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Background: Health-care providers report a lack of training in end-of-life care and limited opportunities exist to learn about the dying process in home settings where most prefer to die., Aim: To evaluate the effectiveness of a Community Action, Research, and Education (CARE) program designed to promote empathy and self-efficacy communicating with and caring for terminally ill patients., Methods: This mixed-methods study collected pre-post data from 18 undergraduates (7 men≤ 11 women) in a 8-week immersive program where they served as primary caregivers in residential homes for the dying providing 200 hours of bedside care to hospice patients during their final days. Quantitative measures assessed empathy using the Jefferson Scale of Empathy-Health Professions (JSE-HPS) version and self-efficacy using a 20-question palliative care skill assessment. Qualitative analyses were conducted on reflective journals to further assess knowledge, skill, and value development., Results: Paired t tests revealed significant increases in empathy ( P < .05) and self-efficacy ( P < .001) to provide end-of-life care. Thematic analysis of reflective journals further demonstrated specific instances of empathy and self-efficacy., Conclusions: Community-run residential homes for the dying offer a unique opportunity for skills training in end-of-life care. The opportunity to serve as a caregiver for the dying improved students' confidence and ability to provide empathic patient- and family-centered end-of-life care to hospice patients in their final days.

Phyllodes tumors (PTs) of the breast are biphasic lesions, comprising an epithelial component set within a neoplastic spindle-celled stroma. These tumors have been classified as benign, borderline, and malignant based on a combination of histological criteria, including stromal cellularity, nuclear pleomorphism, mitotic rate, stromal overgrowth, and margin appearance. The aim of this study was to evaluate the expression of CD34, CD117 (c-kit), and Ki-67 in PT of the breast and attempt to correlate the staining pattern with tumor grade by morphology. Immunohistochemical expression of CD117, CD34, and Ki-67 was studied on formalin-fixed, paraffin-embedded archival tissue material from 33 cases of PT. Histologically, there were 21 benign, 6 borderline, and 6 malignant (high-grade) tumors. All 6 histologically malignant PTs were positive for CD117 (100%), but only 1 marked with CD34 (16.7%). Borderline PTs frequently coexpressed CD34 and CD117 (66.7%). The benign PTs, on the other hand, most commonly (52.4%) showed a CD34(+)/CD117(-) immunoprofile with 33.3% cases coexpressing the markers: that is, CD34(+)/CD117(+). Although most benign PTs (80.6%) showed a Ki-67 of <2%, a few cases showed slightly higher proliferation indices. This study indicates that CD34 and CD117 are differentially expressed in benign and malignant PTs. These markers, therefore, in combination, may be used as an adjunct to morphology in the subclassification of PTs.

Adenovirus-based gene therapy offers a unique opportunity to target gene expression to the liver by systemic delivery. However, systemic administration of a first generation adenoviral construct elicits an inflammatory response leading to TNF-alpha-dependent liver injury. The aim of this study was to evaluate whether the systemic administration of recombinant adenovirus exacerbates a subsequent TNF-alpha-dependent liver injury induced by D-galactosamine and lipopolysaccharide. Surprisingly, low-dose adenovirus administration (10(5) particles) protects, while high-dose adenovirus (10(10) particles) is associated with an exaggerated hepatic inflammatory response from a subsequent D-galactosamine and lipopolysaccharide challenge. This exacerbation is TNF-alpha dependent, since treatment with a TNF inhibitor fully protects against the liver injury. Moreover, intravenous administration of an adenoviral construct expressing the anti-inflammatory protein interleukin-10 reduces TNF-alpha appearance and attenuates the increased hepatocyte injury. Taken together, this report demonstrates potential additive effects of TNF-alpha responses induced by adenovirus and other inflammatory signals, and suggests that the response can be mitigated by relative adenovirus particle dose or by inhibitors, such as TNF-binding protein or interleukin 10.

Development of a new class of drugs designed to selectively inhibit the inducible cyclooxygenase isoenzyme, COX-2, was initially prescribed for individuals diagnosed with osteoarthritis or rheumatoid arthritis. Although these inflammatory disorders are more typically related to the joints of the knee, ankle, or hand, the temporomandibular joint (TMJ) plays a special role due to its involvement in our normal day-to-day activities of eating and communicating. The TMJ, unlike most of the other joints, contains some unique morphological characteristics that support various inflammatory disorders. An overview of these characteristics and the prospective use of the COX-2 inhibitors for temporomandibular joint inflammation are presented.