Quality Indicators for Major Depressive Disorder in Adults: A Review of Performance Measures by the American College of Physicians.

Major depressive disorder (MDD) is a severe mood disorder that affects at least 8.4% of the adult population in the United States. Characteristics of MDD include persistent sadness, diminished interest in daily activities, and a state of hopelessness. The illness may progress quickly and have devastating consequences if left untreated. Eight performance measures are available to evaluate screening, diagnosis, and successful management of MDD. However, many performance measures do not meet the criteria for validity, reliability, evidence, and meaningfulness.The American College of Physicians (ACP) embraces performance measurement as a means to externally validate the quality of care of practices, medical groups, and health plans and to drive reimbursement processes. However, a plethora of performance measures that provide low or no value to patient care have inundated physicians, practices, and systems and burdened them with collecting and reporting of data. The ACP's Performance Measurement Committee (PMC) reviews performance measures using a validated process to inform regulatory and accreditation bodies in an effort to recognize high-quality performance measures, address gaps and areas for improvement in performance measures, and help reduce reporting burden. Out of 8 performance measures, the PMC found only 1 measure (suicide risk assessment) that was valid at all levels of attribution. This paper presents a review of MDD performance measures and highlights opportunities to improve performance measures addressing MDD management.

In vivo natural killer cell depletion during primary simian immunodeficiency virus infection in rhesus monkeys.

The contribution of natural killer (NK) cells to the immune containment of human immunodeficiency virus infection remains undefined. To directly assess the role of NK cells in an AIDS animal model, we depleted rhesus monkeys of >88% of CD3(-) CD16(+) CD159a(+) NK cells at the time of primary simian immunodeficiency virus (SIV) infection by using anti-CD16 antibody. During the first 11 days following SIV inoculation, when NK cell depletion was most profound, a trend toward higher levels of SIV replication was noted in NK cell-depleted monkeys compared to those in control monkeys. However, this treatment did not result in significant changes in the overall levels or kinetics of plasma viral RNA or affect the SIV-induced central memory CD4(+) T-lymphocyte loss. These findings are consistent with a limited role for cytotoxic CD16(+) NK cells in the control of primary SIV viremia.

Use of an anti-CD16 antibody for in vivo depletion of natural killer cells in rhesus macaques.

Non-human primates serve as key animal models for a variety of viral infections. To evaluate the contribution of natural killer (NK) cells to the immune-mediated control of these viruses in macaque monkeys, we have described a method for depleting NK cells in vivo by administration of anti-human CD16 mouse monoclonal antibody. Using a fluorometric NK-cell cytotoxicity assay, we show that most NK-cell cytotoxicity in rhesus monkey peripheral blood mononuclear cells resides in the CD16(+) and/or CD159A(+) subset of lymphocytes. The anti-human CD16 antibody, 3G8, binds to subsets of rhesus monkey lymphocytes and monocytes but not to neutrophils. Intravenous administration of 10-50 mg/kg of 3G8 to normal rhesus monkeys resulted in anti-CD16 antibody persistence in the plasma for 1-3 weeks. This treatment also depleted 80-90% of CD3(-) CD159A(+) lymphocytes, putative NK cells, from blood for at least 1 week and was associated with the loss of NK-cell cytotoxicity when evaluated by in vitro assays. Using this method, transient depletion of NK cells from two rhesus monkeys chronically infected with simian immunodeficiency virus failed to cause changes in virus replication. These studies describe a non-human primate model for in vivo NK-cell depletion and suggest a limited role for cytotoxic CD16(+) NK cells in controlling AIDS virus replication during chronic infection.

Physician gender affects how physician nonverbal behavior is related to patient satisfaction.

BACKGROUND: Physician and patient gender both influence medical communication. Nonverbal behavior is generally under-researched in the medical encounter but plays an important role for patient outcomes such as satisfaction. OBJECTIVE: This article aims at identifying how specific physician nonverbal behaviors predict analogue patient satisfaction depending on physician and patient gender. RESEARCH DESIGN: Eleven physicians in a real medical encounter were videotaped and analogue patients indicated their satisfaction with each physician while viewing the videotapes. SUBJECTS: One hundred sixty-three university students participated (analogue patients). MEASURES: From the videotapes, 17 physician nonverbal behaviors (related to face, body, voice/speech), 2 physician appearance cues, 2 characteristics of the examination room, and 1 patient behavior were coded. For each analogue patient, the correlation between each of these coded characteristics and the patient's satisfaction was calculated, across all physicians and across male and female physicians separately. RESULTS: There was no main effect for patient gender but most coded characteristics showed different relations to patient satisfaction according to physician gender. Analogue patients were most satisfied with female physicians who behaved in line with the female gender role (eg, more gazing, more forward lean, softer voice) while still stressing their professionalism (laboratory coat, medical-looking examination room). For male physicians, satisfaction was high for a broader range of behaviors, partly related to their gender role (eg, louder voice, more distance to patient). CONCLUSIONS: To be satisfied, patients expect female and male physicians to show different patterns of nonverbal behavior. Awareness of these gender-specific expectations should be taken into account in medical training.

Molecular determinants regulating the pairing of NKG2 molecules with CD94 for cell surface heterodimer expression.

The lytic capacity of a NK cell is regulated, in part, by the balance in cell surface expression between inhibitory CD94/NKG2A and activating CD94/NKG2C heterodimers. We demonstrate that, in the absence of DAP12, rhesus monkey NKG2A is preferentially expressed at the cell surface with CD94 due to a single amino acid difference in the transmembrane of NKG2A and NKG2C. Furthermore, in the context of an NKG2A transmembrane, the stalk domain of NKG2C was found to enhance heterodimer formation with CD94 compared with the stalk domain of NKG2A. In the presence of DAP12, the ability of NKG2C to compete for cell surface CD94 heterodimerization is enhanced and approaches that of NKG2A. Finally, allelic differences that affect the ability of rhesus NKG2A to reach the cell surface with CD94 could also be mapped to the transmembrane. These differences in the ability of inhibitory and activating NKG2 molecules to reach the cell surface provide a mechanism for the regulation of NK cell activity.

Tularemia and Q fever.

The zoonotic infections caused by Francisella tularensis and Coxiella burnetii, tularemia and Q fever, respectively, are two less commonly encountered clinical illnesses that are becoming increasingly recognized as epidemiologically important human diseases. The prevalence of tularemia and Q fever can be positively impacted by increased awareness of the clinical entities that arise from infection by these arthropod-borne organisms. Improved recognition of these clinical syndromes will lead to greater diagnostic accuracy in recognizing these diseases in patients. Ultimately, more stringent measures to prevent infection may be required, through raising public awareness, since current therapeutic regimens for these two diseases are limited, and knowledge of the pathogenesis of these two organisms are still in developing stages.