In patients with persistently active rheumatoid arthritis, the combination of etanercept and methotrexate was safe and well tolerated and provided significantly greater clinical benefit than methotrexate alone.

The Extension for Community Healthcare Outcomes (ECHO) Model was developed by the University of New Mexico Health Sciences Center (UNMHSC) as a platform to deliver complex specialty medical care to underserved populations through an innovative educational model of team-based inter-disciplinary development. Using state-of-the-art telehealth technology, best practice protocols, and case based learning, ECHO trains and supports primary care providers to develop knowledge and self-efficacy on a variety of diseases. As a result, they can deliver best practice care for complex health conditions in communities where specialty care is unavailable. ECHO was first developed for the management of hepatitis C virus (HCV), optimal management of which requires consultation with multi-disciplinary experts in medical specialties, mental health and substance abuse. Few practitioners, particularly in rural and underserved areas, have the knowledge to manage its emerging treatment options, side effects, drug toxicities and treatment-induced depression. In addition data was obtained from observation of ECHO weekly clinics and database of ECHO clinic participation and patient presentations by clinical provider, evaluation of the ECHO program incorporates annual survey integrated into the ECHO annual meeting and routine surveys of community providers about workplace learning, personal and professional experiences, systems and environmental factors associated with professional practice, self-efficacy, facilitators and barriers to ECHO. The initial survey data show a significant improvement in provider knowledge, self-efficacy and professional satisfaction through participation in ECHO HCV clinics. Clinicians reported a moderate to major benefit from participation. We conclude that ECHO expands access to best practice care for underserved populations, builds communities of practice to enhance professional development and satisfaction of primary care clinicians, and expands sustainable capacity for care by building local centers of excellence.

Many of the estimated thirty-two million Americans expected to gain coverage under the Affordable Care Act are likely to have high levels of unmet need for various chronic illnesses and to live in areas that are already underserved. In New Mexico an innovative new model of health care education and delivery known as Project ECHO (Extension for Community Healthcare Outcomes) provides high-quality primary and specialty care to a comparable population. Using state-of-the-art telehealth technology and case-based learning, Project ECHO enables specialists at the University of New Mexico Health Sciences Center to partner with primary care clinicians in underserved areas to deliver complex specialty care to patients with hepatitis C, asthma, diabetes, HIV/AIDS, pediatric obesity and mental illness. As of March 2011, 298 Project ECHO teams across New Mexico have delivered more than 10,000 specialty care consultations for hepatitis C and other chronic diseases.

Sonographic needle guidance significantly improves the performance and outcomes of outpatient IA injections in a clinically significant manner.

Prostaglandins (PGs) I of the E series have been shown to inhibit many in vitro measurements of immune function in experimental animals. These include macrophage inhibitory factor production in guinea pigs (1, 2), direct cytolysis in murine lymphocytes (3), hemolytic plaque formation by murine leukocytes (4), and mitogen-induced stimulation of murine lymphocytes (5). In the human, Lomnitzer et al. (6) have shown that PGEI and PGE2 cause reduction in leukocyte inhibitory factor production by phytohemagglutinin(PHA)-stimulated human lymphocytes. Smith et al. (7) demonstrated significant inhibition of [3H]thymidine incorporation into PHA-stimulated human lymphocytes by PGEI, E2, At, and F~. As in the study by Lomnitzer, the final concentration of PGs was relatively high, I0-~-I0-4M. Ferraris and Derubertis have reported (8) that stimulation of 10 ~ human luekocytes with optimal concentrations of PHA produced -10-8M PGE.These data suggest that PGs of the E series might act as endogenous modulators in human immune reactions. PGEI is produced in the mitogen stimulation of human leukocytes, and may in turn inhibit this stimulation. Thus, data are accumulating to support the hypothesis of Bourne et al. (9) that PGs are important regulators of immune function. One troublesome aspect of the studies on human leukocytes is the great disparity between the amount of PGE produced during mitogen stimulation (~10-SM or 5 ng/ml) and the amount required to suppress mitogen stimulation when added to cultures (~10-5M or 5 pg/ml).In the present paper we describe the effects of lower, more physiologic concentrations of PGs on mitogen stimulation of human lymphocytes and lymphocyte subpopulations. We also describe the effect of PG synthetase inhibitors on mitogen-induced stimulation of these cells. We have identified a population of glass adherent mononuclear cells that suppress T-cell mitogenic activity through production of PGs of the E series.

We examined the role of a prostaglandin-producing suppressor cell in the hyporesponsiveness to phytohemagglutinin seen in Hodgkin's disease. Addition of indomethacin to phytohemagglutinin cultures of lymphocytes from six patients with Hodgkin's disease resulted in an increase of 182 +/- 60 per cent in 3H-thymidine incorporation versus a 44 +/- 18% increase in 29 controls (mean +/- S.D., P less than 0.001). Without indomethacin the mean response of the lymphocytes in Hodgkin's disease was 48% of that of control. With indomethacin it was 94% of the control value. Phytohemagglutinin cultures of Hodgkin-disease lymphocytes produced approximately fourfold more prostaglandin E2 after 48 hours than did normal lymphocytes (P less than 0.02). Removal of glass-adherent cells markedly decreased the enhancement seen with indomethacin; it reduced prostaglandin E2 production by more than 80% and eliminated the differences in response to phytohemagglutinin between Hodgkin-disease and normal lymphocytes. Thus, a glass-adherent, prostaglandin-producing suppressor cell is responsible for the hyporesponsiveness to phytohemagglutinin seen with Hodgkin-disease lymphocytes.

SUMMARY Magnetic resonance (MR) imaging and computed tomography (CT) are useful for the evaluation of central nervous system (CNS) lupus. This report describes the use of cranial MR and CT in 21 patients with systemic lupus erythematosus (SLE) with acute neuropsychiatric symptoms manifested by headache, seizures, focal neurological deficits, psychosis, or organic brain syndrome. Computed tomography was found to be insensitive and detected only diffuse atrophy (two cases), cerebral infarct (one case), and intracerebral haemorrhage (one case) in the 21 patients. Cranial MR images obtained with a General Electric 1-5 tesla Signa unit detected labile and fixed areas of increased proton intensity interpreted as focal oedema (eight cases), infarct (10 cases), haemorrhage (one), atrophy (seven), and acute sinusitis (two). Focal oedema was characterised by labile, high intensity lesions in the gray or white matter of the cerebellum, cerebrum, or brain stem, which completely resolved after aggressive corticosteroid treatment. Most high intensity reversible or fixed lesions evident on MR were not apparent on cranial CT images. In several patients sequential MR images were valuable in monitoring the efforts of treatment. Although histological confirmation of the high intensity brain lesions apparent on MR is desirable, prior necropsy studies suggest that pathological confirmation may be difficult owing to the paucity of recognisable brain lesions in patients with CNS lupus. It is concluded that for the evaluation of acute neuropsychiatric SLE MR is useful and provides more information than cranial CT.Acute neuropsychiatric lupus is associated with headache, depression, organic brain syndrome, seizures, psychosis, paresis, and a host of other neurological and psychiatric symptoms.' Because of the non-specific nature of these complaints, systemic lupus erythematosus (SLE) with central nervous system (CNS) symptoms presents a peculiar dilemma to the clinician. Confounding disorders, particularly bacterial meningitis, non-steroidal induced aseptic meningitis, brain abscess, steroid psychosis, and

Objective Magnetic resonance imaging (MRI) often demonstrates brain lesions in neuropsychiatric systemic lupus erythematosus (NPSL). The present study compared post-mortem histopathology with pre-mortem MRI in NPSL. Methods 200 subjects with NPSLE were studied prospectively with MRI over a 10-year period during which 22 subjects died. In 14 subjects, a brain autopsy with histopathology that permitted direct comparison with pre mortem MRI was successfully obtained. Surface anatomy was used to determine the approximate location of individual lesions. Results Pre mortem MRI findings in fatal NPSLE were small focal white matter lesions (100%), cortical atrophy (64%), ventricular dilation (57%), cerebral edema (50%), diffuse white matter abnormalities (43%), focal atrophy (36%), cerebral infarction (29%), acute leukoencephalopathy (25%), intracranial hemorrhage (21%), and calcifications (7%). Microscopic findings in fatal NPSLE included global ischemic changes (57%), parenchymal edema (50%), microhemorrhages (43%), glial hyperplasia (43%), diffuse neuronal/axonal loss (36%), resolved cerebral infarction (33%), microthomboemboli (29%), blood vessel remodeling (29%), acute cerebral infarction (14%), acute macrohemorrhages (14%), and resolved intracranial hemorrhages (7%). Cortical atrophy and ventricular dilation seen by MRI predicted brain mass at autopsy (r = -0.72, p = 0.01, and r = -0.77, p =0.01, respectively). Cerebral autopsy findings, including infarction, cerebral edema, intracranial hemorrhage, calcifications, cysts, and focal atrophy were also predicted accurately by pre mortem MRI. Conclusion Brain lesions in NPSLE detected by MRI accurately represent serious underlying cerebrovascular and parenchymal brain injury on pathology.