In most cases of basal joint osteoarthritis, surgery becomes an option at stages II, III, and IV, as classified by Eaton. Controversy exists regarding which technique achieves the best outcome. This systematic review was undertaken to address the question of which technique, if any, offers the best outcome to patients with osteoarthritis of the first carpometacarpal joint greater than stage II. A thorough search of the electronic databases Cochrane, Cinahl, Healthstar, and MEDLINE/PubMed was undertaken to identify reviews and articles on primary comparative studies of the different surgical options. The methodological quality of the retrieved articles was assessed on the basis of specific criteria. Inclusion criteria were applied to 44 of 254 possibly relevant articles. Eight reviews and 18 comparative studies met the criteria and were reviewed. Each of the techniques, arthrodesis, trapeziectomy with or without biological/synthetic interposition, osteotomy, and joint replacement, was associated with unique benefits and risks. There was great variability in outcome measurements. The majority of retrieved review articles claim that ligamentous reconstruction and tendon interposition may represent the best option; however, validity assessment of these studies revealed methodological flaws. Furthermore, results from the articles on comparative studies indicate that ligamentous reconstruction and tendon interposition may provide no additional benefit when compared with arthrodesis and trapeziectomy alone or with tendon interposition. There is no consensus as to which clinical outcomes are most important in thumb basal joint surgery and how these should be measured. This renders the appraisal and comparison of such studies a challenging task. Until large randomized controlled trials that compare techniques in similar populations with respect to staging and prognostic factors are undertaken and the clinical outcomes are clearly defined, surgeons will continue to claim superiority of one technique over another without supporting evidence.

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Ischemia-reperfusion (I/R) injury causes skeletal muscle infarction and ischemic preconditioning (IPC) augments ischemic tolerance in animal models. To date, this has not been demonstrated in human skeletal muscle. This study aimed to develop an in vitro model to investigate the efficacy of simulated IPC in human skeletal muscle. Human skeletal muscle strips were equilibrated in oxygenated Krebs-Henseleit-HEPES buffer (37 degrees C). Aerobic and reperfusion phases were simulated by normoxic incubation and reoxygenation, respectively. Ischemia was simulated by hypoxic incubation. Energy store, cell viability, and cellular injury were assessed using ATP, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT), and lactate dehydrogenase (LDH) assays, respectively. Morphological integrity was assessed using electron microscopy. Studies were designed to test stability of the preparation (n = 5-11) under normoxic incubation over 24 h; the effect of 1, 2, 3, 4, or 6 h hypoxia followed by 2 h of reoxygenation; and the protective effect of hypoxic preconditioning (HPC; 5 min of hypoxia/5 min of reoxygenation) before 3 h of hypoxia/2 h of reoxygenation. Over 24 h of normoxic incubation, muscle strips remained physiologically intact as assessed by MTT, ATP, and LDH assays. After 3 h of hypoxia/2 h of reoxygenation, MTT reduction levels declined to 50.1 +/- 5.5% (P < 0.05). MTT reduction levels in HPC (82.3 +/- 10.8%) and normoxic control (81.3 +/- 10.2%) groups were similar and higher (P < 0.05) than the 3 h of hypoxia/2 h of reoxygenation group (45.2 +/- 5.8%). Ultrastructural morphology was preserved in normoxic and HPC groups but not in the hypoxia/reoxygenation group. This is the first study to characterize a stable in vitro model of human skeletal muscle and to demonstrate a protective effect of HPC in human skeletal muscle against hypoxia/reoxygenation-induced injury.

Interphase nuclei exhibit a cell type-specific topology of chromatin domains. This topology has been proposed to be established at a specific developmental stage and to be associated, in turn, with cell type-specific gene expression. Using murine, cerebellar Purkinje neurons, we have shown previously that the number and the extent of clustering as well as the spatial, intranuclear distribution of centromeric domains change as a function of postnatal development. Specifically, the redistribution of centromeric domains was determined to be associated temporally with major changes in gene expression. Given that centromeric sequences are not transcribed, we tested the hypothesis that the de novo expression of a specific sequence is similarly associated with a change in its spatial, intranuclear position. In Purkinje neurons, Plc beta3 is expressed de novo between postnatal day 2 and 7. In contrast, the level of expression of Rora remains constant throughout development, following its initial expression at embryonic day 15. Plc beta3 and Rora were labeled by fluorescence in situ hybridization within intact nuclei and their intranuclear, spatial positions quantified by confocal microscopy. When analyzed as the distance from the nuclear centroid, the mean fraction of radial distance of Plc beta3 signals changed from 57.3%+/-2.35 (+/-SEM) (n=50) at P3 to 37.9%+/-2.35 (n=50) at P5. In contrast, the mean fraction of the radial distance of Rora signals did not change during postnatal development, remaining at a mean of 60.1%+/-2.01 (n=208) from the nuclear centroid. While the results do not support a causal relationship between the spatial relocation of Plc beta3 and its de novo expression, their temporal association, as described herein, may be taken to support the hypothesis that its intranuclear, spatial positioning may represent one level of transcriptional control.