Pulmonary Nocardiosis as an Opportunistic Infection in COVID-19.

Unlabelled: Secondary bacterial pneumonia infection is frequent in COVID-19 patients. are responsible for opportunistic pulmonary infections especially after steroid treatment. We describe a case of pulmonary nocardiosis following critical COVID-19 pneumonia in an 83-year-old male.

Comparison of cardiac output optimization with an automated closed-loop goal-directed fluid therapy versus non standardized manual fluid administration during elective abdominal surgery: first prospective randomized controlled trial.

An intraoperative automated closed-loop system for goal-directed fluid therapy has been successfully tested in silico, in vivo and in a clinical case-control matching. This trial compared intraoperative cardiac output (CO) in patients managed with this closed-loop system versus usual practice in an academic medical center. The closed-loop system was connected to a CO monitoring system and delivered automated colloid fluid boluses.

SAR131675, a potent and selective VEGFR-3-TK inhibitor with antilymphangiogenic, antitumoral, and antimetastatic activities.

SAR131675 is a potent and selective VEGFR-3 inhibitor. It inhibited VEGFR-3 tyrosine kinase activity and VEGFR-3 autophosphorylation in HEK cells with IC(50) values of 20 and 45 nmol/L, respectively. SAR131675 dose dependently inhibited the proliferation of primary human lymphatic cells, induced by the VEGFR-3 ligands VEGFC and VEGFD, with an IC(50) of about 20 nmol/L.

Impaired alpha1-adrenergic responses in aged rat hearts.

To determine age-related changes in the cardiac effect of alpha1-adrenergic stimulation, both cardiomyocyte Ca2+-transient and cardiac protein kinase C (PKC) activity were measured in 3-month- (3MO) and 24-month- (24MO) old Wistar rats. Ca2+ transients obtained under 1 Hz pacing by microfluorimetry of cardiomyocyte loaded with indo-1 (405/480 nm fluorescence ratio) were compared in control conditions (Kreb's solution alone) and after alpha1-adrenergic stimulation (phenylephrine or cirazoline, an alpha1-specific agonist). PKC activity and PKC translocation index (particulate/total activity) were also assayed before and after alpha1-adrenergic stimulation.

Interaction of chelerythrine with inositol phosphate metabolism.

Chelerythrine, a potent inhibitor of protein kinase C (PKC), was evaluated for its effect on inositol phosphate (IP) metabolism in newborn rat cardiomyocytes in culture. In a first step, we evaluated the effect of chelerythrine on IP accumulation in basal conditions. For a 10(-4) M dose, 5-phosphatase activity (which dephosphorylates IP3 into IP2) was completely blocked and we observed a large increase in IP accumulation limited to IP2 without any increase in IP3, strongly suggesting that chelerythrine at this dose modifies IP metabolism.

Detection of bradykinin B1 receptors in rat aortic smooth muscle cells.

The tritiated bradykinin B1 receptor agonist [3H]des-Arg(10)-kallidin bound to a single class of high-affinity binding sites (K(d) = 0.5 +/- 0.16 nM; B(max) = 15,000 +/- 8,000 sites/cell) on cultured rat aortic smooth muscle cells.

Characterisation of the effects of SR146131, a novel non-peptide CCK(1) receptor agonist, on IMR-32 human neuroblastoma cells.

The effect of ¿2-[4-(4-chloro-2, 5-dimethoxy-phenyl)-5-[2-cyclohexyl-ethyl)-thiazol-2-ylcarbamoy l]-5, 7-dimethyl-indol-1-yl¿-acetic acid (SR146131), a novel non-peptide agonist of cholecystokinin (CCK) CCK(1) receptors, was compared to the effect of sulphated cholecystokinin octapeptide (CCK-8-S) on CCK(1) receptors of the human neuroblastoma cell line IMR-32. SR146131 inhibited [125I]CCK-8-S binding to IMR-32 cells at nanomolar concentrations. SR146131 and CCK-8-S increased intracellular free Ca(2+) levels ([Ca(2+)](i)) in the same concentration range (EC(50)=6+/-2.

Propofol-induced modifications of cardiomyocyte calcium transient and sarcoplasmic reticulum function in rats.

Background: Propofol is considered to be an anesthetic agent with few or no negative inotropic effects. This study evaluated a possible direct depressant effect of propofol on sarcoplasmic reticulum Ca2+ accumulation and cardiomyocytes.

Methods: The effects of propofol on intracellular Ca2+ transients were evaluated in isolated rat cardiomyocytes using a microfluorometric technique with Indo-1.

Induction of cardiac nitric oxide synthase 2 in rats exposed to chronic hypoxia.

Induction of nitric oxide synthase (NOS2, also designated as iNOS) in the heart is known to occur in response to various stimuli. It is not known, however, whether in vivo hypoxia leads to cardiac NOS2 induction. We thus investigated the effects of normobaric hypoxia (10% O(2)for 8, 15 and 21 days) on NOS2 protein expression and enzyme activity in rat right ventricle (RV) and left ventricle (LV).

Cytosolic myocardial calcium modulation by ATP-dependent potassium channel openers and NO donors.

The goal of this study was to evaluate, in rat cardiomyocytes, the effects on cytosolic calcium of a pure K-adenosine triphosphate (ATP) channel opener, aprikalim, and those of nicorandil, a dual-acting agent that increases cyclic guanosine monophosphate (cGMP) levels and opens K-ATP channels. These effects were compared with those of a pure NO donor, 3-morpholino-sydnonimine (Sin-1). Ventricular myocytes were isolated from the hearts of adult rats.

SR142948A is a potent antagonist of the cardiovascular effects of neurotensin.

The novel compound SR142948A was compared with SR48692 as an antagonist of neurotensin-induced cardiovascular effects both in vitro and in vivo. SR142948A inhibited [125I]-neurotensin binding [median inhibitory concentration (IC50) = 0.24 +/- 0.

Protein kinase C activity and expression in rabbit left ventricular hypertrophy.

Protein Kinase C (PKC) is implicated in the induction of myocardial hypertrophy. Recent studies showed an increased activity and expression of PKC in rat left ventricular hypertrophy, but we demonstrated a decreased PKC activity and content in rabbit heart failure. The present study was designed to evaluate whether these differences were due to species or model differences.

Neurotensin induces the release of prostacyclin from human umbilical vein endothelial cells in vitro and increases plasma prostacyclin levels in the rat.

Human umbilical vein endothelial cells express high affinity neurotensin receptors which are coupled to phosphoinositide turnover and 45Ca2+ efflux (Schaeffer et al., 1995. J.

[Kidney varices: an unusual location].

The authors report the case of a 40-year-old woman who presented with very large right renal varices. Computed tomography and arteriography showed that these varices were situated on the convex surface of the kidney, in front of its anterior surface, and drained venous blood derived from the renal parenchyma. These varices were probably secondary to undiagnosed renal vein thrombosis.

Role of protein phosphatase in the regulation of Na+-K+-ATPase by vasopressin in the cortical collecting duct.

In the cortical collecting duct (CCD), arginin vasopressin (AVP) has been shown to increase the number and activity of basolateral Na+-K+-ATPase by recruiting or activating a latent pool of pumps. However, the precise mechanism of this phenomenon is still unknown. The aim of this study was to investigate whether this AVP-induced increase in basolateral Na+-K+-ATPase could depend on a dephosphorylation process.

Characteristics of a rat cortical collecting duct cell line that maintains high transepithelial resistance.

This study describes the establishment of a rat kidney cortical collecting duct (CCD) clonal cell line (RCCD1 cells) that maintains high transepithelial resistance and specific hormonal sensitivities. Immortalized cells were obtained by infection of primary cultured CCD cells with the wild-type simian virus 40. Grown on Petri dishes, RCCD1 cells are organized as monolayers of cuboid cells separated by tight junctions and form domes.

[Emphysematous pyelonephritis. A case medically treated].

Authors report on a case of emphysematous pyelonephritis in a woman affected with diabetes and renal failure. In order to avoid chronic dialysis, no nephrectomy was performed and the patient was treated only with drugs. Full recovery was obtained, without worsening of the renal function.

Regional alterations of left ventricular contraction and inotropic reserve in conscious dogs with heart failure.

Objective: The goal was to examine left ventricular (LV) regional contraction alterations and especially, regional inotropic reserve changes in tachycardia-induced heart failure (HF).

Methods: Eleven dogs were chronically instrumented to measure LV pressure and its first time derivative (LV dP/dt), left atrial and aortic pressures and to measure antero-apical (AS), -basal (BS) and postero-apical (PS) subendocardial segmental contractions by ultrasonic crystals. Dobutamine (5-15 micrograms/kg per min) and left atrial pacing (150-240 beats/min) were performed in the control state (C) and in HF induced by chronic right ventricular pacing (240 beats/min, 3 weeks).

In situ mitochondrial function in volume overload- and pressure overload-induced cardiac hypertrophy in rats.

Objectives: Little comparative information is available on mitochondrial function changes during experimentally-induced hypertrophy. Respiratory control mechanisms are not exactly the same in situ and in isolated mitochondria. This study assessed in situ mitochondrial function in two myocardial hypertrophy models.

Platelet-activating factor (PAF) is not an essential component of the cascade leading to smooth muscle cell proliferation following vascular injury.

In order to evaluate the relative importance platelet-activating factor (PAF) in the proliferative process leading to restenosis, the effect of SR 27417, a novel highly potent PAF receptor antagonist, on PAF-induced rabbit aortic smooth muscle cell (SMC) proliferation and intimal hyperplasia in rabbit carotid arteries subjected to air-drying endothelial injury was investigated. When added to low concentrations of foetal calf serum, PAF showed a dose-dependent mitogenic effect with regard to rabbit arterial SMC. SR 27417 inhibited PAF-induced SMC growth (IC50 = 2.

Human umbilical vein endothelial cells express high affinity neurotensin receptors coupled to intracellular calcium release.

The binding of 125I-neurotensin (NT) to human umbilical vein endothelial cell monolayers was studied. At 20 degrees C, 125I-NT bound to a single class of binding sites with a dissociation constant of 0.23 +/- 0.

Evidence for the existence of two different ADP-binding sites on rat platelets.

[3H]-2-Methylthio-ADP ([3H]-2-MeS-ADP), a stable analogue of ADP bound to one type of specific binding sites on rat platelets (KD = 0.77 +/- 0.07 nM, Bmax = 160 +/- 11 fmol/10(8) cells).

Thrombin induces endothelial cell growth via both a proteolytic and a non-proteolytic pathway.

Binding of 125I-thrombin to human umbilical vein endothelial cells (HUVECs) was specifically displaced by the synthetic tetradecapeptide SFLLRNPNDKYEPF, named thrombin receptor agonist peptide (TRAP), which has recently been described as a peptide mimicking the new N-terminus created by cleavage of the thrombin receptor, and F-14, a tetradecapeptide representing residues 365-378 of the human alpha-thrombin B chain. Binding of 125I-TRAP to HUVECs was time-dependent, reversible and saturable, showing high affinity (KD = 1.5 +/- 0.

Malformin-A1 inhibits the binding of interleukin-1 beta (IL1 beta) and suppresses the expression of tissue factor in human endothelial cells and monocytes.

Malformin-A1, a cyclic pentapeptide of microbial origin, antagonized in a competitive manner the binding of 125I-IL1 beta (interleukin-1 beta) to human monocytes and cultured human umbilical vein endothelial cells (HUVEC) with IC50 values (doses which reduce specific binding by 50%) of 250 +/- 80 and 230 +/- 25 nM, respectively (N = 3). IL1 increased in a dose-dependent manner the expression of tissue factor, a ubiquitous membrane-anchored glycoprotein that initiates blood coagulation at the surface of HUVEC and human monocytes. Malformin-A1 strongly inhibited IL1-induced tissue factor expression in HUVEC and monocytes with IC50 values of 420 +/- 35 and 105 +/- 25 nM, respectively (N = 3), and reduced IL1-induced expression of intercellular adhesion molecule-1 (ICAM-1, CD54) on HUVEC (IC50 = 125 +/- 18 nM) (N = 4).

Binding of [3H]-2-methylthio ADP to rat platelets--effect of clopidogrel and ticlopidine.

Thienopyridine compounds, including ticlopidine and clopidogrel, have been found to selectively inhibit adenosine 5' diphosphate (ADP)-induced platelet aggregation and adenylyl cyclase ex vivo, but the mechanism of their antiplatelet action remains to be determined. This study was aimed at investigating the effect of clopidogrel and ticlopidine on the binding of [3H]-2-methylthio- adenosine-5'-diphosphate (2-MeS-ADP) to rat platelets. Binding of [3H]-2-MeS-ADP to rat platelets was time-dependent and saturable.