HIV: Inflammatory dermatoses.

Patients living with HIV may experience a variety of inflammatory dermatoses, ranging from exacerbations of underlying conditions to those triggered by HIV infection itself. This article presents a current literature review on the etiology, diagnosis and management of atopic dermatitis, psoriasis, pityriasis rubra pilaris, lichen planus, seborrheic dermatitis, eosinophilic folliculitis, pruritic papular eruption and pruritus, in patients living with HIV.

The Effectiveness of a Self-Directed e-Learning Module on Trainee Knowledge and Confidence during Plastic Surgery Clinical Rotations.

Background: Exposure to plastic surgery is limited during medical school. This makes rotations for clinical clerks and off-service residents challenging. Available resources are often too detailed and overwhelming. Having an accessible, concise, and interactive plastic surgery e-learning module reviewing core plastic surgery topics could help prepare incoming trainees for their rotations. Methods: An e-learning module was created using text, images, and in-house recorded video recordings. Two cohorts were recruited: control cohort (n = 9), who completed their plastic surgery rotation without use of the module, and an interventional cohort (n = 18), who completed the rotation with use of the module. A demographic survey, a 20-question multiple-choice knowledge test, and self-reported confidence score were completed by both cohorts at the end of their plastic surgery rotations. The intervention cohort also completed the knowledge test at the beginning of their rotation to establish baseline. Knowledge and confidence scores were compared using two-tailed, unpaired, nonparametric analyses (Mann-Whitney test). Results: Learners from the intervention cohort reported a 95% module completion rate and found the resource "extremely helpful" (average Likert of 4.8/5). Learners indicated that they were very likely to recommend the resource to others (average Likert 4.9/5). The intervention cohort scored significantly higher on the knowledge test compared with the control cohort (P = 0.008), and on average reported higher confidence levels; however, this was not statistically significant (P = 0.057). Conclusion: An accessible and concise module on core plastic surgery concepts enhances learner knowledge and confidence during plastic surgery clinical rotations.

Role of perivascular and meningeal macrophages in outcome following experimental subarachnoid hemorrhage.

The distribution and clearance of erythrocytes after subarachnoid hemorrhage (SAH) is poorly understood. We aimed to characterize the distribution of erythrocytes after SAH and the cells involved in their clearance. To visualize erythrocyte distribution, we injected fluorescently-labelled erythrocytes into the prechiasmatic cistern of mice. 10 minutes after injection, we found labelled erythrocytes in the subarachnoid space and ventricular system, and also in the perivascular spaces surrounding large penetrating arterioles. 2 and 5 days after SAH, fluorescence was confined within leptomeningeal and perivascular cells. We identified the perivascular cells as perivascular macrophages based on their morphology, location, Iba-1 immunoreactivity and preferential uptake of FITC-dextran. We subsequently depleted meningeal and perivascular macrophages 2 days before or 3 hours after SAH with clodronate liposomes. At day 5 after SAH, we found increased blood deposition in mice treated prior to SAH, but not those treated after. Treatment post-SAH improved neurological scoring, reduced neuronal cell death and perivascular inflammation, whereas pre-treatment only reduced perivascular inflammation. Our data indicate that after SAH, erythrocytes are distributed throughout the subarachnoid space extending into the perivascular spaces of parenchymal arterioles. Furthermore, meningeal and perivascular macrophages are involved in erythrocyte uptake and play an important role in outcome after SAH.

Robust effects of genetic background on responses to subarachnoid hemorrhage in mice.

Outcome varies among patients with subarachnoid hemorrhage but known prognostic factors explain only a small portion of the variation in outcome. We hypothesized that individual genetic variations influence brain and vascular responses to subarachnoid hemorrhage and investigated this using inbred strains of mice.Subarachnoid hemorrhage was induced in seven inbred and a chromosome 7 substitution strain of mouse. Cerebral blood flow, vasospasm of the middle cerebral artery, and brain injury were assessed. After 48 h of subarachnoid hemorrhage, mice showed significant middle cerebral artery vasospasm that correlated positively with reduction in cerebral blood flow at 45 min. Mice also had increased neuronal injury compared to sham controls; A/J and C57BL/6 J strains represented the most and least severe, respectively. However, brain injury did not correlate with cerebral blood flow reduction at 45 min or with vasospasm at 48 h. Chromosome 7 substitution did not influence the degree of vasospasm or brain injury.Our data suggested that mouse genetic background influences outcome of subarachnoid hemorrhage. Investigations into the genetic factors causing these inter-strain differences may provide insight into the etiology of the brain damage following subarachnoid hemorrhage. These findings also have implications for animal modeling of disease and suggest that genetic differences may also modulate outcome in other cardiovascular diseases.

Current management of delayed cerebral ischemia: update from results of recent clinical trials.

Subarachnoid hemorrhage (SAH) accounts for 5-7% of all strokes worldwide and is associated with high mortality and morbidity. Even after surgical intervention, approximately 30% of patients develop long-term cognitive and neurological deficits that significantly affect their capacity to return to work or daily life unassisted. Much of this stems from a secondary ischemic phenomenon referred to as delayed cerebral ischemia (DCI). While DCI has been historically attributed to the narrowing of the large basal cerebral arteries, it is now recognized that numerous pathways contribute to its pathogenesis, including microcirculatory dysfunction, microthrombosis, cortical spreading depression, and early brain injury. This paper seeks to summarize some of the key pathophysiological events that are associated with poor outcome after SAH, provide a general overview of current methods of treating SAH patients, and review the results of recent clinical trials directed at improving outcome after SAH. The scientific basis of these studies will be discussed, in addition to the available results and recommendations for effective patient management. Therapeutic methods under current clinical investigation will also be addressed. In particular, the mechanisms by which they are expected to elicit improved outcome will be investigated, as well as the specific study designs and anticipated time lines for completion.

Molecular alterations in the hippocampus after experimental subarachnoid hemorrhage.

Patients with aneurysmal subarachnoid hemorrhage (SAH) frequently have deficits in learning and memory that may or may not be associated with detectable brain lesions. We examined mediators of long-term potentiation after SAH in rats to determine what processes might be involved. There was a reduction in synapses in the dendritic layer of the CA1 region on transmission electron microscopy as well as reduced colocalization of microtubule-associated protein 2 (MAP2) and synaptophysin. Immunohistochemistry showed reduced staining for GluR1 and calmodulin kinase 2 and increased staining for GluR2. Myelin basic protein staining was decreased as well. There was no detectable neuronal injury by Fluoro-Jade B, TUNEL, or activated caspase-3 staining. Vasospasm of the large arteries of the circle of Willis was mild to moderate in severity. Nitric oxide was increased and superoxide anion radical was decreased in hippocampal tissue. Cerebral blood flow, measured by magnetic resonance imaging, and cerebral glucose metabolism, measured by positron emission tomography, were no different in SAH compared with control groups. The results suggest that the etiology of loss of LTP after SAH is not cerebral ischemia but may be mediated by effects of subarachnoid blood such as oxidative stress and inflammation.