Successful pulmonary endarterectomy after heart transplantation

International audienc

An ecotoxicological view on malaria vector control with ivermectin-treated cattle

International audienceMalaria remains an enduring challenge in sub-Saharan Africa, affecting public health and development. Control measures can include the use of insecticides that target adult Anopheles mosquitoes transmitting the malaria-causing Plasmodium parasite. Such mosquitoes can also bite livestock, allowing vector populations to be maintained at levels that enable parasite transmission. Thus, one way to control the spread of malaria includes the use of endectocide-treated livestock which renders the blood of cattle toxic to such mosquito populations. Here we present an ecotoxicological perspective on malaria vector control, using cattle treated with the endectocide ivermectin to target zoophagic and opportunistic Anopheles coluzzii mosquitoes. Our study employs an innovative, long-acting injectable ivermectin formulation with over 6 months of sustained mosquitocidal activity. Robust vector population modelling underscores its promising field effectiveness. Environmental implications (soil sorption and dissipation) of excreted ivermectin and potential ecotoxicological risks to non-target dung organisms in West Africa are discussed, in addition to actionable, locally inspired risk mitigation measures to protect sub-Saharan soils and agroecosystems from chemical pollution. We highlight how ecotoxicology and environmental chemistry improve livestock-based vector control with ivermectin for effective and more sustainable malaria management

Angiotensin 1-7 in an experimental septic shock model.

Alterations in the renin-angiotensin system have been implicated in the pathophysiology of septic shock. In particular, angiotensin 1-7 (Ang-(1-7)), an anti-inflammatory heptapeptide, has been hypothesized to have beneficial effects. The aim of the present study was to test the effects of Ang-(1-7) infusion on the development and severity of septic shock.info:eu-repo/semantics/publishe

Myocardial effects of angiotensin II compared to norepinephrine in an animal model of septic shock.

Angiotensin II is one of the vasopressors available for use in septic shock. However, its effects on the septic myocardium remain unclear. The aim of the study was to compare the effects of angiotensin II and norepinephrine on cardiac function and myocardial oxygen consumption, inflammation and injury in experimental septic shock.info:eu-repo/semantics/publishe

Additional file 1 of Myocardial effects of angiotensin II compared to norepinephrine in an animal model of septic shock

Additional file 1. Figure S1. Pressure-volume loop illustration. Table S1. Primers used for real-time quantitative polymerase chain reaction (RTQ-PCR) in porcine myocardial tissue. Table S2. Hemodynamic variables in the three groups at the different study time-points. *p-value <0.05 between NE and Ang II. †p-value < 0.05 between NE and Sham. ‡p-value < 0.05 between Ang II and Sham. P-value < 0.05 compared to baseline for NE (§), Ang II (ll) and Sham (**) groups. HR: heart rate; MAP: mean arterial pressure; SV: stroke volume; CO: cardiac output; RAP: right atrial pressure; LVEDV: left ventricular end diastolic volume; LVESV: left ventricular end systolic volume; LVEDP: left ventricularend diastolic pressure; EF: ejection fraction; PRSW: preload recruitable stroke work; Emax: left ventricular maximal elastance; Ea: effective arterial elastance; Ea/Emax: left ventriculo-arterial coupling; V30: LV volume at 30 mmHg on the End Diastolic Pressure Volume Relationship; V100: LV volume at 100 mmHg on the End Systolic Pressure Volume Relationship; NE: norepinephrine; Ang: angiotensin PV loop analysis was obtained at baseline, fluids, vasopressor 1 and vasopressor 2. Table S3. Biological and oxygenation values in the three groups at the different study timepoints. *p-value <0.05 between NE and Ang II. †p-value < 0.05 between NE and Sham. ‡p-value < 0.05 between Ang II and Sham. p-value < 0.05 compared to baseline for NE (§), Ang II (ll) and Sham (**) groups. CO2 gap: veno-arterial difference in CO2 partial pressure; SVO2: mixed venous oxygen saturation; BE: base excess; IL: interleukin; TNF: tumor necrosis factor; NE: norepinephrine; Ang: angiotensin. Table S4. Respiratory variables. Results are presented as mean + SD. *p-value between NE and Ang II groups. †p-value < 0.05 between NE and Sham groups. ‡p-value < 0.05 between Ang II and Sham groups. p-value < 0.05 compared to baseline for NE (§), Ang II (ll) and Sham (**) groups. PaO2: Arterial partial pressure of oxygen; FiO2 fraction of oxygen inspired; Pplat: plateau pressure; Crs:compliance of the respiratory system; EtCO2: end-tidal carbon dioxide; PaCO2: arterial partial pressure of carbon dioxide. Table S5. Blood gas analysis. Values are presented as mean + SD. *p-value between NE and angiotensin II group. †p-value < 0.05 between NE and Sham group. ‡p-value < 0.05 between angiotensin II and Sham group. P-value < 0.05 compared to baseline for NE (§), angiotensin II (ll) and Sham (**) group. Hb: hemoglobin; Ht: hematocrit. PaO2: arterial partial pressure of oxygen. PaCO2: arterial partial pressure of carbon dioxide. Table S6. Biological variables. Values are expressed as mean ± SD. *p-value between NE and Ang II groups. †p-value < 0.05 between NE and Sham groups. ‡p-value < 0.05 between Ang II and Sham groups. p-value < 0.05 compared to baseline for NE (§), Ang II (ll) and Sham (**) groups. ASAT: Aspartate aminotransferase; ALAT Alanine aminotransferase; LDH: Lactate dehydrogenase. Figure S2. A. Left ventricular mRNA expression of molecules implicated in Ca2+ handling and contractile apparatus [ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2 (SERCA2A) and phospholamban (PLB)] B. LV mRNA expression of the ratio Bax/Bcl2 in norepinephrine (black bars) and angiotensin II groups. *pvalue< 0.05. C. Cardiac apoptotic rate: ratio of apoptotic nuclei (TUNEL-positive or brown nuclei) to total nuclei (brown+blue nuclei) (x100 to be expressed as a percentage). D. mRNA expression of cell adhesion molecules (ICAM1, 2 and VCAM1) and eNOS, iNOS, nNOS in norepinephrine and angiotensin II groups compared to sham group. Figure S3. Fold Changes expressed in % between baseline and vasopressor 2 time point

Additional file 2 of Myocardial effects of angiotensin II compared to norepinephrine in an animal model of septic shock

Additional file 2. Uncropped gels

Additional file 1 of Neutralization of extracellular histones by sodium-Β-O-methyl cellobioside sulfate in septic shock

Additional file 1. Additional methods, microcirculation results, histological analysis, and secondary analysis with dead animals excluded

Can we forecast the effects of climate changeon entomophagous biological control agents?

The worldwide climate has been changing rapidly over the past decades. Air temperatures have been increasing in most regions and will probably continue to rise for most of the present century, regardless of any mitigation policy put in place. Although increased herbivory from enhanced biomass production and changes in plant quality are generally accepted as a consequence of global warming, the eventual status of any pest species will mostly depend on the relative effects of climate change on its own versus its natural enemies' complex. Because a bottom-up amplification effect often occurs in trophic webs subjected to any kind of disturbance, natural enemies are expected to suffer the effects of climate change to a greater extent than their phytophagous hosts/preys. A deeper understanding of the genotypic diversity of the populations of natural enemies and their target pests will allow an informed reaction to climate change. New strategies for the selection of exotic natural enemies and their release and establishment will have to be adopted. Conservation biological control will probably become the keystone for the successful management of these biological control agents. © 2013 Society of Chemical Industr