Haemophilus aphrophilus bleb infection after a mitomycin trabeculectomy

Background: Haemophilus aphrophilus is a rare cause of ocular infection. It has been reported once as a cause of late-onset endophthalmitis in a patient with an inadvertent bleb after cataract surgery. We present a case of Haemophilus aphrophilus bleb infection after a mitomycin trabeculectomy.
Methods: A 56-year-old woman presented with a bleb infection 10 weeks after a mitomycin C augmented trabeculectomy at a University tertiary referral practice of one of the authors (GET). The causative organism was Haemophilus aphrophilus , identified by the Toronto Public Health Laboratory, Ontario, Canada.
Results: The bleb infection resolved following topical, subconjunctival and intravenous antibiotic therapy. A formal bleb revision was required to repair a persistent bleb leak.
Conclusion: Patients who have had trabeculectomies augmented with mitomycin C may be predisposed to bleb infection with unusual organisms. Prompt diagnosis and treatment is necessary to control the infection. Increased awareness and communication with laboratory personnel may increase the isolation of this fastidious organism.     

运动对铁吸收的影响及其作用途径

目的:综合分析运动对铁吸收的影响及其作用途径。资料来源:检索Pubmed1950-01/2006-04有关运动对铁吸收的影响及其作用途径的文献,检索词为“iron absorption,iron metabolism,exercise”。同时检索万方数据库1994-01/2006-03有关运动对铁吸收的影响及其作用途径的文献,检索词为“铁吸收,铁代谢,运动”。资料选择:初选后,有关铁吸收、运动对铁吸收影响及其调节机制的文献被选中。发表于2002年后的文献被优先选择,排除重复实验和Meta分析。资料提炼:检索到9000篇文献,大部分是关于铁吸收调节机制的文献,其中40篇有关运动和铁吸收及其调节机制,30篇作为代表性研究文献被引用。资料综合:运动可导致低铁状态,影响运动能力,这种低铁状态的形成及其调节与铁吸收相关。但是,对于运动如何影响铁吸收存在两种截然相反的观点,一种观点认为运动促进铁吸收;另一种观点认为运动降低铁吸收。最近的研究已经显示运动可能通过机体铁水平、一氧化氮、Hepcidin、促红细胞生成素、低氧以及基因突变(如HFE突变)调节铁吸收。结论:有关运动影响铁吸收的研究仍是初步的,在运动情况下如何调节铁吸收尚有待研究,这对于进一步分析运动诱导的低铁状态的本质以及运动员和运动健身人群是否需要以及如何补充铁具有重要意义。     

X型胶原蛋白与骨骼生长发育关系的研究进展

X型胶原是近年来发现的一种新型胶原,它只存在于生长发育期的即将骨化的软骨内,以液态均相的形式分布于细胞外基质,并启动软骨骨化。它具有特异性合成、局限性分布、一过性存在的特征。许多骨骼系统疾病与X型胶原的异常有着密切的关系。     

Apoptosis in peripheral lymphocytes in systemic lupus erythematosus: a review

There is increasing evidence to suggest that abnormalities in apoptosis may play a part in the pathogenesis of systemic lupus erythematosus (SLE). For example, there is now considerable evidence that bel-2 expression is enhanced in a proportion of peripheral T cells, but not in B cells, in SLE patients and correlates with overall disease activity regardless of the activity index employed. Further work is required to establish whether enhanced bel-2 expression by some T cells in SLE patients is related to their activation or intrinsically enhanced by genetic predisposition. Mutations in Fas result in a lymphoproliferative syndrome and may play a role in accelerating autoimmune disease. A report of three children with mutations in Fas has once again focused attention on this regulator of apoptosis. The relationships between inducers and inhibitors of apoptosis may differ in different cell types, and must be elucidated before the implications of observations made in lymphocytes from SLE patients can be fully understood.