Pour une formation pédagogique des enseignants universitaires algériens

Teaching is certainly a vocation, an art, and a gift. The well-experienced university teacher who does master certain pedagogical qualities owe that to the long working hours, training and acquired experiences. In fact, he has developed naturalized skills in analysis aptitudes, understanding, and acting, and progressively became rich and automated skills. These aptitudes can be deceiving on the ground that becoming a ‘good teacher-pedagogue’ is not acquired through professional immersion, or the mastery of a given discipline – thinking that one can teach it efficiently. Nevertheless, it would – further- be mistaking to think that all teachers possess an “innate gift” to miraculously transmit knowledge from their brains to the learners’. We believe that there is need for thinking, hard labor, and more importantly a university pedagogical training to acquire teaching-know-how

ELECTROCHEMICAL BEHAVIOR AND ANALYSIS OF MONURON HERBICIDE IN WATER USING VOLTAMMETRIC METHODS AND PRE ACTIVATED CARBON PASTE ELECTRODE

This research work dealt with the electrochemical behavior and voltammetric analysis of monuron, a phenyl urea herbicide. The sensitive enhancement of the monuron electrochemical signal, using a pre-activated carbon paste electrode, and the explanation of its mechanism were the main findings of this study. Unlike most used herbicides (linuron, diuron, fenuron, etc), monuron was rarely studied before by electrochemical methods. Indeed the square wave voltammetry allowed to optimize and to analyze monuron in water samples; the results showed two linear ranges of concentration: from 1.98 to 0.39 µg mL-1 and from 0.35 to 0.08 µg mL-1, with detection and quantification limits of LOD= 0.016 µg mL-1 and LOQ= 0.054µg mL-1 respectively. Besides these quantitative results, the anodic oxidation of monuron has been explained by an irreversible adsorption-controlled process, following a “one electron – one proton” mechanism

Use of sugars as alternative to chemical control: trials carried out on thrips associated with olive tree

Foliar spraying of infradoses of sugars (glucose, fructose or sucrose) induces plant resistance to pests that are particularly difficult to combat. These include thrips, which can cause flower abortion, stunting and deformation of olives, resulting in significant crop losses. Randomised block trials were conducted during three years (2017 to 2019), on two cultivars Chemlal and Sigoise, in an olive grove in Batna province (Algeria), with the aim of determining the most effective dose and type of sugar on thrips populations, and to evaluate the effectiveness of combining sugar with chemical treatment, as well as the possibility of reducing the dose of the latter. The results showed that sucrose at a concentration of 100 ppm was the most effective and that the efficacy of sucrose was higher than that of glucose and fructose, on both cultivars tested. The combination of sucrose with insecticide resulted in a synergistic effect and a higher efficacy gain than sucrose alone, and that the efficacy of the combination sucrose + insecticide at low dose D1 was identical to the combination sucrose + insecticide at recommended dose D2. It is therefore possible to reduce the chemical insecticide dose while maintaining good treatment efficacy for the control of these pests

Constitutive expression of clathrin hub hinders elicitor-induced clathrin-mediated endocytosis and defense gene expression in plant cells

AbstractEndocytosis has been recently implicated in the signaling network associated with the recognition of microbes by plants. In a previous study, we showed that the elicitor cryptogein was able to induce clathrin-mediated endocytosis (CME) in tobacco suspension cells. Herein, we investigate further the induced CME by means of a GFP-tagged clathrin light chain and a CME inhibitor, the hub domain of clathrin heavy chain. Hub constitutive expression does affect neither cell growth nor constitutive endocytosis but abolishes cryptogein-induced CME. Such an inhibition has no impact on early events in the cryptogein signaling pathway but reduces the expression of defense-associated genes

Stack or trash? Quality assessment of virtual slides

International audienc

Methods for Establishing a Renal Cell Carcinoma Tumor Spheroid Model With Immune Infiltration for Immunotherapeutic Studies

Tumor spheroids play an increasingly important role in cancer research. Their ability to recapitulate crucial features of tumor biology that are lost in the classically used 2D models along with their relative simplicity and handiness have made them the most studied 3D tumor model. Their application as a theranostic tool or as a means to study tumor-host interaction is now well-established in various cancers. However, their use in the field of Renal Cell Carcinoma (RCC) remains very limited. The aim of this work is to present methods to implement a basic RCC spheroid model. These methods cover the steps from RCC tumor dissociation to spheroid infiltration by immune cells. We present a protocol for RCC dissociation using Liberase TM and introduce a culture medium containing Epithelial Growth Factor and Hydrocortisone allowing for faster growth of RCC primary cells. We show that the liquid overlay technique allows for the formation of spheroids from cell lines and from primary cultures. We present a method using morphological criteria to select a homogeneous spheroid population based on a Fiji macro. We then show that spheroids can be infiltrated by PBMCs after activation with OKT3 or IL-15. Finally, we provide an example of application by implementing an immune spheroid killing assay allowing observing increased spheroid destruction after treatment with PD-1 inhibitors. Thus the straightforward methods presented here allow for efficient spheroid formation for a simple RCC 3D model that can be standardized and infused with immune cells to study immunotherapies

Long-term protection and mechanism of pacing-induced postconditioning in the heart

Brief periods of ventricular pacing during the early reperfusion phase (pacing-induced postconditioning, PPC) have been shown to reduce infarct size as measured after 2 h of reperfusion. In this study, we investigated (1) whether PPC leads to maintained reduction in infarct size, (2) whether abnormal mechanical load due to asynchronous activation is the trigger for PPC and (3) the signaling pathways that are involved in PPC. Rabbit hearts were subjected to 30 min of coronary occlusion in vivo, followed by 6 weeks of reperfusion. PPC consisted of ten 30-s intervals of left ventricular (LV) pacing, starting at reperfusion. PPC reduced infarct size (TTC staining) normalized to area at risk, from 49.0 ± 3.3% in control to 22.9 ± 5.7% in PPC rabbits. In isolated ejecting rabbit hearts, replacing LV pacing by biventricular pacing abolished the protective effect of PPC, whereas ten 30-s periods of high preload provided a protective effect similar to PPC. The protective effect of PPC was neither affected by the adenosine receptor blocker 8-SPT nor by the angiotensin II receptor blocker candesartan, but was abrogated by the cytoskeletal microtubule-disrupting agent colchicine. Blockers of the mitochondrial KATP channel (5HD), PKC (chelerythrine) and PI3-kinase (wortmannin) all abrogated the protection provided by PPC. In the in situ pig heart, PPC reduced infarct size from 35 ± 4 to 16 ± 12%, a protection which was abolished by the stretch-activated channel blocker gadolinium. No infarct size reduction was achieved if PPC application was delayed by 5 min or if only five pacing cycles were used. The present study indicates that (1) PPC permanently reduces myocardial injury, (2) abnormal mechanical loading is a more likely trigger for PPC than electrical stimulation or G-coupled receptor stimulation and (3) PPC may share downstream pathways with other modes of cardioprotection

Acute hyperglycemia abolishes cardioprotection by remote ischemic perconditioning

BACKGROUND: Remote ischemic perconditioning (RIPerC) has a promising therapeutic insight to improve the prognosis of acute myocardial infarction. Chronic comorbidities such as diabetes are known to interfere with conditioning interventions by modulating cardioprotective signaling pathways, such as e.g., mTOR pathway and autophagy. However, the effect of acute hyperglycemia on RIPerC has not been studied so far. Therefore, here we investigated the effect of acute hyperglycemia on cardioprotection by RIPerC. METHODS: Wistar rats were divided into normoglycemic (NG) and acute hyperglycemic (AHG) groups. Acute hyperglycemia was induced by glucose infusion to maintain a serum glucose concentration of 15-20 mM throughout the experimental protocol. NG rats received mannitol infusion of an equal osmolarity. Both groups were subdivided into an ischemic (Isch) and a RIPerC group. Each group underwent reversible occlusion of the left anterior descending coronary artery (LAD) for 40 min in the presence or absence of acute hyperglycemia. After the 10-min LAD occlusion, RIPerC was induced by 3 cycles of 5-min unilateral femoral artery and vein occlusion and 5-min reperfusion. After 120 min of reperfusion, infarct size was measured by triphenyltetrazolium chloride staining. To study underlying signaling mechanisms, hearts were harvested for immunoblotting after 35 min in both the NG and AHG groups. RESULTS: Infarct size was significantly reduced by RIPerC in NG, but not in the AHG group (NG + Isch: 46.27 +/- 5.31 % vs. NG + RIPerC: 24.65 +/- 7.45 %, p < 0.05; AHG + Isch: 54.19 +/- 4.07 % vs. 52.76 +/- 3.80 %). Acute hyperglycemia per se did not influence infarct size, but significantly increased the incidence and duration of arrhythmias. Acute hyperglycemia activated mechanistic target of rapamycine (mTOR) pathway, as it significantly increased the phosphorylation of mTOR and S6 proteins and the phosphorylation of AKT. In spite of a decreased LC3II/LC3I ratio, other markers of autophagy, such as ATG7, ULK1 phopsphorylation, Beclin 1 and SQSTM1/p62, were not modulated by acute hyperglycemia. Furthermore, acute hyperglycemia significantly elevated nitrative stress in the heart (0.87 +/- 0.01 vs. 0.50 +/- 0.04 microg 3-nitrotyrosine/mg protein, p < 0.05). CONCLUSIONS: This is the first demonstration that acute hypreglycemia deteriorates cardioprotection by RIPerC. The mechanism of this phenomenon may involve an acute hyperglycemia-induced increase in nitrative stress and activation of the mTOR pathway

The role of gasotransmitters NO, H S, CO in myocardial ischemia/reperfusion injury and cardioprotection by preconditioning, postconditioning, and remote conditioning

Ischemic heart disease is one of the leading causes of morbidity and mortality worldwide. The development of cardioprotective therapeutic agents remains a partially unmet need and a challenge for both medicine and industry, with significant financial and social implications. Protection of the myocardium can be achieved by mechanical vascular occlusions such as preconditioning (PC) when brief episodes of ischemia/reperfusion are subjected prior to ischemia; postconditioning (PostC) when the brief episodes are subjected at the immediate onset of reperfusion, as well as remote conditioning (RC) when the brief episodes are subjected in another vascular territory. The elucidation of the signaling pathways which underlie the protective effects of PC, PostC and RC would be expected to reveal novel molecular targets for cardioprotection that could be manipulated by pharmacological agents to prevent reperfusion injury. Gasotransmitters including nitric oxide (NO), hydrogen sulphide (H2 S) and carbon monoxide (CO) are a growing family of regulatory molecules which impact on physiological and pathological functions. NO, H2 S and CO share several common properties; they are beneficial at low concentrations but hazardous in higher amounts, they relax smooth muscle cells, inhibit apoptosis, and exert anti-inflammatory effects. In the cardiovascular system, both NO, H2 S and CO induce vasorelaxation, and promote cardioprotection. In this review article, we summarize current knowledge on the role of the gasotransmitters NO, H2 S, and CO in myocardial ischemia/reperfusion injury and cardioprotection provided by conditioning strategies and highlight future perspectives in cardioprotection by NO, H2 S, CO, as well as their donor molecules