Bilan initial d’imagerie de l’adénocarcinome pancréatique : données de la littérature sur la place actuelle de la tomographie par émission de positons au 18F-fluorodéoxyglucose (TEP FDG)

In pancreatic adenocarcinoma, initial imaging is essential to better select patients for surgery. Recent literature analysis of F18-Fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET) in pancreatic adenocarcinoma is summarized in the present article. Performances of FDG PET in the fields of lymph node involvement, metastatic involvement and therapeutic efficacy assessment are described for its correct use in pancreatic adenocarcinoma.     

Electromechanical model of excitable tissue to study reentrant cardiac arrhythmias

We introduce the concept of a contracting excitable medium that is capable of conducting non-linear waves of excitation that in turn initiate contraction. Furthermore, these kinematic deformations have a feedback effect on the excitation properties of the medium. Electrical characteristics resemble basic models of cardiac excitation that have been used to successfully study mechanisms of reentrant cardiac arrhythmias in electrophysiology. We present a computational framework that employs electromechanical and mechanoelectric feedback to couple a three-variable FitzHugh–Nagumo-type excitation-tension model to the non-linear stress equilibrium equations, which govern large deformation hyperelasticity. Numerically, the coupled electromechanical model combines a finite difference method approach to integrate the excitation equations, with a Galerkin finite element method to solve the equations governing tissue mechanics. We present example computations demonstrating various effects of contraction on stationary rotating spiral waves and spiral wave break. We show that tissue mechanics significantly contributes to the dynamics of electrical propagation, and that a coupled electromechanical approach should be pursued in future electrophysiological modelling studies.     

IRM-2近交系小鼠对电离辐射抗性的研究

目的观察IRM-2小鼠对电离辐射的耐受性.方法分析测定了IRM-2小鼠对137Csγ射线的LD50及经4.0Gy137Csγ射线照射后不同时间外周血白细胞、骨髓有核细胞总数、骨髓细胞DNA含量和脾结节的变化,并与亲代小鼠ICR和615进行了比较.结果用不同剂量的137Csγ射线照射后,IRM-2小鼠对γ射线的LD50比ICR和615小鼠分别高1.73～1.57Gy和1.44Gy;外周血白细胞数和骨髓有核细胞总数、骨髓细胞DNA含量下降的幅度小且恢复得快;CFU-S的增加也较ICR和615小鼠明显.结论IRM-2小鼠比一般的纯系和杂交品系小鼠具有更强的辐射抗性.     

Evidence for the involvement of the RNA-dependent protein kinase (PKR) in the induction of human cytotoxic T lymphocytes against a synthetic peptide of HIV-1 by regulatory RNA

The studies on the inhibitory effect exerted by Cholera Toxin (CT) on cell growth and proliferation indicate a remarkable heterogeneity of cell response suggesting that the inhibition represents the final event of many different ways or mechanisms . After CT binding, cAMP accumulation may not occur (as in L1210 leukemia cells) or, when occurring (as in SR-4987 stromal cells), may not be coupled with the antiproliferative effect of CT. In WEHI-3B cells CT binds a Gal-GalNac-GM1b receptor and the anticlonogenic effect of CT seems correlated with cAMP accumulation.To demonstrate the central role of cAMP in WEHI-3B cells, starting from the sensitive cell strain we selected and established a clone of WEHI-3B resistant to CT. This revertant clone (WEHI-3B/CT/REV) is currently cultured in the absence of CT and in the proliferation assay shows a dramatic resistance (>46,000 than the parental cells). Stimulation of WEHI-3B/CT/REV cells by cholera toxin failed to enhance cAMP and the ganglioside-CT binding studied on Thin Layer Chromatography (TLC) blots showed that the resistant cells lost the spot correspondent to the migration of Gal-GalNac-GM1b ganglioside. Both the lines respond at the same level to the adenylate cyclase stimulation by forskolin and the incorporation of GM1a did not decrease the resistance of WEHI-3B/CT/REV. These data confirm that Gal-GalNac-GM1b is the most important functional receptor for CT in WEHI-3B cells able to transduce the signal by enhancing cAMP which in turn inhibits cell proliferation (probably by cAMP dependent protein kinase activation). Our study describes the first cell line resistant to CT originated from a susceptible parental strain and provides a new interesting cell model for studying the cAMP dependent mechanisms involved in cell growth regulation.     

脑梗塞的临床表现与CT显示的关系

探讨脑梗塞的临床表现和ＣＴ显示关系。回顾性分析５８例脑梗塞病例的临床资料和ＣＴ图像。ＣＴ显示脑梗塞病灶８小时内阳性显示率最低,５％（１／２０）;２４￣４８小时阳性显示率最高,７８．２％（４３／５５）。脑干及小脑部位梗塞ＣＴ不易显示,ＭＲＩ能明确诊断。根据临床表现和熟悉脑梗塞的病理过程,采取合理的ＣＴ检查和复查时机极为重要,从而提高脑梗塞检查和诊断中ＣＴ检查的敏感性和准确性。提高临床的诊治率,减少后     

CT平扫对肠坏死诊断价值

目的:探讨CT平扫对肠坏死诊断价值,总结肠管坏死征象。方法:分析98例可疑肠坏死患者CT平扫图像,所有患者均经手术证实或未能及时治疗死亡患者CT平扫影像,总结、分析影像特点。结果:全部患者中40例患者存在肠坏死,肠壁厚度改变,包括29例肠壁增厚,8例肠壁菲薄,5例表现为肠壁密度减低,3例表现为肠壁密度增加,25例表现肠管扩张,8例表现肠管塌陷,36例肠管内积液,其中34例见气液平面,4例仅见积气,5例肠壁内见气泡影,38例见腹腔积液,10例见系膜水肿,2例见肠系膜血管密度增高,1例肠系膜静脉内气体,1例门静脉内气体,5例见腹腔游离气体。结论:多排螺旋CT平扫对肠坏死部位及范围的评价有较高的价值,同时CT平扫能明确病因,为及早治疗打下良好基础。     

Direct Mouse Trauma/Burn Model of Heterotopic Ossification

Heterotopic ossification (HO) is the formation of bone outside of the skeleton which forms following major trauma, burn injuries, and orthopaedic surgical procedures. The majority of animal models used to study HO rely on the application of exogenous substances, such as bone morphogenetic protein (BMP), exogenous cell constructs, or genetic mutations in BMP signaling. While these models are useful they do not accurately reproduce the inflammatory states that cause the majority of cases of HO. Here we describe a burn/tenotomy model in mice that reliably produces focused HO. This protocol involves creating a 30% total body surface area partial thickness contact burn on the dorsal skin as well as division of the Achilles tendon at its midpoint. Relying solely on traumatic injury to induce HO at a predictable location allows for time-course study of endochondral heterotopic bone formation from intrinsic physiologic processes and environment only. This method could prove instrumental in understanding the inflammatory and osteogenic pathways involved in trauma-induced HO. Furthermore, because HO develops in a predictable location and time-course in this model, it allows for research to improve early imaging strategies and treatment modalities to prevent HO formation.     

Post-natal heart adaptation in a knock-in mouse model of calsequestrin 2-linked recessive catecholaminergic polymorphic ventricular tachycardia

Cardiac calsequestrin (CASQ2) contributes to intracellular Ca²⁺ homeostasis by virtue of its low-affinity/high-capacity Ca²⁺ binding properties, maintains sarcoplasmic reticulum (SR) architecture and regulates excitation–contraction coupling, especially or exclusively upon β-adrenergic stimulation. Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmogenic disease associated with cardiac arrest in children or young adults. Recessive CPVT variants are due to mutations in the CASQ2 gene. Molecular and ultra-structural properties were studied in hearts of CASQ2^R33Q/R33Q and of CASQ2^−/− mice from post-natal day 2 to week 8. The drastic reduction of CASQ2-R33Q is an early developmental event and is accompanied by down-regulation of triadin and junctin, and morphological changes of jSR and of SR-transverse-tubule junctions. Although endoplasmic reticulum stress is activated, no signs of either apoptosis or autophagy are detected. The other model of recessive CPVT, the CASQ2^−/− mouse, does not display the same adaptive pattern. Expression of CASQ2-R33Q influences molecular and ultra-structural heart development; post-natal, adaptive changes appear capable of ensuring until adulthood a new pathophysiological equilibrium.