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George Trendelenburg

Publications and source records attributed to George Trendelenburg.

7 recordsLinked to original sources
PubMed2006

Multiple brain abscesses following surgical treatment of a perianal abscess.

We report a case of multiple brain abscesses (BAs) in a 67-year-old man with symptoms of progredient disorientation and amnestic aphasia. Onset of symptoms occurred one week after surgical treatment of a perianal abscess. No other source of infection was identified and the abscesses were limited to the brain. The immune status was normal but a patent foramen ovale (pFO) was found. The patient was treated with high-dose antibiotics, leading to a complete radiological disappearance of the BAs. Hematogenous spread of infectious emboli from a perianal focus exclusively to the brain is very rare. In our patient, the mechanisms of infectious spread into the brain might have occurred via a cardiac right-to-left shunt or alternatively via the non-valvular vertebral venous system. In this manuscript, both pathways are critically reviewed.

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PubMed2005

Neuroprotective role of astrocytes in cerebral ischemia: focus on ischemic preconditioning.

Following focal cerebral ischemia ("stroke") a complex and dynamic interaction of vascular cells, glial cells, and neurons determines the extent of the ensuing lesion. Traditionally, the focus has been on mechanisms of damage, while recently it has become clear that endogenous mechanisms of protection are equally important for the final outcome. Glial cells, in particular astrocytes, have always been viewed as supporters of neuronal function. Only recently a very active role for glial cells has been emerging in physiology and pathophysiology. Not surprisingly, then, specific protective pathways have been identified by which these cells can protect or even help to regenerate brain tissue after acute insults. However, as exemplified by the existence of the glial scar, which forms around lesioned brain tissue, is composed mainly of astrocytes and plays a key role in regeneration failure, it is an oversimplification to assign merely protective functions to astrocytes. The present review will discuss the role of astrocytes in ischemic brain injury with a focus on neuroprotection in general. In this context we will consider particularly the phenomenon of "ischemic tolerance," which is an experimental paradigm helpful in discriminating destructive from protective mechanisms after cerebral ischemia.

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PubMed2003

Improved protocol for SAGE tag-to-gene allocation.

Serial analysis of gene expression (SAGE) is a powerful method for large-scale analysis of gene expression patterns. SAGE yields digital information on transcript abundance by the use of short sequence fragments (tags). Because SAGE does not require a priori knowledge of the expressed genes in the starting material, SAGE can be used for gene discovery. Unfortunately, correct tag-to-gene discovery. Unfortunately, correct tag-to-gene allocation after SAGE remains problematic when the short sequence of the tag corresponds to more than one gene in the reference database or when novel yet uncloned genes were detected. To overcome this problem, we developed an improved protocol for the proper identification of tag-corresponding genes. It relies on the isolation of 3'-terminal cDNA restriction fragments by the use of paramagnetic streptavidin beads and the ligation of linkers before the amplification step. Our protocol benefits from additional information encoded in each SAGE tag: its location 3'-terminal to the last NlaIII restriction site in the cDNA. In contrast to previously described protocols, stringent PCR conditions can be applied because of the length of the specific primers, which are composed of linker- and tag-specific sequences. Additionally, we demonstrate that our protocol yields quantitative information that can be used for further expression analysis of specific SAGE tags.

Animals↗
PubMed2002

Serial analysis of gene expression identifies metallothionein-II as major neuroprotective gene in mouse focal cerebral ischemia.

We applied serial analysis of gene expression (SAGE) to study differentially expressed genes in mouse brain 14 hr after the induction of focal cerebral ischemia. Analysis of >60,000 transcripts revealed 83 upregulated and 94 downregulated transcripts (more than or equal to eightfold). Reproducibility was demonstrated by performing SAGE in duplicate on the same starting material. Metallothionein-II (MT-II) was the most significantly upregulated transcript in the ischemic hemisphere. MT-I and MT-II are assumed to be induced by metals, glucocorticoids, and inflammatory signals in a coordinated manner, yet their function remains elusive. Upregulation of both MT-I and MT-II was confirmed by Northern blotting. MT-I and MT-II mRNA expression increased as early as 2 hr after 2 hr of transient ischemia, with a maximum after 16 hr. Western blotting and immunohistochemistry revealed MT-I/-II upregulation in the ischemic hemisphere, whereas double labeling demonstrated the colocalization of MT with markers for astrocytes as well as for monocytes/macrophages. MT-I- and MT-II-deficient mice developed approximately threefold larger infarcts than wild-type mice and a significantly worse neurological outcome. For the first time we make available a comprehensive data set on brain ischemic gene expression and underscore the important protective role of metallothioneins in ischemic damage of the brain. Our results demonstrate the usefulness of SAGE to screen functionally relevant genes and the power of knock-out models in linking function to expression data generated by high throughput techniques.

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