Comparison of the Wide-Awake Approach and Conventional Approach in Extensor Indicis Proprius-to-Extensor Pollicis Longus Tendon Transfer for Chronic Extensor Pollicis Longus Rupture.

BACKGROUND: The wide-awake approach enables surgeons to perform optimal tensioning of a transferred tendon intraoperatively. The authors hypothesized that the extensor indicis proprius-to-extensor pollicis longus tendon transfer using the wide-awake approach would yield better results than conventional surgery. METHODS: A retrospective analysis was performed of the prospectively collected data of 29 consecutive patients who underwent extensor indicis proprius-to-extensor pollicis longus tendon transfer. Patients were treated with the wide-awake approach (group A, n = 11) and conventional surgery under general anesthesia (group B, n = 18). The groups were compared retrospectively for thumb interphalangeal and metacarpophalangeal joint motion, grip and pinch strength, specific extensor indicis proprius-to-extensor pollicis longus evaluation method (SEEM), and Disabilities of the Arm, Shoulder and Hand questionnaire score at 6 weeks and 2, 4, 6, and 12 months postoperatively. RESULTS: Group A showed significantly better interphalangeal joint flexion and total arc of motion at 6 weeks and 2, 4, and 6 months, and significantly better metacarpophalangeal joint flexion and total arc of motion at all time points. Interphalangeal and metacarpophalangeal joint extension showed no difference at all time points. Group A showed significantly better specific extensor indicis proprius-to-extensor pollicis longus evaluation method scores at 2 and 4 months, and Disabilities of the Arm, Shoulder and Hand questionnaire scores at 4, 6, and 12 months. Grip and pinch strength showed no difference at all time points. The complication rate and duration until return to work were not different between groups. CONCLUSION: Compared with the conventional approach, the wide-awake approach showed significantly better results in the thumb's range of motion and functional outcomes, especially in the early postoperative periods. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, III.

Association between Resting Heart Rate and Colorectal Cancer: Results from a Case-Controlled Study.

Previous studies evaluating associations between resting heart rate (RHR) and cancer-related mortality/prognosis have yielded conflicting results. We investigated whether elevations in RHR are associated with colorectal cancer (CRC). We conducted a case-controlled study involving 1241 CRC patients and 5909 cancer-free controls from the Korean National Health and Nutrition Examination Survey. After propensity score (PS) matching, 1207 CRC patients and 1207 matched controls were analyzed. Associations between RHR and CRC, colon, and rectal cancer were analyzed in appropriate patient subgroups using multiple and conditional logistic regression. Receiver operating characteristics analysis yielded the optimal RHR cut-point to predict CRC. RHR was significantly higher in CRC, colon, and rectal cancer patients than in controls (72.7 bpm in CRC, 72.8 bpm in colon cancer, 72.3 bpm in rectal cancer, and 68.7 bpm in controls; all p < 0.001). Analysis of data prior to PS matching yielded the following odds ratios (ORs) per RHR increment for CRC, colon, and rectal cancer: 1.043 (95% confidence intervals (CIs): 1.036-1.049), 1.045 (95% CI: 1.037-1.053), and 1.040 (95% CI: 1.030-1.051), respectively, in unadjusted models, and 1.043 (95% CI: 1.034-1.051), 1.046 (95% CI: 1.037-1.055), and 1.040 (95% CI: 1.027-1.052), respectively, in multivariable adjusted models. Patients with CRC, colon, and rectal cancer have a significantly higher RHR compared to cancer-free controls.

Prevalence and Risk Factors of Chronic Rhinosinusitis in the Elderly Population of Korea.

BACKGROUND: Although a significant number of the clinical features and pathophysiologic mechanisms of chronic rhinosinusitis (CRS) have been described, only a few studies have been published on characterization of CRS in the field of aging. OBJECTIVE: We investigated the prevalence and risk factors of CRS in elderly (≥65 years old) Koreans using large-scale nationwide epidemiological data and compared the risk factors of elderly with those of younger adult participants (19-64 years old). METHODS: Data from 25 529 participants who completed the 2008-2012 Korean National Health and Nutrition Examination Survey were analyzed. Diagnosis of CRS was done according to the EP3OS 2012 guideline for epidemiologic study. Risk factors of CRS were compared in the aspects of sociodemographics, general health behaviors, clinical characteristics, and comorbidities of participants. RESULTS: The prevalence of CRS was significantly higher in 5590 elderly than in 19 939 younger adults (6.55% vs 5.69%; P = .016. Some variables of socioeconomic status and mental health in the adult group were associated with increased risk of CRS but did not show association in the elderly group. We observed a significant association between CRS prevalence and comorbid allergic rhinitis, asthma, and atopic dermatitis in both groups ( P < .05). However, in the elderly group, the associations were significantly weaker with regard to allergic rhinitis ( P-interaction = .03) and asthma ( P-interaction = .002). CONCLUSION: These results suggest that elderly populations have distinct pathophysiology and clinical presentations from adult CRS, and management for elderly patients with CRS may require different or additional therapeutic approaches.

Total synthesis, structural revision, and absolute configuration of (-)-clavosolide [corrected] A.

[reaction: see text] Enantioselective synthesis of 3, a revised structure for clavosolide A, was completed. Both (1)H and (13)C NMR spectra of the natural and synthetic compounds were identical, and optical rotation measurements identified the absolute configuration of the natural clavosolide A as [corrected] 3.

Common genes responsible for differentiation and senescence of human mucosal and epidermal keratinocytes.

Serial subcultures of normal human oral keratinocytes (NHOKs) and normal human epidermal keratinocytes (NHEKs) to the postmitotic stage result in terminal differentiation and replicative senescence. In order to investigate the common mode of differentiation and/or senescence between mucosal and epidermal keratinocytes, gene expression profiling on both NHOKs and NHEKs was performed by a cDNA microarray analysis. Primary NHOKs and NHEKs were serially subcultured, and the expression level of 3,063 genes was compared between the exponentially growing and senescent cultures. The senescent NHOKs and NHEKs highly expressed 55 and 37 genes, respectively. Among these genes, 16 genes were common in both NHOKs and NHEKs while the other genes were upregulated either in the NHOKs or in the NHEKs. Furthermore, the expression levels of the common genes did not change in the human diploid fibroblasts during the subcultures. These results suggest that subculture-induced differentiation and/or replicative senescence in NHOKs and NHEKs has similar characteristics, but that the pathways leading to these processes are distinct and keratinocyte specific.

High extracellular Ca2+ alone stimulates osteoclast formation but inhibits in the presence of other osteoclastogenic factors.

High ambient Ca2+ at bone resorption sites have been implicated to play an important role in the regulation of bone remodeling. The present study was performed to clarify the mode of high extracellular Ca2+ (Ca2+(e))-induced modulation of osteoclastogenesis and the expression of receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG), thereby to define its role in osteoclast formation. Mouse bone marrow cells were cocultured with osteoblastic cells in the absence or presence of osteoclastogenic factors such as 1,25-dihydroxyvitaminD3 (1,25-(OH)2vitD3)and macrophage colony-stimulating factor/soluble RANKL. Ca2+ concentration in media (1.8 mM) was adjusted to 3, 5, 7 or 10 mM. Osteoclast formation was confirmed by the appearance of tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cells and the expression of osteoclast phenotypic markers (calcitonin receptor, vitronectin receptor, cathepsin K, matrix metalloproteinase-9, carbonic anhydrase 2). High Ca2+(e) alone significantly stimulated osteoclast formation in a dose-dependent manner. However, in the presence of highly osteoclastogenic factors, high Ca2+(e) significantly inhibited osteoclastogenesis. High Ca2+(e) alone continuously up-regulated RANKL expression while only transiently increased OPG expression. However, in the presence of 1,25-(OH)(2)vitD(3), high Ca2+(e) did not change the 1,25-(OH)2vitD3-induced RANKL expression while increased OPG expression. Taken together, these findings suggest that high Ca2+(e) alone increase osteoclastogenesis but inhibit in the presence of other osteoclastogenic factors. In addition, high CaCa2+(e)-induced osteoclastogenesis may be mediated by osteoblasts via up-regulation of RANKL expression. Meanwhile up-regulated OPG might participate in the inhibitory effect of high Ca2+(e) on 1,25-(OH)2vitD3-induced osteoclastogenesis.

p44/42 MAPK activation is necessary for receptor activator of nuclear factor-kappaB ligand induction by high extracellular calcium.

Although extracellular calcium (Ca(2+)(o)) has been suggested to modulate bone remodeling, the exact mechanism is unclear. This study was performed to explore the signaling pathways of high Ca(2+)(o) that are responsible for controlling the expression of receptor activator of NF-kappaB ligand (RANKL) in mouse osteoblastic cells. As previously reported, high Ca(2+)(o) increased RANKL expression. However, the G protein-coupled Ca(2+)(o)-sensing receptor (CaSR) was not detected in the primary cultured mouse osteoblastic cell. The inhibition of the pertussis-sensitive G protein, phospholipase C, protein kinase C, intracellular calcium mobilization, p38 MAPK, or phosphoinositide 3-kinase did not block RANKL induction caused by high Ca(2+)(o). In contrast, the inhibition of p44/42 MAPK pathway reduced the RANKL expression induced by high Ca(2+)(o). Moreover, high Ca(2+)(o) activated p44/42 MAPK and MEK1/2. These results suggest that RANKL induction by high Ca(2+)(o) might not be mediated by CaSR and its putative downstream signaling pathways, but the pathway employing p44/42 MAPK is involved in the high Ca(2+)(o)-induced RANKL expression in mouse osteoblastic cells.