The objective of this study was to determine the visco-hyperelastic constitutive law of brain tissue under dynamic impacts. A method combined by finite element simulations and optimization algorithm was employed for the determination of material variables. Firstly, finite element simulations of brain tissue dynamic uniaxial tension, with a maximum stretch rate of 1.3 and strain rates of 30 s–1 and 90 s–1, were developed referring to experimental data. Then, fitting errors between the engineering stress-strain curves predicted by simulations and experimental average curves were assigned as objective functions, and the multi-objective genetic algorithm was employed for the optimation solution. The results demonstrate that the brain tissue finite element models assigned with the novel obtained visco-hyperelastic material law could predict the brain tissue’s dynamic mechanical characteristic well at different loading rates. Meanwhile, the novel material law could also be applied in the human head finite element models for the improvement of the biofidelity under dynamic impact loadings.
Fibrinogen (Fg) in human plasma plays an important role in hemostasis, vascular repair and tissue integrity. The surface chemistry of extracellular matrix or biological materials affects the orientation and distribution of Fg, and changes the exposure of integrin binding sites, thereby affecting its adhesion function to platelets. Here, the quantity, morphology and side chain exposure of Fg adsorbed on hydrophilic, hydrophobic and avidin surfaces were measured by atomic force microscopy (AFM) and flow cytometry (FCM), then the rolling behavior of platelets on Fg was observed through a parallel plate flow chamber system. Our results show that the hydrophobic surface leads to a large amount of cross-linking and aggregation of Fg, while the hydrophilic surface reduces the adsorption and accumulation of Fg while causing the exposure and spreading of the α chain on Fg and further mediating the adhesion of platelets. Fg immobilized by avidin / biotin on hydrophilic surface can maintain the monomer state, avoid over exposure and stretching of α chain, and bind to the platelets activated by the A1 domain of von Willebrand factor instead of inactivated platelets. This study would be helpful for improving the blood compatibility of implant biomaterials and reasonable experimental design of coagulation in vitro.
The human gut microbiota regulates many host pathophysiological processes including metabolic, inflammatory, immune and cellular responses. In recent years, the incidence and mortality of lung cancer have increased rapidly, which is one of the biggest challenges in the field of cancer treatment today, especially in non-small cell lung cancer. Animal models and clinical studies have found that the gut microbiota of non-small cell lung cancer patients is significantly changed compared with the healthy people. The gut microbiota and metabolites can not only play a pro-cancer or tumor suppressor role by regulating immune, inflammatory responses and so on, but also be related with radiotherapy and chemotherapy of non-small cell lung cancer and the resistance of immunotherapy. Therefore, gut microbiota and related metabolites can be both potential markers for early diagnosis and prognosis in patients with non-small cell lung cancer and novel therapeutic targets for targeted drugs. This study will review the latest research progress of effect of gut microbiota on non-small cell lung cancer, and provide a new diagnosis and treatment ideas for non-small cell lung cancer.
Lung cancer has a high morbidity and mortality, and invasion is one of the major factors that cause recurrence and death in lung cancer patients. Tumor-associated macrophages (TAMs) are cells that have the potential to secrete cytokines, growth hormones, inflammatory substrates, and protein hydrolases, which are associated with the growth, invasion and metastasis of tumors. In this article, we will explore the various chemicals that are manufactured to promote the invasion of lung cancer, as well as the numerous clinical therapeutic features that TAMs possess in the treatment of lung cancer. In addition, we look at the possibility that TAMs might be beneficial in the treatment of lung cancer. We have an innovative investigation of the huge variety of complex substances generated by TAMs, with the goal of determining whether or not the molecules under investigation have the potential to serve as new therapeutic targets. Throughout the whole of the presentation, a significant focus is placed on doing in-depth research to ascertain whether TAMs have the capability to reinforce as viable carriers for unique and creative medications. This not only provides novel concepts for the creation of new targeted therapies but also leads to the development of brand-new, cutting-edge methods for the manufacture of individualized medicines and drug carriers.
ObjectiveTo summary the application and effectiveness of the posterior radial collateral artery (PRCA) compound flap in reconstruction of soft tissue defect after tongue cancer excision. MethodsBetween August 2011 and October 2011, 5 patients with squamous cell carcinoma underwent tongue defects reconstruction with compound flap with extended lateral arm free flap (ELAFF) and triceps muscle flap (TMF) after ablation in one-stage. All patients were male with an average age of 59 years (range, 43-71 years). The disease duration was 25-60 days (mean, 42 days). After extended resection, 3 cases had 1/3 tongue and mouth floor defect, and 2 cases had 1/2 tongue and mouth floor defect. The size of ELAFF ranged from 7 cm × 5 cm to 9 cm × 5 cm, and the size of TMF ranged from 3 cm × 3 cm to 4 cm × 4 cm. The donor sites were directly sutured. ResultsAll compound flaps survived. The wounds at donor sites and recipient sites healed primarily. The patients were followed up 6 months. After operation, the tongue had good appearance and motion; the patients had clear voice and no dysphagia. No recurrence was observed during follow-up. Local numbness appeared at the donor sites, but the function of the elbows was normal. ConclusionThe application of the compound flap of ELAFF and TMF based on PRCA perforator is a better option to reconstruct tongue defects for its reliable blood supply, appropriate thickness, easy operative procedures, and less complication.
ObjectiveTo establish a model of portal hypertension with hypersplenism in SD rats by portal vein binding combined with splenic vein ligation. MethodsSixty healthy male SD rats were randomly divided into three groups: sham operation group （only laparotomy, n=20）, portal vein binding group (only binding, n=20), and portal vein binding combined with splenic vein ligation group (combined operation group, n=20). The counts of platelet, erythrocyte, and leukocyte were examined just before operation and once a week after operation for 7 weeks. Portal pressure, shortaxis, and longaxis diameter of spleen were examined just before operation and seven weeks after operation. At the seventh week, all the animals were sacrificed, spleen index and pathology changes of each group were examined. ResultsErythrocyte and platelet counts in combined operation group were significantly lower than those in the other two groups on the third week （Plt;0.05）, and there was no significant difference in leukocyte count among three groups （Pgt;0.05）. Compared with the preoperative value, portal pressure increased significantly on the seventh week in both portal vein binding group and combined operation group, and was higher than that in the sham operation group （Plt;0.05）. The two diameters of spleen also increased significantly in combined operation group on the seventh week （Plt;0.05）, and were larger than those in the other two groups （Plt;0.05）. The same result was found in spleen index （Plt;0.05）. Typical pathological changes of hypersplenism presented only in combined operation group on the seventh week after operation. ConclusionsPortal vein binding combined with splenic vein ligation can induce experimental secondary hypersplenism successfully. This procedure is simple and stable, and helpful to the scientific research.
【摘要】 目的 了解老年門診患者癡呆癥的發生率及其相關危險因素。方法 對2007年7月—2009年5月,年齡≥60歲644例門診患者進行簡易智能表(MMSE簡易評分)評價,并收集患者文化程度、吸煙、基礎疾病、用藥史進行危險因素相關分析。結果 樣本人群老年癡呆癥的發病率為16.0%。與老年性癡呆密切相齡、高血壓、腦卒中史、聽力受損和視力受損。結論 高齡、高血壓、腦卒中是老年性癡呆主要的危險因素,當前的醫療衛生機構應該積極有效地采取措施,控制可變因素,減少老年性癡呆的發生。
Objective To systemically review the efficacy and safety of strontium chloride for bone metastases from prostate cancer. Methods PubMed, The Cochrane Library, EMbase, VIP, CBM, CNKI and WanFang Data databases were electronically searched to collect randomized controlled trials (RCTs) about strontium chloride for bone metastases from prostate cancer from inception to November 2016. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies, then, meta-analysis was performed by using RevMan 5.3 software. Results A total of 7 RCTs involving 1 532 patients were included. The results of meta-analysis showed that strontium chloride was superior to placebo in the rate of pain relief (RR=1.79, 95%CI 1.35 to 2.37, P<0.000 1), but more likely to cause slight leucopenia (Peto OR=5.02, 95%CI 1.49 to 16.95,P=0.009). However, no significant difference was found in overall survival time between two groups (RR=0.87, 95%CI 0.58 to 1.30, P=0.49). In addition, strontium chloride was superior to radiotherapy in rate of bone pain relief (RR=1.28, 95%CI 1.12 to 1.47, P=0.0004), but it would cause thrombocy (Peto OR=2.61, 95%CI 1.04 to 6.57, P=0.04). Conclusion Current evidence shows that the strontium chloride is superior to placebo in the rate of pain relief, but it will cause slight leucopenia. The strontium chloride is superior to radiotherapy in rate of bone pain relief. Due to limited quality and quantity of the included studies, more high quality studies are needed to verify the above conclusion.
ObjectiveTo investigate the effect of maresin-1 (MaR1) on lung inflammation and MAPK signaling pathway in asthmatic mice.MethodsTwenty-four female BALB/c mice were randomly divided into normal group, asthma model group, MaR1 group and dexamethasone group. The asthma model was successfully established by using ovalbumin (OVA) combined with aluminum hydroxide, and then MaR1 and dexamethasone were respectively given to asthmatic mice. Serum, bronchoalveolar lavage fluid (BALF) and lung tissue were collected for further analysis. Pathological changes of lung tissue in mice were detected by hematoxylin-eosin and periodic acid-Schi?. Proportion of inflammatory cells in BALF classified by Swiss-Giemsa staining. Th2-related inflammatory cytokines, interleukin (IL)-4, IL-5, IL-13 and IgE in serum and BALF were detected by enzyme linked immunosorbent assay. The protein concentration of p-p38 and p-JNK in lung tissues were detected by Western blot.ResultsCompared with the normal group, the asthma model group had increased both airway inflammation and the number of goblet cells significantly (P<0.05). The number of various inflammatory cells in BALF had also increased significantly (P<0.05). The levels of IL-4, IL-5 and IL-13 in BALF and IgE and OVA-specific-IgE in serum were significantly increased (P<0.05). The protein contents of p-p38 and p-JNK in lung tissues were significantly increased (P<0.05). Compared with the asthma model group, both MaR1 and dexamethasone group had reduced inflammation and mucus secretion in lung tissue, number of inflammatory cells in BALF (P<0.05), levels of related inflammatory cytokines in BALF and IgE in serum (P<0.05), and expression of p-p38 and p-JNK proteins in lung tissue (P<0.05).ConclusionsMaR1 can inhibit the production and release of both Th2-related inflammatory cytokines and IgE, effectively reduce the inflammatory response and mucus production in lung tissues of asthmatic mice, with similar effect to dexamethasone. The mechanism may be related to the down-regulation of MAPKs signaling pathway.
Objective To observe the expression of S100A8 and S100A9 in alveolar macrophages (AMs) of chronic obstructive pulmonary disease (COPD) rats, and explore the effect on the release of inflammatory mediators from AMs in COPD rats. Methods Twelve adult male Wistar rats were randomly divided into a normal control group and a COPD group. The COPD model was established by exposing the rats to cigarette smoke and intratracheal injection of endotoxin for 1 month. The pathological changes of lung tissue of rats were observed under light microscope. Total cells counts and the number of AMs, lymphocytes, neutrophils in bronchoalveolar lavage fluid (BALF) of two groups were examined by Wright's staining methods. Rat AMs from the control group and the COPD group were isolated and cultured, and then treated with different doses of S100A8 and S100A9 for 6 hours and 12 hours. The levels of interleukin (IL)-8, IL-6 and tumour necrosis factor-α (TNF-α) in the AMs supernatants were measured by enzyme linked immunosorbent assay. The expression of S100A8 and S100A9 mRNA in AMs of rats were observed by in situ hybridization. The immunohistochemical method was used to observed the expression of S100A8/A9 protein of AMs. Results After cigarette smoking combined with intratracheal injection of endotoxin for 1 month, the lung tissue of rats showed typical pathological changes of COPD. Total cell counts and the number of AMs, lymphocytes, neutrophils in BALF of the COPD rats were significantly higher than those of the normal rats (P<0.05). Among them, the increase in the number of AMs was the most obvious. Compared with the control group, the expression of S100A8 mRNA, S100A9 mRNA and S100A8/A9 protein in AMs of the COPD group were up-regulated significantly (P<0.05). After the AMs of COPD rats were treated with S100A8 and S100A9, the contents of IL-8, IL-6 and TNF-α in AMs supernatants increased significantly in a time- and dose-dependent manner. When the AMs were treated with the same dose of S100A8 and S100A9 for the same time, the levels of IL-8, IL-6 and TNF-α in the AMs supernatant of the COPD group were higher than those of the normal control group. Conclusions The expression of S100A8 and S100A9 in cultured COPD rat AMs is significantly increased. S100A8 and S100A9 can promote the secretion and release of inflammatory factors IL-6, IL-8 and TNF-α from AMs of COPD rats in a time and dose-dependent manner. The effects of S100A8 and S100A9 on the secretion of IL-6, IL-8 and TNF-α in AM of COPD rats are significantly enhanced compared with those of normal rats.