Calcification of the iliac arteries: a marker for leakage risk in rectal anastomosis-a blinded clinical trial.

PURPOSE: Anastomotic leakage (AL) is associated with increased morbidity and mortality after colorectal surgery. Calcification of the arteries has been identified as a risk factor for cardiovascular events and can be reliably measured on computed tomography using software assistance. The aim of this prospective study was to prove the value of calcium scoring of the iliac arteries as a predictor of AL after rectal anastomosis. METHODS: Consecutive patients who underwent colorectal resection with rectal anastomosis were analyzed. Diagnostic computed tomography images were used to detect calcification of the arteries supplying the rectal anastomosis. Logistic regression analysis was used to determine the relationship between vascular calcification and AL. RESULTS: Of 139 included and analyzed patients, AL occurred in 15 (11%). The volume and calcium scores were significantly higher in the infrarenal aorta, the left and right common iliac artery, and the left internal iliac artery. In univariate analysis, calcification of the left internal iliac artery and both internal iliac arteries combined correlated with the occurrence of the primary endpoint. A receiver operating curve analysis led to the cut-off values of 30 and 6 for the volume score and calcium score, respectively. They provide a negative predictive value of 0.97 and a positive predictive value of 0.19. CONCLUSIONS: Calcification in the iliac arteries appears to be a good marker for the risk of leakage after rectal anastomosis. The calcification scoring system is easy to calculate after computed tomography and may aid in patient selection to create a protective ileostomy.

HspB5/αB-crystallin increases dendritic complexity and protects the dendritic arbor during heat shock in cultured rat hippocampal neurons.

The small heat shock protein ΗspΒ5 (αB-crystallin) exhibits generally cytoprotective functions and possesses powerful neuroprotective capacity in the brain. However, little is known about the mode of action of ΗspΒ5 or other members of the HspB family particularly in neurons. To get clues of the neuronal function of HspBs, we overexpressed several HspBs in cultured rat hippocampal neurons and investigated their effect on neuronal morphology and stress resistance. Whereas axon length and synapse density were not affected by any HspB, dendritic complexity was enhanced by HspB5 and, to a lesser extent, by HspB6. Furthermore, we could show that this process was dependent on phosphorylation, since a non-phosphorylatable mutant of HspB5 did not show this effect. Rarefaction of the dendritic arbor is one hallmark of several neurodegenerative diseases. To investigate if HspB5, which is upregulated at pathophysiological conditions, might be able to protect dendrites during such situations, we exposed HspB5 overexpressing neuronal cultures to heat shock. HspB5 prevented heat shock-induced rarefaction of dendrites. In conclusion, we identified regulation of dendritic complexity as a new function of HspB5 in hippocampal neurons.