Evaluation of a patient-centred, needs-based approach to support shared decision making in contraceptive counselling: the COCO study.

Objectives: The Contraceptive Counselling (COCO) study tested whether a structured approach to assessing patient needs and expectations improved method choice and satisfaction with the contraceptive decision-making process.

Methods: Physicians and women were invited to complete needs-based contraceptive counselling sessions using a structured questionnaire. Physicians recorded the individual responses online; women evaluated the process using an immediate post-consultation questionnaire and then via a structured online interview 6 months later.

Concise Review: MSC Adhesion Cascade-Insights into Homing and Transendothelial Migration.

Mesenchymal stem cells (MSCs) are promising candidates for adult cell therapies in regenerative medicine. To fully exert their potential, efficient homing and migration toward lesion sites play an important role. Local transplantation deposits MSC in spatial proximity to the lesion, but often requires invasive procedures.

Specific Mechanisms Underlying Right Heart Failure: The Missing Upregulation of Superoxide Dismutase-2 and Its Decisive Role in Antioxidative Defense.

Aims: Research into right ventricular (RV) physiology and identification of pathomechanisms underlying RV failure have been neglected for many years, because function of the RV is often considered less important for overall hemodynamics and maintenance of blood circulation. In view of this, this study focuses on identifying specific adaptive mechanisms of the RV and left ventricle (LV) during a state of chronic nitric oxide (NO) deficiency, one of the main causes of cardiac failure. NO deficiency was induced in rats by L-NAME feeding over a 4 week period.

Astrocytic mitochondrial membrane hyperpolarization following extended oxygen and glucose deprivation.

Astrocytes can tolerate longer periods of oxygen and glucose deprivation (OGD) as compared to neurons. The reasons for this reduced vulnerability are not well understood. Particularly, changes in mitochondrial membrane potential (Δψ(m)) in astrocytes, an indicator of the cellular redox state, have not been investigated during reperfusion after extended OGD exposure.

Continuous adenosine A2A receptor antagonism after focal cerebral ischemia in spontaneously hypertensive rats.

Antagonism of the adenosine A2A receptor (A2AR) has been shown to elicit substantial neuroprotective properties when given immediately after cerebral ischemia. We asked whether the continuous application of a selective A2AR antagonist within a clinically relevant time window will be a feasible and effective approach to treat focal cerebral ischemia. To answer this question, we subjected 20 male spontaneously hypertensive rats to permanent middle cerebral artery occlusion and randomized them equally to a verum and a control group.

Object-based analysis of astroglial reaction and astrocyte subtype morphology after ischemic brain injury.

The astrocytic response to ischemic brain injury is characterized by specific alterations of glial cell morphology and function. Various studies described both beneficial and detrimental aspects of activated astrocytes, suggesting the existence of different subtypes. We investigated this issue using a novel object-based approach to study characteristics of astrogliosis after stroke.

Changes in T2 relaxation time after stroke reflect clearing processes.

Background And Purpose: CT and MR imaging techniques are frequently used for the diagnosis and progress monitoring of ischemic stroke in clinical practice and research. After stroke, both methods are characterized by a transient pseudo-normalized imaging signal, the so-called fogging phenomenon. This study evaluates potential pathophysiological changes associated with fogging, as well as its influence on the correct determination of the ischemic lesion in a rat stroke model.

Intravenous human umbilical cord blood transplantation for stroke: impact on infarct volume and caspase-3-dependent cell death in spontaneously hypertensive rats.

Transplantation of human umbilical cord blood cells (HUCBC) produces reliable behavioral and morphological improvements in animal models of stroke. However, the mechanisms of action still have not been fully elucidated. The aim of the present study is the evaluation of potential neuroprotective effects produced by HUCBC in terms of reduced infarct volume and caspase-3-dependent cell death.

Hypoxia tolerance in animals: biology and application.

Many invertebrates and ectothermic vertebrates successfully cope with a fluctuating supply of ambient oxygen-and consequently, a highly variable tissue oxygenation-through increasing their antioxidant barriers. During chronic deprivation of oxygen, however, the hypometabolic defense mode of the fruit fly Drosophila, the hypoxia-induced behavioral hypothermia of the crayfish Pacifastacus leniusculus, and the production of ethanol during anoxia by the crucian carp Carassius carassius all indicate that these animals are also capable of utilizing a suite of genetic and physiological defenses to survive otherwise lethal reductions in tissue oxygenation. Normally, much of an organism's gene response to hypoxia is orchestrated via the hypoxia-inducible transcription factor HIF.

Ribose treatment reduced the infarct size and improved heart function after myocardial infarction in rats.

Objective: In this study the effect of ribose on heart function and infarct-size was analyzed 6 h after myocardial infarction (MI) in rats.

Methods: Continuous i.v.

Crucial role of interleukin-6 in the development of norepinephrine-induced left ventricular remodeling in mice.

Background: Elevated serum concentration of interleukin (IL)-6 is a predictor for poor prognosis in congestive heart failure. It was shown previously in rats, that IL-6 expression in the left ventricle (LV) was followed by LV hypertrophy.

Methods: Using IL-6 deficient mice (IL-6(-/-)), we studied the role of IL-6 in a model of norepinephrine (NE)-induced LV hypertrophy.

S100A1 deficiency results in prolonged ventricular repolarization in response to sympathetic activation.

S100A1 is a Ca(2+)-binding protein and predominantly expressed in the heart. We have generated a mouse line of S100A1 deficiency by gene trap mutagenesis to investigate the impact of S100A1 ablation on heart function. Electrocardiogram recordings revealed that after beta-adrenergic stimulation S100A1-deficient mice had prolonged QT, QTc and ST intervals and intraventricular conduction disturbances reminiscent of 2 : 1 bundle branch block.

Cord blood cell therapy alters LV remodeling and cytokine expression but does not improve heart function after myocardial infarction in rats.

Objective: In this study the ability of unrestricted somatic stem cells (USSC) and mononuclear cord blood cells (MN-CBC) was tested to improve heart function and left ventricular (LV) remodeling after myocardial infarction (MI).

Methods: The cells were delivered by i.v.

Tissue inhibitor of matrix metalloproteinase-1 in norepinephrine-induced remodeling of the mouse heart.

Background: Matrix metalloproteinases (MMPs) play an important role in myocardial remodeling. Their activity is regulated by the tissue inhibitors of metalloproteinases (TIMPs). The present study analyzed the contribution of changes in functional and molecular parameters to early cardiac remodeling in mice hearts.

Contrast enhanced echocardiographic follow-up of cardiac remodeling and function after myocardial infarction in rats.

Echocardiography is a reliable and commonly used method to examine cardiac diseases. Recent employment of modern technologies provides new opportunities to study left ventricular (LV) remodeling after myocardial infarction (MI) also in small rodents. LV volumes as most important prognostic parameters can be estimated by noncontrast enhanced echocardiography in rats from M-mode or single cross sections only.

Embryonic endothelial progenitor cells expressing a broad range of proangiogenic and remodeling factors enhance vascularization and tissue recovery in acute and chronic ischemia.

Clonal embryonic endothelial progenitor cells (eEPCs) isolated from embryonic day 7.5 mice home specifically to hypoxic areas in mouse tumor metastases but spare normal organs and do not form carcinomas. Based on these results, we assessed the potential of eEPCs to enhance vascularization and limit organ dysfunction after ischemia in syngenic and xenotypic organisms.

Heart function and molecular biological parameters are comparable in young adult and aged rats after chronic myocardial infarction.

Objective: To test the hypothesis that IL-1beta and IL-6 play a pivotal role after myocardial infarction (MI) particularly in aged rats.

Methods: Chronic MI was induced in young adult (3.5 months) and aged (18 months) female Sprague-Dawley rats by ligation of the left coronary artery.

Hematopoietic stem cells do not repair the infarcted mouse heart.

Objective: Recent reports suggest that hematopoietic stem cells (HSC) can transdifferentiate into cardiomyoctes and contribute to myocardial regeneration after injury. This concept has recently been challenged by studies in which bone-marrow (BM)-derived cells do not acquire a cardiac phenotype after direct injection into ischemic myocardium.

Methods: In this study, we analyzed the effect of increased circulating adult BM cells by stimulation with stem cell factor (SCF; 200 microg/kg/d for 7 days) and granulocyte-colony stimulating factor (G-CSF, 50 microg/kg/d for 7 days) or by peripheral delivery of isolated adult BM cells on morphological and hemodynamic parameters of mouse hearts 6 weeks after induction of chronic myocardial infarction (MI).

Norepinephrine-induced changes in cardiac transforming growth factor-beta isoform expression pattern of female and male rats.

Transforming growth factor-beta (TGF-beta) is a ubiquitous growth-regulating protein with an essential role in tissue repair and formation of extracellular matrix (ECM). To better understand the role of different isoforms of TGF-beta in the cardiac remodeling process induced by norepinephrine (NE), the expression of TGF-beta1, TGF-beta2, and TGF-beta3 was studied and compared with the expression of collagen. NE (0.

Cardiac remodeling in erythropoietin-transgenic mice.

Background: Transgenic (tg) mice with chronic overexpression of the human erythropoietin gene are characterized by an increased hematocrit of about 0.80 in adulthood. This is accompanied by cardiac dysfunction and premature death.

Norepinephrine-induced acute heart failure in transgenic mice overexpressing erythropoietin.

Objective: Overexpression of erythropoietin (Epo) in mice (Epo-tg6) leads to an increase in hematocrit and blood volume, and strongly reduces endurance upon exercise. It was the aim of this study to characterize the mechanisms underlying the reduced cardiac performance.

Methods: Left (LV) and right (RV) ventricular function was measured with and without norepinephrine (NE) stimulation in 12 anaesthetized Epo-tg6 and in 13 wild-type (WT) control mice.

Norepinephrine-induced cardiac hypertrophy and fibrosis are not due to mast cell degranulation.

The norepinephrine (NE)-induced hypertrophy of the left ventricle (LV) in the rat is preceded by increased interleukin (IL)-6 expression and associated with LV fibrosis. We have examined whether the elevated level of IL-6 may be due to mast cell degranulation. Therefore we tested the effect of cromoglycate sodium salt (cromolyn), an inhibitor of mast cell degranulation with anti-inflammatory and membrane-stabilizing activity, on the increased expression of IL-6 mRNA and of mRNAs of proteins involved in the remodelling of the extracellular matrix (ECM) which is induced by NE (0.

Effect of propranolol on cardiac cytokine expression after myocardial infarction in rats.

The pro-inflammatory cytokines interleukin (IL)-1beta and IL-6 have been shown to be upregulated in the myocardium after injury and after adrenergic receptor stimulation. Together with other cytokines, such as the transforming growth factor (TGF)-beta, the pro-inflammatory cytokines have been implicated in the initiation of tissue repair and wound healing after myocardial infarction (MI). In the present study, the effect of beta-adrenergic receptor blockade with propranolol (2 mg/kg x h s.

Catheterization of pulmonary artery in rats with an ultraminiature catheter pressure transducer.

Utilizing new materials and miniaturization techniques, an ultraminiature catheter pressure transducer for catheterization of the pulmonary artery (PA) has been developed and applied in intact, spontaneously breathing, anesthetized rats. The catheter arrangement consists of three components: 1) an SPR-671 ultraminiature pressure transducer (measuring catheter), 2) a plastic introducer (sheath) that is slipped over the measuring catheter, and 3) an external wire mounted on the outside of the introducer for bending its tip. The measuring catheter is first inserted through the right jugular vein into the right ventricle.