Symptoms of Depression Are Associated With Opioid Use Regardless of Pain Severity and Physical Functioning Among Treatment-Seeking Patients With Chronic Pain.

Depression may be a critical factor in the initiation and maintenance of opioids. This study investigated the association among opioid use, pain, and depression in patients evaluated at a university-based outpatient pain clinic. Of the 2,104 new patients included, 55.89% reported current opioid use and showed a worse phenotypic profile (eg, higher pain severity, worse physical functioning) compared with nonopioid users. In addition, more opioid users reported symptoms suggestive of depression than those not taking opioids (43.6% vs 26.8%, P < .001). In a multivariate logistic regression model, increased pain severity was associated with increased probability of taking opioids; however, this was moderated by depression (estimate = -.212, P < .001). For nondepressed patients, the predicted probabilities of opioid use increased as pain severity increased. In contrast, among patients with symptoms of depression, the probability of taking opioids did not change based on pain severity. Similarly, although increased physical function was associated with increased probability of opioid use, this was moderated by depression (estimate = .033, P = .034). Patients with symptoms of depression were more likely to be taking opioids at higher levels of functioning (Ps < .03). Perspective: This study investigated the association among opioid use, pain, and depression at a university-based outpatient pain clinic. Depression emerged as a moderator of the relationship among opioid use, pain severity, and physical functioning. These findings lend support to the hypothesis that patients may be self-medicating affective pain with opioids.

Left ventricular aneurysm repair with use of a bovine pericardial patch.

Left ventricular aneurysm, which can impair systolic function, has a reported incidence of 10% to 35% in patients after myocardial infarction. In a 58-year-old woman who had a history of myocardial infarction, we excised a large left ventricular aneurysm and restored left ventricular geometry with use of a bovine pericardial patch. The aneurysm's characteristics and the patient's preoperative left ventricular ejection fraction of 0.25 had indicated surgical intervention. The patient had an uneventful postoperative course, and her left ventricular ejection fraction was 0.50 to 0.55 on the 4th postoperative day. This case illustrates the value of surgical treatment for patients who have a debilitating left ventricular aneurysm.

Endovascular repair of the ascending aorta: when and how to implement the current technology.

BACKGROUND: The purpose of our study was to examine when and how to implement the current endoluminal stent graft technology to treat ascending aortic disease. METHODS: During a 7-year period (March 2006 through July 2013), 7 consecutive patients (median age, 69 years; range, 61.5 to 80.5 years) with multiple comorbidities underwent endoluminal repair of the ascending aorta. Six had an ascending aortic pseudoaneurysm, and 1 had iatrogenic coarctation. The median number of prior sternotomies was 2 (range, 1 to 4). RESULTS: Technical success was achieved in all but 1 patient, with 1 death (14.3%) at 30 days. The endoluminal technology used included the Gore TAG (W.L. Gore and Associates, Flagstaff, AZ) thoracic graft (including the new C-TAG) in 6 patients, the Talent stent graft (Medtronic, Santa Rosa, CA) in 1, an Excluder cuff (W.L. Gore) in 2, and an Amplatzer occluder (AGA Medical Corp, Plymouth, MN) in 1. More than 1 stent was placed in 4 patients. Three patients required innominate artery stenting, and 1 required additional left common carotid artery stenting. One patient (14.3%) required intraoperative conversion to open surgical repair. Median follow-up was 14.4 months (interquartile [25th to 75th percentile] range, 5.5 to 22.6 months) with 66.6% overall survival. No aortic-related death was reported during the follow-up period. CONCLUSIONS: Stent grafting of the ascending aorta is feasible but limited and is reserved for high-risk individuals. Technical expertise is essential, and follow-up is mandatory. Technical points, tips, and challenges of the current endovascular technology to effectively treat the ascending aorta are described.

Fungicidal sesquiterpene dialdehyde cinnamates from Pseudowintera axillaris.

Bioactivity-directed separation of a foliage extract from the New Zealand shrub Pseudowintera axillaris led to a compound with fungicidal activity against the plant pathogen Phytophthora infestans. This was identified as a new sesquiterpene dialdehyde cinnamate named paxidal. Two 6-hydroxy derivatives were present at lower levels in the extract. A further nine derivatives were synthesized from these natural products for a structure-activity study against a range of important food crop pathogens. The cinnamate group was important for fungicidal effects, and protection of the dialdehyde as a dimethyl acetal gave more potent, broader spectrum activity.

Adhesion of lymphocytes to bladder cancer cells: the role of the alpha(E)beta(7) integrin.

The alpha(E)beta(7)integrin (defined by CD103) is expressed by most intra-epithelial lymphocytes (IEL) but by fewer than 2% peripheral blood lymphocytes (PBL). An important ligand for this molecule is the epithelial cell adhesion molecule E-cadherin. Loss of E-cadherin is associated with increased invasion and metastasis in bladder cancer. This study examines the role of the alpha(E)beta(7)-E-cadherin interaction in lymphocyte targeting of bladder cancer cells. Lymphocytes were activated in vitro by mixed lymphocyte reaction (MLR) and CD103 was upregulated by treatment with transforming growth factor beta (TGFbeta). The CD103(+) lymphocytes were used in a flow cytometric adhesion assay with bladder cancer cell lines, differing in expression of E-cadherin and intercellular adhesion molecule-1 (ICAM-1). Antibody blockade was used to confirm the relative importance of CD103 and ICAM-1 to intercellular adhesion. Lymphocytes with upregulated CD103 compared to control lymphocytes showed enhanced adhesion to an E-cadherin expressing bladder cancer cell line ( P=0.0003). This increased adhesion could be abrogated by anti-CD103 adhesion blockade. For ICAM-1 expressing bladder cells, adhesion of lymphocytes could be markedly reduced using anti-ICAM-1 blockade. In conclusion, the upregulation of CD103 by lymphocytes increases adhesion to E-cadherin expressing bladder cancer targets. Loss of E-cadherin in bladder cancer progression may provide a mechanism both for increased invasion and effective immune evasion.