A Novel 3D-Printed Device for Precise Percutaneous Placement of Cannulated Compression Screws in Human Femoral Neck Fractures.

BACKGROUND: The aim of this study was to investigate the application of computer-aided design and 3D printing technology for percutaneous fixation of femoral neck fractures using cannulated compression screws. METHODS: Using computed tomography data, an individualized proximal femur model was created with a 3D printer. The reduction of the femoral neck fracture and the placement of the cannulated compression screws were simulated on a computer. A 3D printing guide plate was designed to match the proximal femur. After demonstrating the feasibility of the 3D model before the surgical procedure, the guide needles and cannulated compression screws were inserted with the aid of the 3D-printed guide plate. RESULTS: During the procedure, the 3D-printed guide plate for each patient matched the bone markers of the proximal femur. With the aid of the 3D-printed guide plate, three cannulated compression screws were accurately inserted into the femoral neck to treat femoral neck fractures. After screw placement, intraoperative X-ray examination showed results that were consistent with the preoperative design. The time taken to complete the procedure in the guide plate group was 35.3 ± 2.1 min, the intraoperative blood loss was 6.3 ± 2.8 mL, and X-ray fluoroscopy was only performed 9.1 ± 3.5 times. Postoperative radiographs showed adequate reduction of the femoral neck fractures. The entry point, entry direction, and length of the three cannulated compression screws were consistent with the preoperative design, and the screws did not penetrate the bone cortex. CONCLUSION: Using computer-aided design and 3D printing technology, personalized and accurate placement of cannulated compression screws can be realized for the treatment of femoral neck fractures. This technique can shorten the time required for the procedure and reduce damage to the femoral neck cortex, intraoperative bleeding, and the exposure of patients and healthcare staff to radiation.

Shikonin Ameliorates LPS-Induced Cardiac Dysfunction by SIRT1-Dependent Inhibition of NLRP3 Inflammasome.

Shikonin (SHI) is an anti-inflammatory agent extracted from natural herbs. It is still unknown whether SHI ameliorates lipopolysaccharide (LPS)-induced cardiac dysfunction. This study aims to explore the protective effects of SHI on LPS-induced myocardial injury and its mechanism. The LPS-induced cardiac dysfunction mouse model was employed to investigate the protective effects of SHI. In the present study, we found that SHI treatment improved the survival rate and cardiac function and remarkably ameliorated the release of inflammatory cytokines and macrophage infiltration in heart tissue of LPS-treated mice. SHI also reduced lactate dehydrogenase (LDH) and cardiac troponin (cTn) release, cell inflammation, and apoptosis in LPS plus adenosine triphosphate (ATP)-treated H9c2 cells. In addition, SHI significantly upregulated silent information regulator 1 (SIRT1) expression and suppressed the upregulation of NOD-like receptor protein 3 (NLRP3), cleaved caspase-1, and caspase-1 activity in heart tissues induced by LPS. Meanwhile, we got the same results in LPS plus ATP-treated H9c2 cells in vitro. Further, SIRT1 inhibitor or siRNA partially blocked SHI-mediated upregulation of SIRT1 expression and downregulation of NLRP3, cleaved caspase-1, and caspase-1 activity in heart tissues induced by LPS. Therefore, we conclude that SHI ameliorates LPS-induced cardiac dysfunction by inhibiting SIRT1-dependent activation of NLRP3 inflammasomes and might be a promising therapeutic strategy for the treatment of LPS-induced cardiac dysfunction.

Association of Plasma Pentraxin-3 Levels on Admission with In-hospital Mortality in Patients with Acute Type A Aortic Dissection.

BACKGROUND: Acute aortic dissection is a life-threatening cardiovascular emergency. Pentraxin-3 (PTX3) is proposed as a prognostic marker and found to be related to worse clinical outcomes in various cardiovascular diseases. This study sought to investigate the association of circulating PTX3 levels with in-hospital mortality in patients with acute Type A aortic dissection (TAAD). METHODS: A total of 98 patients with TAAD between January 2012 and December 2015 were enrolled in this study. Plasma concentrations of PTX3 were measured upon admission using a high-sensitivity enzyme-linked immunosorbent assay system. Patients were divided into two groups as patients died during hospitalization (Group 1) and those who survived (Group 2). The clinical, laboratory variables, and imaging findings were analyzed between the two groups, and predictors for in-hospital mortality were evaluated using multivariate analysis. RESULTS: During the hospital stay, 32 (33%) patients died and 66 (67%) survived. The patients who died during hospitalization had significantly higher PTX3 levels on admission compared to those who survived. Pearson's correlation analysis demonstrated that PTX3 correlated positively with high-sensitivity C-reactive protein (hsCRP), maximum white blood cell count, and aortic diameter. Multivariate logistic regression analysis demonstrated that PTX3 levels, coronary involvement, cardiac tamponade, and a conservative treatment strategy are significant independent predictors of in-hospital mortality in patients with TAAD. The receiver operating characteristic curve analysis further illustrated that PTX3 levels on admission were strong predictors of mortality with an area under the curve of 0.89. A PTX3 level ≥5.46 ng/ml showed a sensitivity of 88% and a specificity of 79%, and an hsCRP concentration ≥9.5 mg/L had a sensitivity of 80% and a specificity of 69% for predicting in-hospital mortality. CONCLUSION: High PTX3 levels on admission are independently associated with the in-hospital mortality in patients with TAAD.

A Simple Emergency Prediction Tool for Acute Aortic Dissection.

BACKGROUND: A simple emergency risk prediction tool should be developed for clinicians to quickly identify the prognosis of patients with acute aortic dissection. METHODS: We enrolled 280 patients with acute aortic dissection admitted to emergency department between May 2010 and February 2013. Multivariate logistic regression analysis was performed to identify independent predictors of in-hospital death. RESULTS: The in-hospital mortality of our patients with acute aortic dissection was 32.5%, in-hospital deaths with surgery less than the survived (34.1% VS 54.5%). Multivariate analysis identified that age (≥65 years old), Type A, blood pressure (mean systolic blood pressure ≤ 90 mmHg), neutrophil percentage (≥ 80%) and serum D-dimer (≥ 5.0 mg/L) were significant predictors of death. With the simple emergency risk prediction tool, scores of all in-hospital deaths were ≥ 3, whereas almost all of the survivors (97.9%) had scores < 15. A score of 10 offered the best threshold value, with the highest sensitivity (81.3%) and specificity (86.8%). CONCLUSIONS: The in-hospital mortality rate of patients with acute aortic dissection is high and can be predicted. Early surgery would be beneficial for in-hospital survive. This tool should be available for clinicians in the emergency department to quickly identify the prognosis of patients with acute aortic dissection.

[Analysis on an early diagnosis grading model for acute aortic dissection].

OBJECTIVE: To investigate the value of an early diagnosis grading model derived from the clinical manifestation, laboratory and imaging data for the diagnosis of aortic dissection (AD). METHODS: An early diagnosis grading model was established based on the clinical manifestation, laboratory and imaging data from 182 AD patients who admitted to our department during the last 3 years, 184 patients with chest and back pain served as controls. RESULTS: The sensitivity and specificity of diagnosing AD with the score of 5 is 96.7% and 81.0%, respectively. CONCLUSION: The emergency diagnose of AD could be improved based on the established early grading model based on the stabbing and severe pain, rapid blood pressure increase, asymmetry of the blood pressure and/or the pulse, widened aortic knob, mediastinum or descending aorta on X-ray, and significantly increased D-dimmer level.

[Effect of depsides salts from salvia miltiorrhiza on functions of platelet and vascular endothelial cell of patients with chronic obstructive pulmonary disease in acute exacerbation stage].

OBJECTIVE: To investigate the influence of depsides salts from salvia miltiorrhiza (DSM) on the functions of platelet and vascular endothelial cell in severe chronic obstructive pulmonary diseases (COPD) patients with acute exacerbation. METHODS: Forty patients with severe COPD in acute exacerbation stage were randomly divided into two groups: conventional treatment (CT) group and DSM treatment (DSM) group, each consisting of 20 cases, and 20 healthy adults served as control group. All COPD patients were given conventional treatment, while for the patients in DSM group 0.2 g depsides DSM was given through intravenous drip everyday in addition for 2 weeks. The levels of the plasma platelet membrane glycoprotein 140 (GMP140) and von Willebrand factor (vMF) in the blood samples were determined with enzyme linked immunosorbent assay (ELISA) and the level of CD62P/CD61 with flow cytometry (FCM). RESULTS: The level of GMP140 [CT group: (17.51+/-2.75) microg/L, DSM group: (16.94+/-2.57) microg/L], vMF [CT group: (13.64+/-2.37) microg/L, DSM group: (14.14+/-2.17) microg/L] and CD62P/CD61 [CT group: (20.24+/-2.64)% , DSM group: (19.54+/-2.69)%] were elevated significantly in severe COPD patients with acute exacerbation compared to the control group before treatment [(11.21+/-1.11)%, (9.25+/-1.80) microg/L, (6.13+/-1.17) microg/L, all P<0.01]. After intervention, the levels of the above three indexes in both treatment groups were significantly decreased, and the decrease in DSM group [GMP140: (3.91+/- 0.57) microg/L , vWF: (3.86+/-0.71) microg/L, CD62P/CD61: (3.69+/-0.62)%] was more prominent than the CT group [GMP140: (2.30+/-0.33) microg/L, vWF: (2.72+/- 0.45) microg/L , CD62P/CD61: (2.24+/-0.45)%, all P<0.01], but they were higher than normal levels. CONCLUSION: DSM has the effect of inhibiting the activation of vascular endothelial cells and platelet. The medicine may be used to prevent thrombotic diseases.

[Effect of ulinastain on the expression of hemeoxygenase-1 in oleic acid-induced acute lung injury in rats].

OBJECTIVE: To explore the effect of ulinastain on the expression of hemeoxy genase-1 (HO-1) in oil acid-induced acute lung injury in rats. METHODS: The animal model of acute lung injury was established by oil acid. Thirty SD rats were randomly divided into 3 groups: the blank control group (A), the acute lung injury group (B) and the acute lung injury group (C) followed by injecting 100 mL/kg ulinastatin. Each group consisted of 10 rats. Group A were given 0.2 mL/kg natural solution through the trial vein; Group B and C were given 0.2 mL/kg oil-acid through trial vein, while group C were injected 100mL/kg ulinastatin by the peritoneal cavity after injecting oil acid. After 4 hours, the rates of respiration were counted and blood samples were cramped out through the heart puncture for blood gas analysis. The expressions of hemeoxygenase-1 and the pathologic construction changes were determined by HE staining in the lower right lung of rats in the 3 groups. RESULTS: The respiration dysfunction caused by oil acid could be prominently improved by ulinastain. There was only a little expression of hemeoxygenase-1 in the lung of Group A, but the expression increased in Group B and significatively increased in Group C. CONCLUSION: Ulinastatin may protect the rats from acute lung injury through increasing the expression of HO-1.

[Construction and activity evaluation of pSUPER RNAi system that inhibits Smad3].

OBJECTIVE: To construct the expressing vector of siRNA which can inhibit the Smad3 activity. METHODS: Sixty-four bases of 2 pair oligos for hairp in RNA expression which targeted Smad3 gene were chemically synthesized and annealed. pSUPER vector was linearized with BgL II and Hin d III treated with alkaline phosphatase (CIP). Anneled oligos were inserted into the downstream of the treated pSUPER's pol III H1 promoter to construct RNAi plasmid (pSUPER Smad3). Oligos with a scrambled sequence were used as a negative control. pSUPER Smad3 was transfected into human renal tubular epithelial cells (HKC). RESULTS: Recombinant pSUPER Smad3 vector was identified by the digestion with Eco R I and Hin d III, and confirmed by the sequencing analysis with T3 primer. Sixty-four bases had been inserted into the expected site. Furthermore, the insertion sequence was exactly corrected. The activity evaluation indicated that mRNA and protein of Smad3 but not Smad2 were inhibited by pSUPER Smad3 in HKC. CONCLUSION: The pSUPER Smad3 system has been constructed successfully, and has high inhibition and specificity in vitro.