Both arytenoid subluxation and recurrent laryngeal nerve paralysis (RLNP) may result from injury to the larynx, and they may be difficult to distinguish clinically. A patient with arytenoid subluxation who was initially believed to have RLNP was treated with medialization laryngoplasty 1 year after the injury. Preoperative magnetic resonance imaging and computed tomography effectively demonstrated the cricoarytenoid subluxation, which was confirmed by intraoperative electromyography (EMG) showing normal electrical activity in the thyroarytenoid muscle. Photographs from preoperative fiberoptic laryngoscopy are presented to identify the appearance of arytenoid subluxation. Computed tomographic findings and photographs from laryngoscopy of two patients with RLNP documented by intraoperative EMG evaluation are presented to help distinguish the clinical appearance of this disorder from arytenoid subluxation. An integrated approach to the diagnosis and treatment of arytenoid subluxation is presented.
CCN5 is a secreted heparin-and estrogenregulated matricellular protein that inhibits vertebrate smooth muscle cell proliferation and motility. CCN5 is expressed throughout murine embryonic development in most organs and tissues. However, after embryonic development is complete, we hypothesized that CCN5 distribution would be largely restricted to small set of tissues, including smooth muscle cells of the arteries, uterus, airway, and digestive tract. Because CCN5 inhibits proliferation of smooth muscle cells in vitro, it might function to prevent excessive growth in vivo. In contrast, another member of the CCN family, CCN2, promotes smooth muscle cell proliferation in vitro, and thus it was expected that its expression levels would be low in uninjured normal adult tissues. Frozen sections from adult tissues and organs were analyzed immunohistochemically using anti-CCN5 and anti-CCN2 antibodies. Both proteins were detected in arteries, the uterus, bronchioles, and the digestive tract as expected, and also in many other tissues including the pancreas, spleen, liver, skeletal muscle, ovary, testis, thymus, brain, olfactory epithelium, and kidney. CCN5 and CCN2 protein was found in smooth muscle, endothelial cells, epithelial cells, skeletal muscle, cells of the nervous system, and numerous other cell types. In many cells, both CCN5 and CCN2 was present in the nucleus. Rather than having opposite patterns of localization, CCN5 and CCN2 often had similar sites of expression. The wide distribution of both CCN5 and CCN2 suggests that both proteins have additional biological functions beyond those previously identified in specific cellular and pathological models.
Background. Cardiovascular disease is the major cause of death in the end-stage renal disease population. Novel risk factors such as homocysteine (Hcy) are of considerable interest in this group as hyperhomocysteinaemia is highly prevalent in the setting of renal impairment. Folic acid-vitamin B group therapies are only partially effective treatments. Hcy is highly protein-bound and thus poorly dialysed. Dialyzers with albumin-leaking properties have been shown to result in lowering of plasma Hcy. As the FX-class (Advanced Fresenius Polysulfone dialyzer) has greater clearance of larger molecular weight substances but is non-albumin-leaking, we explored the capacity of this new technology membrane to reduce plasma Hcy levels. Methods. A prospective randomized cross-over trial in 35 prevalent haemodialysis patients, one group receiving 12 weeks dialysis using FX dialyzer then 12 weeks with standard high flux dialysis (SHF) and the other group SHF followed by FX dialyzer. All patients received vitamin B 6 25 mg and folic acid 5 mg daily throughout the study. Results. The primary outcome was plasma Hcy pre-dialysis at week 12. FX vs SHF showed no significant difference, 25±6.6 vs 25.9±5.8 mg/l, Á95% CI ¼ À2.77 to 4.59, P ¼ 0.31. There was a nonsignificant trend toward a decrease in Hcy in both groups (27.43±7.68 to 25.91±5.78 mmol/l for SHF, P ¼ 0.23 and 26.0±4.58 to 25.0±6.61 mmol/l for FX, P ¼ 0.28). Analysis by repeated measures method demonstrated a statistically significantly lower Hcy with FX vs SHF dialyzer (adjusted b ¼ À1.30, 95% CI ¼ À2.41 to À0.19, P ¼ 0.022). K t /V urea was higher in FX vs SHF (1.35±0.18 vs 1.22±0.2; P ¼ 0.013). Folate and B 6 levels did not change. Conclusions. The primary outcome analysis did not show any significant difference in pre-Hcy comparing FX and SHF membranes. Although our secondary analysis demonstrated a statistically significant difference between membranes, the magnitude of the difference (1.3 mmol/l) is not clinically significant. Thus the use of the FX dialyzer did not result in a clinically significant benefit in relation to improving pre-dialysis Hcy compared with standard high-flux dialysis.
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