Cardioprotective effects of sinomenine in myocardial ischemia/reperfusion injury in a rat model

BackgroundIschemia reperfusion (I/R) play an imperative role in the expansion of cardiovascular disease. Sinomenine (SM) has been exhibited to possess antioxidant, anticancer, anti-inflammatory, antiviral and anticarcinogenic properties. The aim of the study was scrutinized the cardioprotective effect of SM against I/R injury in rat.MethodsRat were randomly divided into normal control (NC), I/R control and I/R + SM (5, 10 and 20 mg/kg), respectively. Ventricular arrhythmias, body weight and heart weight were estimated. Antioxidant, inflammatory cytokines, inflammatory mediators and plasmin system indicator were accessed.ResultsPre-treated SM group rats exhibited the reduction in the duration and incidence of ventricular fibrillation, ventricular ectopic beat (VEB) and ventricular tachycardia along with suppression of arrhythmia score during the ischemia (30 and 120 min). SM treated rats significantly (P < 0.001) altered the level of antioxidant parameters. SM treatment significantly (P < 0.001) repressed the level of creatine kinase MB (CK-MB), creatine kinase (CK) and troponin I (Tnl). SM treated rats significantly (P < 0.001) repressed the tissue factor (TF), thromboxane B2 (TXB2), plasminogen activator inhibitor 1 (PAI-1) and plasma fibrinogen (Fbg) and inflammatory cytokines and inflammatory mediators.ConclusionOur result clearly indicated that SM plays anti-arrhythmia effect in I/R injury in the rats via alteration of oxidative stress and inflammatory reaction.     

1例直肠癌患者术后继发腹壁多处坏死性软组织感染的护理

总结1例直肠癌患者术后继发腹壁多处坏死性软组织感染的护理经验。护理要点：感染性休克的早期识别和有效控制;坏死性软组织感染的识别及护理,控制全身性感染再次发生;分阶段落实个体化镇痛,改善疼痛症状;分阶段动态落实营养支持方案;实施全程心理干预。经过122 d的精心护理,8处伤口全部愈合,患者恢复良好。     

Thermochromic Tissue-Mimicking Phantoms for Thermal Ablation Based on Polyacrylamide Gel

In recent years, thermal ablation has played an increasingly important role in treating various tumors in the clinic. A practical thermochromic phantom model can provide a favorable platform for clinical thermotherapy training of young physicians or calibration and optimization of thermal devices without risk to animals or human participants. To date, many tissue-mimicking thermal phantoms have been developed and are well liked, especially the polyacrylamide gel (PAG)–based phantoms. This review summarizes the PAG-based phantoms in the field of thermotherapy, details their advantages and disadvantages and provides a direction for further optimization. The relevant physical parameters (such as electrical, acoustic, and thermal properties) of these phantoms are also presented in this review, which can assist operators in a deeper understanding of these phantoms and selection of the proper recipes for phantom fabrication.     

Anomaly of cornea and ocular adnexa in spinster homolog 2 (Spns2) knockout mice

Spinster 2 (Spns2) is a transporter that pumps sphingosine-1-phosphate (S1P), a bioactive lipid mediator synthesized in the cytoplasm, out of cells into the inter cellular space. S1P is a signal that modulates cellular behavior during embryonic development, inflammation and tissue repair, etc. A Spns2-null (KO) mouse is born with failure of eyelid closure (eyelid-open-at birth; EOB) and develop corneal fibrosis in adulthood. It remains elusive whether corneal lesion is caused by exposure to keratitis (lagophthalmos) of EOB phenotype or the loss of Spns2 directly perturbs the corneal tissue morphogenesis and intra-eyelid structures. Therefore, we investigated differences between the cornea and ocular adnexa morphogenesis in KO and wild-type (WT) embryos and adults as well.The loss of Spns2 perturbs cornea morphogenesis during embryonic development as early as E16.5 besides EOB phenotype. Histology showed that the corneal stroma was thinner with less extracellular matrix accumulation, e.g., collagen and keratocan in the KO mouse. Epithelial stratification, expression of keratin 12 and formation of desmosomes and hemidesmosomes were also perturbed in these KO corneas. Lacking Spns2 impaired morphogenesis of the Meibomian glands and of orbicularis oculi muscles. KO glands were labeled for ELOVL4 and PPARγ and were Oil-Red O-positive, suggesting KO acinar cells possessed functionality as the glands.This is the first report on the roles of Spns2 in corneal and Meibomian gland morphogenesis. Corneal tissue destruction in an adult KO mouse might be due to not only lagophthalmos but also to an impaired morphogenesis of cornea, Meibomian glands, and orbicularis oculi muscle.     

Stem cells for babies and their surgeons: The future is now

Pediatric surgeons are ideal allies for the translation of basic science including stem cell therapies. In the spirit of Robert E. Gross, of applying creative solutions to pediatric problems with technical expertise, we describe the impending cellular therapies that may be derived from stem and progenitor cells. Understanding the types and capabilities of stem and progenitor cells is important for pediatric surgeons to join and facilitate progress for babies. We are developing an induced pluripotent stem cell therapy for enteric neuropathies such as Hirschsprung disease that might be helpful for children in the near future. Our goals, which we hope to share with other surgeons and scientists, include working to establish safe clinical trials and meeting regulatory standards in a thoughtful way that balances patients need and unknown risks.     

CYP2C19*3基因多态性对癫痫患者奥卡西平活性代谢产物MHD浓度的影响

目的：分析CYP2C19*3基因多态性与癫痫患者奥卡西平（oxcarbazepine，OXC）活性代谢产物10，11-二氢-10-羟基卡马西平（monohydroxycarbazepine，MHD）血药浓度的相关性。方法：纳入120例OXC单药治疗1个月以上且症状控制良好的癫痫患者，采集清晨服药前空腹血，采用高效液相色谱法测定MHD稳态谷浓度。通过PCR和sanger测序判定患者CYP2C19*3基因型。结果：120例癫痫患者快代谢患者64例，MHD血浆浓度为（18.17±7.34）μg·mL^-1；中代谢型患者36例，MHD血浆浓度为（19.31±9.17）μg·mL^-1；慢代谢型患者20例，MHD血浆浓度为（25.79±7.51）μg·mL^-1，3种基因型的MHD浓度有显著性差异（F=7.077，P=0.0013）。多因素分析显示，日剂量作为影响血药浓度的重要指标呈现出显著相关性（P<0.05）。结论：CYP2C19*3基因多态性影响MHD血药浓度，并且日剂量越高，MHD血药浓度越大，两者成显著正相关，临床应进行血药浓度监测。     

Hemorrhage promotes chronic adverse remodeling in acute myocardial infarction: a T1, T2 and BOLD study

Hemorrhage is recognized as a new independent predictor of adverse outcomes following acute myocardial infarction. However, the mechanisms of its effects are less understood. The aim of our study was to probe the downstream impact of hemorrhage towards chronic remodeling, including inflammation, vasodilator function and matrix alterations in an experimental model of hemorrhage. Myocardial hemorrhage was induced in the porcine heart by intracoronary injection of collagenase. Animals (N = 18) were subjected to coronary occlusion followed by reperfusion in three groups (six/group): 8 min ischemia with hemorrhage (+HEM), 45 min infarction with no hemorrhage (I ? HEM) and 45 min infarction with hemorrhage (I + HEM). MRI was performed up to 4 weeks after intervention. Cardiac function, edema (T₂, T₁), hemorrhage (T₂*), vasodilator function (T₂ BOLD), infarction and microvascular obstruction (MVO) and partition coefficient (pre‐ and post‐contrast T₁) were computed. Hemorrhage was induced only in the +HEM and I + HEM groups on Day 1 (low T₂* values). Infarct size was the greatest in the I + HEM group, while the +HEM group showed no observable infarct. MVO was seen only in the I + HEM group, with a 40% occurrence rate. Function was compromised and ventricular volume was enlarged only in the hemorrhage groups and not in the ischemia‐alone group. In the infarct zone, edema and matrix expansion were the greatest in the I + HEM group. In the remote myocardium, T₂ elevation and matrix expansion associated with a transient vasodilator dysfunction were observed in the hemorrhage groups but not in the ischemia‐alone group. Our study demonstrates that the introduction of myocardial hemorrhage at reperfusion results in greater myocardial damage, upregulated inflammation, chronic adverse remodeling and remote myocardial alterations beyond the effects of the initial ischemic insult. A systematic understanding of the consequences of hemorrhage will potentially aid in the identification of novel therapeutics for high‐risk patients progressing towards heart failure.     

An insight into electrical resistivity of white matter and brain tumors

BackgroundThere is a lack of information regarding electrical properties of white matter and brain tumors.ObjectiveTo investigate the feasibility of in-vivo measurement of electrical resistivity during brain surgery and establish a better understanding of the resistivity patterns of brain tumors in correlation to the white matter.MethodsA bipolar probe was used to measure electrical resistivity during surgery in a prospective cohort of patients with brain tumors. For impedance measurement, the probe applied a constant current of 0.7 μA with a frequency of 140 Hz. The measurement was performed in the white matter within and outside peritumoral edema as well as in non-enhancing, enhancing and necrotic tumor areas. Resistivity values expressed in ohmmeter (Ω1m) were compared between different intracranial tissues and brain tumors.ResultsNinety-two patients (gliomas WHO II:16, WHO III:10, WHO IV:33, metastasis:33) were included. White matter outside peritumoral edema had higher resistivity values (13.3 ± 1.7 Ω1m) than within peritumoral edema (8.5 ± 1.6 Ω1m), and both had higher values than brain tumors including non-enhancing (WHO II:6.4 ± 1.3 Ω1m, WHO III:6.3 ± 0.9 Ω1m), enhancing (WHO IV:5 ± 1 Ω1m, metastasis:5.4 ± 1.3 Ω1m) and necrotic tumor areas (WHO IV:3.9 ± 1.1 Ω1m, metastasis:4.3 ± 1.3 Ω1m), p=<0.001. No difference was found between low-grade and anaplastic gliomas, p = 0.808, while resistivity values in both were higher than the highest values found in glioblastomas, p = 0.003 and p = 0.004, respectively.ConclusionsThe technique we applied enabled us to measure electrical resistivity of white matter and brain tumors in-vivo presumably with a significant effect with regard to dielectric polarization. Our results suggest that there are significant differences within different areas and subtypes of brain tumors and that white matter exhibits higher electrical resistivity than brain tumors.