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71.
Chronic neck and shoulder pain. Focusing on myofascial origins   总被引:1,自引:0,他引:1  
Chronic neck and shoulder pain is a complex, multifactorial problem. Often many months have passed since its onset. During this time the patient may have seen many physicians and tried many medications, some with abuse potential. Most patients are depressed and have lost their ability to cope with the stresses of daily life. The goals of therapy are to enable patients to deal with the problem and to bring them to the point where pain is no longer the dominant factor in their lives. For patients with chronic neck and shoulder pain of myofascial origin, this is accomplished with a multi-disciplinary approach that incorporates use of psychotherapeutic techniques, nonsteroidal antiinflammatory medications, antidepressant drugs, trigger-point injection, and several physical therapy modalities.  相似文献   
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Depressed scars of the head and neck can be predictably and satisfactorily revised by the combination of local subcutaneous flaps with the accepted techniques of superficial scar revision.  相似文献   
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Because epithelial cells are the major cell type productively infected with Chlamydia during genital tract infections, the overall goal of our research was to understand the contribution of infected epithelial cells to the host defense. We previously showed that Toll-like receptor 3 (TLR3) is the critical pattern recognition receptor in oviduct epithelial (OE) cells that is stimulated during Chlamydia infection, resulting in the synthesis of beta interferon (IFN-β). Here, we present data that implicates TLR3 in the expression of a multitude of other innate-inflammatory immune modulators including interleukin-6 (IL-6), CXCL10, CXCL16, and CCL5. We demonstrate that Chlamydia-induced expression of these cytokines is severely disrupted in TLR3-deficient OE cells, whereas Chlamydia replication in the TLR3-deficient cells is more efficient than in wild-type OE cells. Pretreatment of the TLR3-deficient OE cells with 50 U of IFN-β/ml prior to infection diminished Chlamydia replication and restored the ability of Chlamydia infection to induce IL-6, CXCL10, and CCL5 expression in TLR3-deficient OE cells; however, CXCL16 induction was not restored by IFN-β preincubation. Our findings were corroborated in pathway-focused PCR arrays, which demonstrated a multitude of different inflammatory genes that were defectively regulated during Chlamydia infection of the TLR3-deficient OE cells, and we found that some of these genes were induced only when IFN-β was added prior to infection. Our OE cell data implicate TLR3 as an essential inducer of IFN-β and other inflammatory mediators by epithelial cells during Chlamydia infection and highlight the contribution of TLR3 to the inflammatory cytokine response.  相似文献   
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Toomey M  Biddle C 《AANA journal》2006,74(5):379-384
The phenomenon of itching has received surprisingly little scientific scrutiny despite its commonality--hence its designation as a kind of neglected, "orphan symptom." Recent research and clinical understanding has shed light on itching, helping to illuminate its previously shaded landscape. This course reviews the nature of itching, its physiology, major triggers of particular interest to anesthetists (especially when using neuraxial agents), and interventions directed at its resolution. A variety of chemical mediators and modulators have important roles in the genesis and experience of itching. Although many medical comorbidities can cause itch, the ubiquitous use of neuraxial opioids in the perioperative care of patients has been attended by a dramatic increase in the number of patients experiencing, and complaining of, itching as a consequence of our management. Patient satisfaction inventories have placed the sensation of refractory itch among the most distressing, non-life-threatening complications that are experienced. Intractable itch can be so incapacitating that it deserves the same degree of clinical attention as pain.  相似文献   
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Solid pseudopapillary neoplasm of the pancreas (SPNP) is a rare tumor with low malignant potential found in adolescent girls and young women. The pathogenesis of SPNP remains uncertain and its management is controversial. Genetic changes associated with SPNP have seldom been reported. We describe here the cytogenetic investigation of a case of SPNP in a 13-year-old girl whose tumor cells revealed two unrelated clones: one clone characterized by complex karyotypic changes, including breakpoints in two common fragile sites at chromosome 2, band q33, and chromosome 4, band q31, and the second clone defined by partial monosomy for chromosome X. Loss of heterozygosity for HRAS was also identified by array comparative genomic hybridization (a-CGH). These cumulative changes seem insufficient for activation of cell transformation, but could possibly play a role in priming the cell for future mutagenic events.  相似文献   
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