The incidence of infectious maxillary sinusitis (IMS) and its clinical relevance was prospectively studied in 162 consecutive critically ill patients who were mechanically ventilated for a period longer than 7 d. All had a paranasal computed tomographic (CT) scan within 48 h of admission and were divided into three groups according to the radiologic aspect of their maxillary sinuses: Group 1 = normal maxillary sinuses (n = 40), Group 2 = maxillary mucosal thickening (n = 26), Group 3 = radiologic maxillary sinusitis (RMS) defined as the presence of an air fluid level and/or opacification of maxillary sinuses (n = 96). Group 1 patients were randomized between nasal and oral endotracheal intubation with a gastric intubation performed via the same route and had a second paranasal CT scan 7 d later. Endotracheal and gastric tubes were left in their original position in Group 2 patients and a second paranasal CT scan was performed 7 d later. All patients of Group 3 underwent a transnasal puncture for bacteriologic analysis of maxillary sinus content. Forty-five spontaneously breathing patients served as a control group. In all patients with RMS, the occurrence of bronchopneumonia (BPN) was prospectively assessed for 7 d following the initial CT scan. Upon inclusion, only 25% of the patients had normal maxillary sinuses whereas all patients in the control group had normal paranasal CT scans. After 7 d, 46% of Group 2 patients had evidence of RMS. Risk factors for RMS were nasal placement and duration of endotracheal and gastric intubation.(ABSTRACT TRUNCATED AT 250 WORDS)
In the removal of tumours that develop within the third ventricle, most approaches are not entirely satisfactory. Therefore, a new approach has been devised: transfrontal exposure of the anterior portion of the frontal horn; coagulation and section of the striothalamic vein in order to open up the roof of the third ventricle; use of a blunt spatula introduced in the foramen of Monro and pushed backwards under the choroïd plexus. This approach has been used in ten cases. Postoperative mortality has been nil; the surgical approach has not apparently been responsible for any sequelae. It is simple and gives a good view of the third ventricle.
Organismal aging entails a gradual decline of normal physiological functions and a major contributor to this decline is withdrawal of the cell cycle, known as senescence. Senescence can result from telomere diminution leading to a finite number of population doublings, known as replicative senescence (RS), or from oncogene overexpression, as a protective mechanism against cancer. Senescence is associated with large-scale chromatin re-organization and changes in gene expression. Replication stress is a complex phenomenon, defined as the slowing or stalling of replication fork progression and/or DNA synthesis, which has serious implications for genome stability, and consequently in human diseases. Aberrant replication fork structures activate the replication stress response leading to the activation of dormant origins, which is thought to be a safeguard mechanism to complete DNA replication on time. However, the relationship between replicative stress and the changes in the spatiotemporal program of DNA replication in senescence progression remains unclear. Here, we studied the DNA replication program during senescence progression in proliferative and pre-senescent cells from donors of various ages by single DNA fiber combing of replicated DNA, origin mapping by sequencing short nascent strands and genome-wide profiling of replication timing (TRT). We demonstrate that, progression into RS leads to reduced replication fork rates and activation of dormant origins, which are the hallmarks of replication stress. However, with the exception of a delay in RT of the CREB5 gene in all pre-senescent cells, RT was globally unaffected by replication stress during entry into either oncogene-induced or RS. Consequently, we conclude that RT alterations associated with physiological and accelerated aging, do not result from senescence progression. Our results clarify the interplay between senescence, aging and replication programs and demonstrate that RT is largely resistant to replication stress.
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