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Background: Maxillary expansion (ME) is a common practice in orthodontics that aims to increase the constricted maxillary arch width. Relapse often occurs, however, and better treatment strategies are needed. In order to develop a more effective method, this study was designed to further examine the process of tissue remodeling during ME, to identify the changes in expression of several proteins of interest, and to clarify the molecular mechanism responsible for tissue remodeling.

OBJECTIVE: This study investigated levels of interleukin (IL)-34, a proinflammatory cytokine, in patients with coronary artery disease (CAD). METHODS: Following coronary artery angiography, 91 patients with CAD (including stable and unstable angina pectoris) were divided into two groups, the CAD group (coronary artery stenosis ≥ 50%) and the control group (coronary artery stenosis < 50%). Serum levels of factors including IL-34 and high sensitivity C-reactive protein (hs-CRP) were measured. RESULTS: IL-34 and hs-CRP levels were significantly higher in the CAD group than in the control group (191.3 ± 17.9 pg/ml versus 125.4 ± 14.8 pg/ml and 3.08 ± 1.81 mg/ml versus 1.42 ± 1.01 mg/ml, respectively), with a significantly positive correlation between IL-34 and hs-CRP levels in the CAD group. Multiple regression analysis showed that IL-34 and hs-CRP levels were independent predictors of CAD (IL-34: odds ratio [OR] 2.073, 95% confidence intervals (CI) 1.419, 2.672; hs-CRP: OR 1.878, 95% CI 1.172, 2.531). CONCLUSIONS: IL-34 levels were significantly increased in patients with CAD, and positively correlated with hs-CRP levels, suggesting that IL-34 may be an independent predictor of CAD.

Objective To evaluate the effects of early administration of Sacubitril/Valsartan (Sac/Val) in patients with ST-elevation myocardial infarction after primary percutaneous coronary intervention (pPCI). Methods This prospective, controlled, single-center study randomized 186 ST-segment elevation myocardial infarction patients to one of the following two groups: Sac/Val group: early administration of Sac/Val within 24 hours after pPCI; control group: conventional angiotensin-converting enzyme inhibitors (ACEI) application. The creatine Kinase (CK) peak after the surgery, the incidence of acute heart failure during hospitalization, level of NT-proBNP and left ventricular ejection fraction (LVEF) measured by ultrasound before discharge and soluble suppression of tumorigenicity2 (sST2), LVEF, infarct size determined by single photon emission computed tomography (SPECT), readmission rate within 6 months were recorded and compared between two groups. Results Compared to the control group, Sac/Val could decrease the CK peak and the incidence of acute heart failure after pPCI; the level of NT-proBNP was lower and LVEF was higher before discharge in the Sac/Val group. After 6 months, the patients who had taken Sac/Val had a higher LVEF, a smaller infarct size determined by SPECT, lower sST2 and readmission rate. Conclusion Patients with ST-elevation myocardial infarction after primary percutaneous coronary intervention could benefit from early administration of Sacubitril/Valsartan, the effect was superior to conventional ACEI.

Splenomegaly and pancytopenia are common in Wilson’s disease (WD) and splenectomy is one of the conventional treatments for splenomegaly and the associated pancytopenia. However, splenectomy remained controversial for hypersplenism in WD as it was reported that splenectomy leaded to serious emotional and neurological deterioration in WD patients with hypersplenism. In the current study, we present our experiences in 70 WD patients with hypersplenism who had undergone splenectomy, outlining the safety and efficacy of splenectomy in WD. The clinical database of 70 WD patients with hypersplenism who had undergone splenectomy in our hospital between 2009 and 2013 were reviewed and followed-up regularly. Before splenectomy, all the patients accepted a short period of anti-copper treatment with intravenous sodium 2, 3-dimercapto-1-propane sulfonate (DMPS). All the patients demonstrated a marked improvement in platelet and leucocyte counts after splenectomy. No severe postoperative complication was observed. In particular, none of the 37 patients with mixed neurologic and hepatic presentations experienced neurological deterioration after splenectomy, and none of the patients with only hepatic presentations newly developed neurological symptoms. During the one year follow-up period, no patient presented hepatic failure or hepatic encephalopathy, no hepatic patient newly developed neurological presentations, and only 3 patients with mixed neurologic and hepatic presentations suffered neurological deterioration and these 3 patients had poor compliance of anti-copper treatment. Quantative analysis of the neurological symptoms in the 37 patients using the Unified Wilson’s Disease Rating Scale (UWDRS) showed that the neurological symptoms were not changed in a short-term of one week after splenectomy but significantly improved in a long-term of one year after splenectomy. Additionally, compared to that before splenectomy, the esophageal gastric varices in most patients significantly improved one year after splenectomy. Thus, we may conclude that splenectomy is a safe and effective therapeutic measure for hypersplenism in WD patients who had been preoperatively treated with DMPS for powerful anti-copper therapy.

These findings imply that stimulating PC6 can change the amplitude of the intrinsic cortical activity of the brain. In particular, a continuous and temporally consistent effect of acupuncture within PCC not the common brain circuit of pain including ACC and cerebellum was observed. Considering the cognitive functions and deficits of the relevant areas in mild cognitive impairment and Alzheimer disease, acupuncture on PC6 could potentially affect both psychiatric and neurological disorders. Thus, stimulating PC6 may be a candidate method for improving cognitive impairment.

BackgroundAfter acute myocardial infarction, the recovery of ischemic myocardial blood flow may cause myocardial reperfusion injury, which reduces the efficacy of myocardial reperfusion. Ways to reduce and prevent myocardial ischemia/reperfusion (I/R) injury are of great clinical significance in the treatment of patients with acute myocardial infarction. TRAF1 (tumor necrosis factor receptor–associated factor 1) is an important adapter protein that is implicated in molecular events regulating immunity, inflammation, and cell death. Little is known about the role and impact of TRAF1 in myocardial I/R injury.Methods and Results TRAF1 expression is markedly induced in wild‐type mice and cardiomyocytes after I/R or hypoxia/reoxygenation stimulation. I/R models were established in TRAF1 knockout mice and wild type mice (n=10 per group). We demonstrated that TRAF1 deficiency protects against myocardial I/R–induced loss of heat function, inflammation, and cardiomyocyte death. In addition, overexpression of TRAF1 in primary cardiomyocytes promotes hypoxia/reoxygenation‐induced inflammation and apoptosis in vitro. Mechanistically, TRAF1 promotes myocardial I/R injury through regulating ASK1 (apoptosis signal‐regulating kinase 1)–mediated JNK/p38 (c‐Jun N‐terminal kinase/p38) MAPK (mitogen‐activated protein kinase) cascades.ConclusionsOur results indicated that TRAF1 aggravates the development of myocardial I/R injury by enhancing the activation of ASK1‐mediated JNK/p38 cascades. Targeting the TRAF1–ASK1–JNK/p38 pathway provide feasible therapies for cardiac I/R injury.

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