鸡败血支原体pMGA多基因家族及其免疫逸机制的研究进展

pMGA多基因家族主要编码一类黏附素／血凝素蛋白，存在于鸡败血支原体的细胞表面，其主要功能是促进支原体黏附到宿主细胞上。近年来的相关研究发现，编码pMGA的基因数量从32－70不等，主要转录水平上通过（GAA）n 基序的数量改变引发pMGA基因的选择性转录，造成pMGA的抗原发生变异，从而干扰宿主正常免疫功能的发挥，使支原体对宿主产生严重的免疫逃逸。其中，（GAA）n基序已被证实在pMGA基因表达调控中起重要作用，这一三联体重复基序数目的多少直接影响到pMGA基因的ON／OFF不，本文通过对鸡败血支原体pMGA多基因家分子生物学研究进展浅要综述，以提出pMGA基因可能的转录调控机制，这对研究鸡败血支原体的分子致病机理及其免疫机制大有裨益。     

Responses to submaximal treadmill exercise and training in the horse: changes in haematology, arterial blood gas and acid base measurements, plasma biochemical values and heart rate

Four standardbred horses with subcutaneously relocated carotid arteries were given a seven week training programme of treadmill exercise at a gradient of 19 per cent in order to assess if there were any effects of exercise and training on haematology, arterial blood gas and acid base measurements, plasma biochemistry and heart rate. The exercise consisted of one minute walking at 110 metres/minute followed by five minutes trotting at 200 metres/minute, twice daily in the first week. The period of trotting exercise was increased by one minute per week so that by the seventh week the horses were being given 12 minutes trotting twice daily. Before training commenced venous blood samples, for complete blood counts and plasma biochemistry, and arterial samples, for blood gas, acid base and lactate measurements, were taken at rest, after five minutes and 15 minutes of treadmill exercise (200 metres/minute) and 30 minutes and 60 minutes after completing the exercise. Heart rate was measured by telemetric electrocardiogram at similar intervals. This exercise test and blood collection were repeated after one, three, five and seven weeks of training. The only significant changes were a decrease in exercise lactate with training, increases in exercise and recovery total protein. The haematological response to treadmill exercise included an increase in certain red cell parametes and a leucocytosis which was caused by both a neutrophilia and a lymphocytosis. These effects had largely disappeared by 30 minutes after exercise and all values had returned to resting values by one hour after exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Requirement for coronin 1 in T lymphocyte trafficking and cellular homeostasis

The evolutionarily conserved actin-related protein (Arp2/3) complex is a key component of actin filament networks that is dynamically regulated by nucleation-promoting and inhibitory factors. Although much is known about actin assembly, the physiologic functions of inhibitory proteins are unclear. We generated coronin 1-/- mice and found that coronin 1 exerted an inhibitory effect on cellular steady-state F-actin formation via an Arp2/3-dependent mechanism. Whereas coronin 1 was required for chemokine-mediated migration, it was dispensable for T cell antigen receptor functions in T cells. Moreover, actin dynamics, through a mitochondrial pathway, was linked to lymphocyte homeostasis.     

Liver lobe torsion in dogs: 13 cases (1995-2004)

OBJECTIVE: To determine history, results of diagnostic testing, surgical findings, complications, and outcome for dogs with liver lobe torsion (LLT). DESIGN: Retrospective case series. ANIMALS: 12 dogs (1 with 2 episodes). PROCEDURE: Signalment, clinical signs, clinicopathologic findings, radiographic and ultrasonographic findings, surgical and histologic findings, complications, and hospitalization time were evaluated. RESULTS: The most common clinical signs were nonspecific abnormalities (eg, vomiting, lethargy, and anorexia) of acute or chronic duration. All dogs were large-breed dogs (median body weight, 37.2 kg [82 lb]). Biochemical abnormalities included high alanine amino-transferase (n = 12) and aspartate aminotransferase (11) activities. Results of abdominal ultrasonography were supportive of the diagnosis in 5 of 8 cases. Affected lobes included the left medial lobe (n = 4), left lateral lobe (3), papillary process of the caudate lobe (2), caudate lobe (1), and right lateral lobe (1). Exploratory celiotomy and liver lobectomy were performed in 12 of 13 cases, and in 11 of those 12 cases, the dog survived. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that development of nonspecific clinical signs of vomiting, lethargy, and anorexia in conjunction with high serum hepatic enzyme activities and mature neutrophilia in a medium-sized or large-breed dog should increase the index of suspicion for LLT. Abdominal ultrasonography with Doppler assessment may be useful in establishing the diagnosis. The long-term outcome for dogs that survive the hospitalization period is excellent.     

Effects of mutations in Drosophila nicotinic acetylcholine receptor subunits on sensitivity to insecticides targeting nicotinic acetylcholine receptors

Several strains of Drosophila melanogaster possess mutant alleles in nicotinic acetylcholine receptor (nAChR) subunits, Dα1 and Dβ2 that confer resistance to neonicotinoids such as imidacloprid and nitenpyram, and Dα6, that confers resistance to spinosyns. These mutant strains were bioassayed with a selected set of nAChR active insecticides including neonicotinoids, spinosad, and sulfoxaflor, a new sulfoximine insecticide. All of the neonicotinoids examined, except dinotefuran showed reduced insecticidal efficacy on larvae of the Dα1 mutant, suggesting that this subunit may be important in the action of these insecticides. All of the neonicotinoids, including dinotefuran, showed reduced insecticidal efficacy on larvae possessing the Dβ2 mutation. A similar pattern of broad neonicotinoid resistance to that of Dβ2 alone was also observed for larvae with both the mutations (Dα1 + Dβ2). The Dβ2 mutation exhibited a lower level of cross-resistance to sulfoxaflor (<3-fold) than to any of the neonicotinoids (>13-fold). In contrast, there was no cross-resistance for any of the neonicotinoids or sulfoxaflor in adult flies with the Dα6 mutation, which confers high levels of resistance to spinosad. Thus in the D. melanogaster strains studied, target site resistance observed for the neonicotinoids and the spinosyns does not translate directly to resistance towards sulfoxaflor.     

How cells know the size of their organelles

Cells have developed ways to sense and control the size of their organelles. Size-sensing mechanisms range from direct measurements provided by dedicated reporters to indirect functional readouts, and they are used to modify organelle size under both normal and stress conditions. Organelle size can also be controlled in the absence of an identifiable size sensor. Studies on flagella have dissected principles of size sensing and control, and it will be exciting to see how these principles apply to other organelles.