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This study compared the results of the minimally invasive coracoclavicular (CC) fixation with a single TightRope (MITR) procedure and the hook plate (HP) procedure for acute acromioclavicular (AC) joint dislocation treatment. Sixteen patients with a mean age of 44.9 ± 11 years were treated with the MITR procedure. Nineteen patients with a mean age of 40.2 ± 8.7 years were treated using the HP procedure. Clinical outcomes were evaluated with the Visual Analog Scale (VAS) for pain, Constant–Murley Score (CMS), and University of California at Los Angeles (UCLA) Shoulder score. Vertical displacement of the clavicle with reference to the height of the acromion was measured in standard anteroposterior radiographs. The mean follow-up was 27 months in the MITR group and 30 months in the HP group. No statistically significant differences were found between the MITR group and the HR group in terms of VAS score (0.4 ± 0.6 vs 0.7 ± 0.6, P = 0.138), UCLA Shoulder score (33.9 ± 2.5 vs 33.7 ± 1.5, P = 0.843), or CMS (95.7 ± 7.3 vs 93.7 ± 6.6, P = 0.400). No redislocation was identified in the HP group, while redislocation occurred in 1 of 16 (6.3%) patients in the MITR group. One patient in the HP group (5.3%) had acromial osteolysis, while no acromial osteolysis was found in the MITR group. No other adverse events, such as infections, tunnel widening, fractures, or implant-related complications, were observed. Both procedures provided satisfactory results. The HP procedure provided better reduction, while the MITR procedure provided a slightly lower tendency of pain. Long-term follow-up is needed to investigate the clinical outcomes and radiological outcomes of both groups.

Spiral artery remodeling is an important physiological process in the pregnant uterus which increases blood flow to the fetus. Impaired spiral artery remodeling contributes to preeclampsia, a major disease in pregnancy. Corin, a transmembrane serine protease, is up-regulated in the pregnant uterus to promote spiral artery remodeling. To date, the mechanism underlying uterine corin up-regulation remains unknown. Here we show that Krüppel-like factor (KLF) 17 is a key transcription factor for uterine corin expression in pregnancy. In cultured human uterine endometrial cells, KLF17 binds to the CORIN promoter and enhances the promoter activity. Disruption of the KLF17 gene in the endometrial cells abolishes CORIN expression. In mice, Klf17 is up-regulated in the pregnant uterus. Klf17 deficiency prevents uterine Corin expression in pregnancy. Moreover, Klf17-deficient mice have poorly remodeled uterine spiral arteries and develop gestational hypertension and proteinuria. Together, our results reveal an important function of KLF17 in regulating Corin expression and uterine physiology in pregnancy.

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Background. Doxorubicin (DOX) is a commonly used chemotherapeutic drug but is limited in clinical applications by its cardiotoxicity. Neiguan acupoint (PC6) is a well-recognized acupoint for the treatment of cardiothoracic disease. However, whether acupuncture at PC6 could be effective in preventing DOX-induced cardiotoxicity is still unknown. Methods. A set of experiments were performed with myocardial cells, wild type, inducible nitric oxide synthase knockout (iNOS-/-), and myocardial-specific ablation arginase 2 (Myh6-ARG 2-/-) mice. We investigated the protective effect and the underlying mechanisms for electroacupuncture (EA) against DOX-induced cardiotoxicity by echocardiography, immunostaining, biochemical analysis, and molecular biotechnology in vivo and in vitro analysis. Results. We found that DOX-mediated nitric oxide (NO) production was positively correlated with the iNOS level but has a negative correlation with the arginase 2 (ARG 2) level in both myocardial cells and tissues. Meanwhile, EA at PC6 alleviated cardiac dysfunction and cardiac hypertrophy in DOX-treated mice. EA at PC6 blocked the upregulation of NO production in accompanied with the downregulated iNOS and upregulated ARG 2 levels in myocardial tissue induced by DOX. Furthermore, knockout iNOS prevented cardiotoxicity and EA treatment did not cause the further improvement of cardiac function in iNOS-/- mice treated by DOX. In contrast, deficiency of myocardial ARG 2 aggravated DOX-induced cardiotoxicity and reduced EA protective effect. Conclusion. These results suggest that EA treatment at PC6 can prevent DOX-induced cardiotoxicity through modulating NO production by modulating the iNOS/ARG 2 balance in myocardial cells.

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