Publications

BACKGROUND

Mental health assessments in post-conflict zones have relied heavily on Western psychiatric scales. Yet, a strict dependence on the paradigms of Western psychiatry risks inappropriately prioritizing syndromes, such as PTSD, which, however important, are eclipsed by local concerns.

MATERIAL AND DISCUSSION

In Dearborn, Michigan, home to the largest population of Iraqi refugees in the United States, 60 Iraqi refugee life stories were collected in order to adapt the Harvard Trauma Questionnaire (HTQ) to the Iraqi context.

CONCLUSION

The methodology described proved to be a useful approach to developing a trauma measure that is culturally grounded in a multi-dimensional model of mental health.

BACKGROUND

Safe delivery of care depends on effective communication among all health care providers, especially during transfers of care. The traditional medical chart does not adequately support such communication. We designed a patient-tracking tool that enhances provider communication and supports clinical decision making.

AIM

To develop a problem-based patient-tracking tool, called Sign-out, Information Retrieval, and Summary (SynopSIS), in order to support patient tracking, transfers of care (ie, sign-outs), and daily rounds.

SETTING

Tertiary-care, university-based teaching hospital.

PROGRAM DESCRIPTION

SynopSIS compiles and organizes information from the electronic medical record to support hospital discharge and disposition decisions, daily provider decisions, and overnight or cross-coverage decisions. It reflects the provider's patient-care and daily work-flow needs.

PROGRAM EVALUATION

We plan to use Web-based surveys, audits of daily use, and interdisciplinary focus groups to evaluate SynopSIS's impact on communication between providers, quality of sign-out, patient continuity of care, and rounding efficiency.

CONCLUSIONS

We expect SynopSIS to improve care by facilitating communication between care teams, standardizing sign-out, and automating daily review of clinical and laboratory trends. SynopSIS redesigns the clinical chart to better serve provider and patient needs.

Sudden cardiac death is a major public health problem affecting 500,000 patients annually in the United States alone. The major risk factor for sudden cardiac death is the presence of coronary artery disease, usually in the setting of reduced ejection fraction. Globally, the incidence is expected to rise sharply as the prevalence of coronary artery disease and heart failure continue to increase. However, sudden cardiac death is a heterogeneous condition and may be caused by acute ischemia, structural defects, myocardial scar, and/or genetic mutations. Sudden death may occur even in a grossly normal heart. Beta-blockers can reduce the risk of sudden cardiac death, while implantable cardioverter defibrillators are effective at terminating malignant arrhythmias. Ejection fraction remains the major criterion to stratify patients for defibrillator implantation but this strategy alone is insensitive and nonspecific. Novel clinical, electrophysiologic, and genetic markers have been identified that may increase precision in patient selection for primary prevention therapy. This review discusses the epidemiology, mechanisms, etiologies, therapies, treatment guidelines, and future directions in the management of sudden cardiac death.

Mycobacterium tuberculosis is an exceptionally successful human pathogen. A major component of this success is the ability of the bacteria to infect immunocompetent individuals and to evade eradication by an adaptive immune response that includes production of the macrophage-activating cytokine, IFN-gamma. Although IFN-gamma is essential for arrest of progressive tuberculosis, it is insufficient for efficacious macrophage killing of the bacteria, which may be due to the ability of M. tuberculosis to inhibit selected macrophage responses to IFN-gamma. In vitro studies have determined that mycobacterial lipoproteins and other components of the M. tuberculosis cell envelope, acting as agonists for TLR2, inhibit IFN-gamma induction of MHC class II. In addition, M. tuberculosis peptidoglycan and IL-6 secreted by infected macrophages inhibit IFN-gamma induction of MHC class II in a TLR2-independent manner. To determine whether TLR2-dependent inhibition of macrophage responses to IFN-gamma is quantitatively dominant over the TLR2-independent mechanisms in vivo, we prepared mixed bone marrow chimeric mice in which the hemopoietic compartment was reconstituted with a mixture of TLR(+/+) and TLR2(-/-) cells. When the chimeric mice were infected with M. tuberculosis, the expression of MHC class II on TLR2(+/+) and TLR2(-/-) macrophages from the lungs of individual infected chimeric mice was indistinguishable. These results indicate that TLR2-dependent and -independent mechanisms of inhibition of responses to IFN-gamma are equivalent in vivo, and that M. tuberculosis uses multiple pathways to abrogate the action of an important effector of adaptive immunity. This work was supported by National Institutes of Health Grants AI 065357-AI 020010.