gag-GFP融合蛋白重组质粒,并将其转染293T细胞,采用western blot检测不同时间点VLPs的产生及释放。并进一步通过活细胞和3D成像技术观察Gag-GFP在细胞中的表达动态及VLPs的组装过程。结果表明:Gag和GFP蛋白融合表达不影响VLPs的组装,转染约6 h后EIAV Gag蛋白进行合成并在细胞胞质聚集完成组装形成VLPs。该实验结果为进一步研究EIAV在细胞中的组装路线和机制奠定了重要基础。     

一例犬吉氏巴贝斯虫感染引起的免疫介导溶血性贫血的诊治

犬免疫介导溶血性贫血是一种与自身红细胞抗体有关的溶血性贫血,发病原因可分为原发性和继发性,论文主要介绍了一例由吉氏巴贝斯虫感染后继发的犬自身免疫溶血性贫血的诊断、治疗和预后。     

A retrospective study of aplastic pancytopenia in the dog: 9 cases (1996-2003)

BACKGROUND: Aplastic pancytopenia is defined by the presence of pancytopenia in blood and a hypocellular bone marrow with the hematopoietic space replaced by adipose tissue. Several causes of acquired aplastic pancytopenia are known; however, in some cases, an underlying cause is never determined. OBJECTIVE: The objective of this retrospective study was to identify the incidence, potential causes, and outcome of aplastic pancytopenia in dogs. METHODS: Bone marrow cytologic and core biopsy reports were reviewed to identify dogs diagnosed with aplastic pancytopenia between July 1, 1996 and June 30, 2003. Four-hundred eighty-six bone marrow reports that included aspirate and core biopsy evaluations were reviewed. Signalment, treatment given, previous and current disease conditions, clinical signs of disease, clinical laboratory data, therapy, response to therapy, and survival time were recorded. RESULTS: Nine dogs (1.85% of bone marrow samples reviewed) met the criteria for inclusion. Two dogs (22%) had associated diseases that included monocytic ehrlichiosis and Sertoli cell tumor. In 7 dogs (78%), the cause of aplastic pancytopenia could not be definitively determined, although an idiosyncratic drug reaction to griseofulvin was suspected in 1 of the dogs. The median age of dogs diagnosed with aplastic pancytopenia was 3.2 years, and apparent breed or sex predilection was not identified. Median HCT, total WBC count, and platelet count on the day of presentation were 21.8%, 1.0 x 10(3)/microL, and 2.0 x 10(3)/microL, respectively. Six of 9 dogs diagnosed with aplastic pancytopenia died or were euthanized within 21 days. Two dogs had complete hematologic recovery. One dog was living 3 years after diagnosis, but hematologic recovery was never documented. CONCLUSIONS: Aplastic pancytopenia is diagnosed infrequently and idiopathic aplastic pancytopenia may account for up to 67% or more of canine cases. Although the prognosis is guarded, some dogs with aplastic pancytopenia recover.     

Development and characterization of a potential diagnostic monoclonal antibody against capsid protein VP1 of the chicken anemia virus

Chicken anemia virus (CAV) is an important viral pathogen that causes anemia and severe immunodeficiency syndrome in chickens worldwide. In this study, a potential diagnostic monoclonal antibody against the CAV VP1 protein was developed which can precisely recognize the CAV antigen for diagnostic and virus recovery purposes. The VP1 gene of CAV encoding the N-terminus-deleted VP1 protein, VP1Nd129, was cloned into an Escherichia (E.) coli expression vector. After isopropyl-β-D-thiogalactopyronoside induction, VP1Nd129 protein was shown to be successfully expressed in the E. coli. By performing an enzyme-linked immunoabsorbent assay using two coating antigens, purified VP1Nd129 and CAV-infected liver tissue lysate, E3 monoclonal antibody (mAb) was found to have higher reactivity against VP1 protein than the other positive clones according to the result of limiting dilution method from 64 clones. Using immunohistochemistry, the presence of the VP1-specific mAb, E3, was confirmed using CAV-infected liver and thymus tissues as positive-infected samples. Additionally, CAV particle purification was also performed using an immunoaffinity column containing E3 mAb. The monoclonal E3 mAb developed in this study will not only be very useful for detecting CAV infection and performing histopathology studies of infected chickens, but may also be used to purify CAV particles in the future.     

藏系绵羊钼诱导铜缺乏的研究

自2000年以来,青海省乌兰地区藏绵羊出现以异食、消瘦和贫血为特征的疾病。经分析该地区土壤、牧草和动物的矿物质元素含量,发现在患病区,土壤钼含量为（4.63±1.51）μg/g,牧草为（4.89±1.79）μg/g,极显著高于正常地区。患病动物血液平均铜含量为（0.23±0.07）μg/g,被毛铜平均含量为（3.27±0.71）μg/g,而正常区的动物为（0.97±0.23）μg/g和（6.78±1.57）μg/g,差异极显著;患病动物血液铜最高值为0.53μg/g,血液铜最低值为0.031μg/g。而正常地区藏绵羊血液铜含量最高值为1.33μg/g,血液铜最低值为0.83μg/g。同时患病动物血清铜蓝蛋白显著低于正常动物,并且有小红细胞贫血。结果表明,藏绵羊以异食、消瘦和贫血为特征的营养代谢疾病为钼诱导的次级铜缺乏。