We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Find out more about the Kindle Personal Document Service.
Background: Late-life depression has been associated with vascular diseases and with increases in circulating cytokines and cell adhesion molecules in the prefrontal cortex. We hypothesized that soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) would be increased in late-life major depression.
Methods: Serum levels of sICAM-1 and sVCAM-1 were measured in subjects over 60 with major depression (N = 23), subsyndromal depression (N = 20) and controls (N = 25). Depression severity was assessed using the Montgomery-Åsberg (MDRS) and Geriatric Depression (GDS) rating scales.
Results: There was no significant increase in sICAM-1 (p = 0.240) or sVCAM-1 (p = 0.600) in depression nor was there any correlation of either molecule with depression severity. Adjusting for differences in cognitive impairment did not alter these findings. There was also no difference between subjects with an early onset of depression (before 60) and those with late-onset depression.
Conclusions: These findings do not provide evidence that previously reported increases in serum cytokines in depression are due to peripheral vascular disease. Although we assessed subjects for vascular diseases it is possible that subtle but important differences between groups may still have been present and may have contributed to our negative findings.
Our results suggest central nervous system mechanisms, such as related to HPA axis activation, may be responsible for the enhanced inflammatory response in depression.
Neuroimaging studies have demonstrated changes in the dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex (ACC) in major depression.
We investigated the expression of cell adhesion molecules (CAMs) in the prefrontal cortex in depression.
Immunohistochemistry to localise CAMs in post-mortem tissue from 20 subjects with major depression and 20 controls, and image analysis to quantify their expression.
We found significant increases in CAMs in the grey matter ofthe DLPFC in the depression group but no comparable differences in the ACC or occipital cortex. In the white matter there was a non-significant increase in intercellular adhesion molecule-1 in the DLPFC in the depression group but no increase in the other areas or for vascular cell adhesion molecule-1 in any area. Paired tests showed specificity for the DLPFC in the depression group only.
Theincreasein CAM expression in the DLPFC suggests an inflammatory reaction and is consistent with ischaemia.
To investigate and control a nosocomial outbreak of Burkholderia cepacia lower respiratory tract infection.
Outbreak investigation and case-control study.
A 260-bed community hospital.
Participants were mechanically ventilated intensive care patients without cystic fibrosis. A case was defined as a hospitalized patient with a sputum culture positive for B cepacia between January 1 and November 6, 1998.
Respiratory therapy infection control policies and practices were reviewed; laboratory and environmental studies and a retrospective case-control study were conducted. Case-patients were matched with control-patients on age, gender, diagnosis, and type of intensive care unit.
Nine case-patients were identified; B cepacia likely caused pneumonia in seven and colonization in two. Two respiratory therapy practices probably contributed to the transmission of B cepacia: multidose albuterol vials were used among several patients, and nebulizer assemblies often were not dried between uses. B cepacia was grown from cultures of three previously opened multidose vials; pulsed-field gel electrophoresis patterns of B cepacia from seven case-patients and two multidose vials were indistinguishable. Case-patients had longer durations of heated humidified mechanical ventilation (mean, 9.8 days vs 4.4 days; P=.03) and were more likely to have exposure to one particular respiratory therapist than controls (odds ratio, undefined; 95% confidence interval, 4.7-∞ P=.001). The association with the respiratory therapist, a temporary employee, persisted after controlling for duration of heated humidified ventilation. No new B cepacia infections were identified after control measures were implemented.
B cepacia probably was transmitted among patients through use of extrinsically contaminated multidose albuterol vials. Respiratory therapy departments must pay close attention to infection control practices, particularly among new or temporary staff.
Email your librarian or administrator to recommend adding this to your organisation's collection.