Natural History of a Disease: Patent Ductus Arteriosus Diagnosed on an Elderly Woman.

Patent ductus arteriosus (PDA) is a rare finding in adults. The ductus arteriosus (DA) is responsible for shunting blood from the pulmonary artery into the aorta bypassing the lungs in fetal life (the placenta is responsible for fetal oxygenated blood). Its closure happens after birth, once fetal circulation transitions to normal postnatal circulation and blood oxygenates in the lungs. If the DA does not close, the PDA may continue to shunt blood from the systemic (higher pressure) to the pulmonary (lower pressure) circulation causing remodeling of the left ventricle and eventually heart failure. A PDA is suspected when there is a systolic/diastolic murmur in the left sternal border; a transthoracic or transesophageal echocardiogram may visualize the shunt and measure the systemic/pulmonary shunt ratio. We described a case of an 84-year-old elderly woman who presented with an acute heart failure exacerbation as the first symptom of PDA and was found to have left ventricular hypertrophy, right ventricular hypertrophy, and pulmonary hypertension as the initial presentation.

Autonomic Symptoms in Older Adults Are Common and Associated With Health-Related Quality of Life.

Background: Autonomic symptoms are common in older adults, and a large body of literature focusing on age-related diseases shows that autonomic symptoms in these diseases constrain Health-Related Quality of Life (HRQoL). To our best knowledge, the association between autonomic symptoms in older adults, independent of specific diseases, and HRQoL has not yet been assessed. Aim: To assess the frequency and the effect of autonomic symptoms in general, as well as orthostatic intolerance, vasomotor, secretomotor, gastrointestinal, bladder, and pupillomotor symptoms, on HRQoL in older adults. Methods: Cross-sectional data of the fourth visit of the Tübinger evaluation of Risk factors for Early detection of Neurodegeneration (TREND) study were included. Autonomic symptoms, as assessed with the Composite Autonomic Symptom Score 31 (COMPASS 31), were quantified and compared with HRQoL, as assessed with the EuroQol five-level version (EQ-5D-5L). Statistical analyses included Spearman's rank correlation and multiple linear regression analysis. Results: The analysis included 928 participants with a median of 68 years; 47% were women. Of those, 85% reported at least one autonomic symptom. Gastrointestinal and secretomotor symptoms were most common. The COMPASS 31 total score and all subdomains were significantly associated with reduced HRQoL. Among the subdomains, the strongest correlations with HRQoL were found for gastrointestinal and bladder symptoms. Overall, autonomic symptoms alone explained 20% of the variance of HRQoL; when depressive mood was added, the model explained 32%. Conclusion: Autonomic symptoms are associated with HRQoL and depressive symptoms in older adults.

Functional connectivity of the vigilant-attention network in children and adolescents with attention-deficit/hyperactivity disorder.

The ability to maintain attention to simple tasks (i.e., vigilant attention, VA) is often impaired in attention-deficit/hyperactivity disorder (ADHD), but the underlying pathophysiological mechanisms at the brain network level are not clear yet. We therefore investigated ADHD-related differences in resting-state functional connectivity within a meta-analytically defined brain network of 14 distinct regions subserving VA (comprising 91 connections in total), as well as the association of connectivity with markers of behavioural dysfunction in 17 children (age range: 9-14 years) with a diagnosis of ADHD and 21 age-matched neurotypical controls. Our analyses revealed selective, rather than global, differences in the intrinsic coupling between nodes of the VA-related brain network in children with ADHD, relative to controls. In particular, ADHD patients showed substantially diminished intrinsic coupling for 7 connections and increased coupling for 4 connections, with many differences involving connectivity with the anterior insula. Moreover, connectivity strength of several aberrant connections was found to be associated with core aspects of ADHD symptomatology, such as poor attention, difficulties with social functioning, and impaired cognitive control, attesting to the behavioural relevance of specific connectivity differences observed in the resting state.

Multipotent Adult Progenitor Cells, but Not Tissue Inhibitor of Matrix Metalloproteinase-3, Increase Tissue Sparing and Reduce Urological Complications following Spinal Cord Injury.

Following spinal cord injury (SCI), inflammation amplifies damage beyond the initial insult, providing an opportunity for targeted treatments. An ideal protective therapy would reduce both edema within the lesion area and the activation/infiltration of detrimental immune cells. Previous investigations demonstrated the efficacy of intravenous injection of multipotent adult progenitor cells (MAPC®) to modulate immune response following SCI, leading to significant improvements in tissue sparing, locomotor and urological functions. Separate studies have demonstrated that tissue inhibitor of matrix metalloproteinase-3 (TIMP3) reduces blood-brain barrier permeability following traumatic brain injury in a mouse model, leading to improved functional recovery. This study examined whether TIMP3, delivered alone or in concert with MAPC cells, improves functional recovery from a contusion SCI in a rat model. The results suggest that intravenous delivery of MAPC cell therapy 1 day following acute SCI significantly improves tissue sparing and impacts functional recovery. TIMP3 treatment provided no significant benefit, and further, when co-administered with MAPC cells, it abrogated the therapeutic effects of MAPC cell therapy. Importantly, this study demonstrated for the first time that acute treatment of SCI with MAPC cells can significantly reduce the incidence of urinary tract infection (UTI) and the use of antibiotics for UTI treatment.

Effects of Dietary Acute Tryptophan Depletion (ATD) on NPY Serum Levels in Healthy Adult Humans Whilst Controlling for Methionine Supply-A Pilot Study.

Central nervous serotonin (5-HT) can influence behaviour and neuropsychiatric disorders. Evidence from animal models suggest that lowered levels of neuropeptide Y (NPY) may have similar effects, although it is currently unknown whether decreased central nervous 5-HT impact NPY concentrations. Given that the production of NPY is dependent on the essential amino acid methionine (MET), it is imperative to account for the presence of MET in such investigations. Hence, this study sought to examine the effects of acute tryptophan depletion (ATD; a dietary procedure that temporarily lowers central nervous 5-HT synthesis) on serum concentrations of NPY, whilst using the potential renal acid load indicator (PRAL) to control for levels of MET. In a double-blind repeated measures design, 24 adult humans randomly received an AA-load lacking in TRP (ATD) on one occasion, and a balanced control mixture with TRP (BAL) on a second occasion, both with a PRAL of nearly 47.3 mEq of MET. Blood samples were obtained at 90, 180, and 240 min after each of the AA challenges. ATD, and therefore, diminished substrate availability for brain 5-HT synthesis did not lead to significant changes in serum NPY concentrations over time, compared to BAL, under an acute acidotic stimulus.

Effects of a structured 20-session slow-cortical-potential-based neurofeedback program on attentional performance in children and adolescents with attention-deficit hyperactivity disorder: retrospective analysis of an open-label pilot-approach and 6-month follow-up.

OBJECTIVE: The aim of this approach was to conduct a structured electroencephalography-based neurofeedback training program for children and adolescents with attention-deficit hyperactivity disorder (ADHD) using slow cortical potentials with an intensive first (almost daily sessions) and second phase of training (two sessions per week) and to assess aspects of attentional performance. PATIENTS AND METHODS: A total of 24 young patients with ADHD participated in the 20-session training program. During phase I of training (2 weeks, 10 sessions), participants were trained on weekdays. During phase II, neurofeedback training occurred twice per week (5 weeks). The patients' inattention problems were measured at three assessment time points before (pre, T0) and after (post, T1) the training and at a 6-month follow-up (T2); the assessments included neuropsychological tests (Alertness and Divided Attention subtests of the Test for Attentional Performance; Sustained Attention Dots and Shifting Attentional Set subtests of the Amsterdam Neuropsychological Test) and questionnaire data (inattention subscales of the so-called Fremdbeurteilungsbogen für Hyperkinetische Störungen and Child Behavior Checklist/4-18 [CBCL/4-18]). All data were analyzed retrospectively. RESULTS: The mean auditive reaction time in a Divided Attention task decreased significantly from T0 to T1 (medium effect), which was persistent over time and also found for a T0-T2 comparison (larger effects). In the Sustained Attention Dots task, the mean reaction time was reduced from T0-T1 and T1-T2 (small effects), whereas in the Shifting Attentional Set task, patients were able to increase the number of trials from T1-T2 and significantly diminished the number of errors (T1-T2 & T0-T2, large effects). CONCLUSION: First positive but very small effects and preliminary results regarding different parameters of attentional performance were detected in young individuals with ADHD. The limitations of the obtained preliminary data are the rather small sample size, the lack of a control group/a placebo condition and the open-label approach because of the clinical setting and retrospective analysis. The value of the current approach lies in providing pilot data for future studies involving larger samples.

Intravenous multipotent adult progenitor cell treatment decreases inflammation leading to functional recovery following spinal cord injury.

Following spinal cord injury (SCI), immune-mediated secondary processes exacerbate the extent of permanent neurological deficits. We investigated the capacity of adult bone marrow-derived stem cells, which exhibit immunomodulatory properties, to alter inflammation and promote recovery following SCI. In vitro, we show that human multipotent adult progenitor cells (MAPCs) have the ability to modulate macrophage activation, and prior exposure to MAPC secreted factors can reduce macrophage-mediated axonal dieback of dystrophic axons. Using a contusion model of SCI, we found that intravenous delivery of MAPCs one day, but not immediately, after SCI significantly improves urinary and locomotor recovery, which was associated with marked spinal cord tissue sparing. Intravenous MAPCs altered the immune response in the spinal cord and periphery, however biodistribution studies revealed that no MAPCs were found in the cord and instead preferentially homed to the spleen. Our results demonstrate that MAPCs exert their primary effects in the periphery and provide strong support for the use of these cells in acute human contusive SCI.

Studying the effects of dietary body weight-adjusted acute tryptophan depletion on punishment-related behavioral inhibition.

BACKGROUND: Alterations in serotonergic (5-HT) neurotransmission are thought to play a decisive role in affective disorders and impulse control. OBJECTIVE: This study aims to reproduce and extend previous findings on the effects of acute tryptophan depletion (ATD) and subsequently diminished central 5-HT synthesis in a reinforced categorization task using a refined body weight-adjusted depletion protocol. DESIGN: Twenty-four young healthy adults (12 females, mean age [SD]=25.3 [2.1] years) were subjected to a double-blind within-subject crossover design. Each subject was administered both an ATD challenge and a balanced amino acid load (BAL) in two separate sessions in randomized order. Punishment-related behavioral inhibition was assessed using a forced choice go/no-go task that incorporated a variable payoff schedule. RESULTS: Administration of ATD resulted in significant reductions in TRP measured in peripheral blood samples, indicating reductions of TRP influx across the blood-brain barrier and related brain 5-HT synthesis. Overall accuracy and response time performance were improved after ATD administration. The ability to adjust behavioral responses to aversive outcome magnitudes and behavioral adjustments following error contingent punishment remained intact after decreased brain 5-HT synthesis. A previously observed dissociation effect of ATD on punishment-induced inhibition was not observed. CONCLUSIONS: Our results suggest that neurodietary challenges with ATD Moja-De have no detrimental effects on task performance and punishment-related inhibition in healthy adults.

Effects of dietary tryptophan and phenylalanine-tyrosine depletion on phasic alertness in healthy adults - A pilot study.

BACKGROUND: The synthesis of the neurotransmitters serotonin (5-HT) and dopamine (DA) in the brain can be directly altered by dietary manipulation of their relevant precursor amino acids (AA). There is evidence that altered serotonergic and dopaminergic neurotransmission are both associated with impaired attentional control. Specifically, phasic alertness is one specific aspect of attention that has been linked to changes in 5-HT and DA availability in different neurocircuitries related to attentional processes. The present study investigated the impact of short-term reductions in central nervous system 5-HT and DA synthesis, which was achieved by dietary depletion of the relevant precursor AA, on phasic alertness in healthy adult volunteers; body weight-adapted dietary tryptophan and phenylalanine-tyrosine depletion (PTD) techniques were used. METHODS: The study employed a double-blind between-subject design. Fifty healthy male and female subjects were allocated to three groups in a randomized and counterbalanced manner and received three different dietary challenge conditions: acute tryptophan depletion (ATD, for the depletion of 5-HT; N=16), PTD (for the depletion of DA; N=17), and a balanced AA load (BAL; N=17), which served as a control condition. Three hours after challenge intake (ATD/PTD/BAL), phasic alertness was assessed using a standardized test battery for attentional performance (TAP). Blood samples for AA level analyses were obtained at baseline and 360 min after the challenge intake. RESULTS: Overall, there were no significant differences in phasic alertness for the different challenge conditions. Regarding PTD administration, a positive correlation between the reaction times and the DA-related depletion magnitude was detected via the lower plasma tyrosine levels and the slow reaction times of the first run of the task. In contrast, higher tryptophan concentrations were associated with slower reaction times in the fourth run of the task in the same challenge group. CONCLUSION: The present study is the first to demonstrate preliminary data that support an association between decreased central nervous system DA synthesis, which was achieved by dietary depletion strategies, and slower reaction times in specific runs of a task designed to assess phasic alertness in healthy adult volunteers; these findings are consistent with previous evidence that links phasic alertness with dopaminergic neurotransmission. A lack of significant differences between the three groups could be due to compensatory mechanisms and the limited sample size, as well as the dietary challenge procedures administered to healthy participants and the strict exclusion criteria used. The potential underlying neurochemical processes related to phasic alertness should be the subject of further investigations.

Reduced Responsiveness to Social Provocation in Autism Spectrum Disorder.

Deficits in emotion processing and social interaction are prominent symptoms of autism spectrum disorder (ASD). ASD has also been associated with aggressive tendencies towards self and others. The prevalence of aggressive behavior in this disorder, its etiology and its impact on social life are still unclear. This study investigated behavioral and physiological effects of social provocation in patients with ASD and healthy controls. We used a modified Taylor Aggression Paradigm in 24 high-functioning patients with ASD and 24 healthy controls. Participants were instructed to play against a fictitious human opponent. Money withdrawals toward the participant represented provocation and money deduction by the participant denoted aggressive behavior. Throughout the measurement, electrodermal activity (EDA) was recorded. Healthy controls showed higher aggressive responses to high provocation compared to low provocation, which demonstrated the effectiveness of the used procedure in eliciting aggression. Patients' responses were not influenced by the level of social provocation, although in both groups aggression was higher after lost compared to won trials. Physiologically, controls showed fewer but higher EDA amplitudes when responding aggressively, whereas patients displayed the opposite pattern of more but lower EDA amplitudes. The modified Taylor Aggression Paradigm successfully elicited aggression and revealed different behavioral and neurophysiological responses in patients and healthy controls. Patients' aggressive behavior as well as their physiological responses were less modulated by level of provocation compared to controls. Therapeutic attempts for patients might concentrate on improving empathic abilities and the understanding of social situations, including provocation and aggressive behavior.

Modulation of the proteoglycan receptor PTPσ promotes recovery after spinal cord injury.

Contusive spinal cord injury leads to a variety of disabilities owing to limited neuronal regeneration and functional plasticity. It is well established that an upregulation of glial-derived chondroitin sulphate proteoglycans (CSPGs) within the glial scar and perineuronal net creates a barrier to axonal regrowth and sprouting. Protein tyrosine phosphatase σ (PTPσ), along with its sister phosphatase leukocyte common antigen-related (LAR) and the nogo receptors 1 and 3 (NgR), have recently been identified as receptors for the inhibitory glycosylated side chains of CSPGs. Here we find in rats that PTPσ has a critical role in converting growth cones into a dystrophic state by tightly stabilizing them within CSPG-rich substrates. We generated a membrane-permeable peptide mimetic of the PTPσ wedge domain that binds to PTPσ and relieves CSPG-mediated inhibition. Systemic delivery of this peptide over weeks restored substantial serotonergic innervation to the spinal cord below the level of injury and facilitated functional recovery of both locomotor and urinary systems. Our results add a new layer of understanding to the critical role of PTPσ in mediating the growth-inhibited state of neurons due to CSPGs within the injured adult spinal cord.

Entrapment via synaptic-like connections between NG2 proteoglycan+ cells and dystrophic axons in the lesion plays a role in regeneration failure after spinal cord injury.

NG2 is purportedly one of the most growth-inhibitory chondroitin sulfate proteoglycans (CSPGs) produced after spinal cord injury. Nonetheless, once the severed axon tips dieback from the lesion core into the penumbra they closely associate with NG2+ cells. We asked if proteoglycans play a role in this tight cell-cell interaction and whether overadhesion upon these cells might participate in regeneration failure in rodents. Studies using varying ratios of CSPGs and adhesion molecules along with chondroitinase ABC, as well as purified adult cord-derived NG2 glia, demonstrate that CSPGs are involved in entrapping neurons. Once dystrophic axons become stabilized upon NG2+ cells, they form synaptic-like connections both in vitro and in vivo. In NG2 knock-out mice, sensory axons in the dorsal columns dieback further than their control counterparts. When axons are double conditioned to enhance their growth potential, some traverse the lesion core and express reduced amounts of synaptic proteins. Our studies suggest that proteoglycan-mediated entrapment upon NG2+ cells is an additional obstacle to CNS axon regeneration.

Conductive shield for ultra-low-field magnetic resonance imaging: Theory and measurements of eddy currents.

Eddy currents induced by applied magnetic-field pulses have been a common issue in ultra-low-field magnetic resonance imaging. In particular, a relatively large prepolarizing field-applied before each signal acquisition sequence to increase the signal-induces currents in the walls of the surrounding conductive shielded room. The magnetic-field transient generated by the eddy currents may cause severe image distortions and signal loss, especially with the large prepolarizing coils designed for in vivo imaging. We derive a theory of eddy currents in thin conducting structures and enclosures to provide intuitive understanding and efficient computations. We present detailed measurements of the eddy-current patterns and their time evolution in a previous-generation shielded room. The analysis led to the design and construction of a new shielded room with symmetrically placed 1.6-mm-thick aluminum sheets that were weakly coupled electrically. The currents flowing around the entire room were heavily damped, resulting in a decay time constant of about 6 ms for both the measured and computed field transients. The measured eddy-current vector maps were in excellent agreement with predictions based on the theory, suggesting that both the experimental methods and the theory were successful and could be applied to a wide variety of thin conducting structures.

Intracoronary and systemic melatonin to patients with acute myocardial infarction: protocol for the IMPACT trial.

INTRODUCTION: Ischaemia-reperfusion injury following acute myocardial infarctions (AMI) is an unavoidable consequence of the primary percutaneous coronary intervention (pPCI) procedure. A pivotal mechanism in ischaemia-reperfusion injury is the production of reactive oxygen species following reperfusion. The endogenous hormone, melatonin, works as an antioxidant and could potentially minimise the ischaemia-reperfusion injury. Given intracoronarily, it enables melatonin to work directly at the site of reperfusion. We wish to test if melatonin, as an antioxidant, can minimise the reperfusion injury following pPCI in patients with AMI. MATERIAL AND METHODS: The IMPACT trial is a multicentre, randomised, double-blinded, placebo-controlled study. We wish to include 2 × 20 patients with ST-elevation myocardial infarctions undergoing pPCI within six hours from symptom onset. The primary end-point is the Myocardial Salvage Index assessed by cardiovascular magnetic resonance imaging on day 4 (± 1) after pPCI. The secondary end-points are high-sensitivity troponin, creatinekinase myocardial band and clinical events. CONCLUSION: The aim of the IMPACT trial is to evaluate the effect of melatonin on reperfusion injuries following pPCI. Owing to its relatively non-toxic profile, melatonin is an easily implementable drug in the clinical setting, and melatonin has the potential to reduce morbidity in patients with AMI. FUNDING: This study received no financial support from the industry. TRIAL REGISTRATION: www.clinicaltrials.gov, clinical trials identifier: NCT01172171.

Prototype phantoms for characterization of ultralow field magnetic resonance imaging.

PURPOSE: Prototype phantoms were designed, constructed, and characterized for the purpose of calibrating ultralow field magnetic resonance imaging (ULF MRI) systems. The phantoms were designed to measure spatial resolution and to quantify sensitivity to systematic variation of proton density and relaxation time, T1 . METHODS: The phantoms were characterized first with conventional magnetic resonance scanners at 1.5 and 3 T, and subsequently with a prototype ULF MRI scanner between 107 and 128 µT . RESULTS: The ULF system demonstrated a 2-mm spatial resolution and, using T1 measurements, distinguished aqueous solutions of MnCl2 differing by 20 µM [Mn(2+) ]. CONCLUSION: The prototype phantoms proved well-matched to ULF MRI applications, and allowed direct comparison of the performance of ULF and clinical systems.

Clinical-grade multipotent adult progenitor cells durably control pathogenic T cell responses in human models of transplantation and autoimmunity.

A major goal of immunotherapy remains the control of pathogenic T cell responses that drive autoimmunity and allograft rejection. Adherent progenitor cells, including mesenchymal stromal cells (MSCs) and multipotent adult progenitor cells (MAPCs), represent attractive immunomodulatory cell therapy candidates currently active in clinical trials. MAPCs can be distinguished from MSCs on the basis of cellular phenotype, size, transcriptional profile, and expansion capacity. However, despite their ongoing evaluation in autoimmune and allogeneic solid organ transplantation settings, data supporting the immune regulatory potential of clinical-grade MAPCs are limited. In this study, we used allogeneic islet transplantation as a model indication to assess the ability of clinical-grade MAPCs to control T cell responses that drive immunopathology in human autoimmune disease and allograft rejection. MAPCs suppressed T cell proliferation and Th1 and Th17 cytokine production while increasing secretion of IL-10 and were able to suppress effector functions of bona fide autoreactive T cells from individuals with type 1 diabetes mellitus, including killing of human islets. Furthermore, MAPCs favored the proliferation of regulatory T cells during homeostatic expansion driven by γ-chain cytokines and exerted a durable, yet reversible, control of T cell function. MAPC suppression required licensing and proceeded via IDO-mediated tryptophan catabolism. Therefore, the common immune modulatory characteristics of clinical-grade MAPCs shown in this study suggest that they can be regarded as an alternative source of adult progenitor cells with similar clinical usefulness to MSCs. Taken collectively, these findings may guide the successful deployment of both MSCs and MAPCs for the amelioration of human autoimmunity and allograft rejection.

Mesenchymal stromal cells as a means of controlling pathological T-cell responses in allogeneic islet transplantation.

PURPOSE OF REVIEW: To evaluate the potential for mesenchymal stromal cells (MSCs) to regulate T-cell responses responsible for graft destruction following allogeneic islet transplantation (AIT). RECENT FINDINGS: Despite a high level of primary graft function being observed in most individuals following AIT, the majority of recipients require exogenous insulin within 5 years, presumably due to graft attrition. Although this process is not fully understood, recent evidence suggests that a combination of chronic allograft rejection and/or the recrudescence of anti-islet autoimmunity govern islet loss. Emerging reports highlight that the pathology of AIT may involve the proliferation, effector function and homeostatic expansion of alloreactive and autoreactive T-cell pools. MSCs exhibit several desirable characteristics, which may advocate their use in AIT. This includes the capacity to suppress alloreactive and autoimmune T-cell responses, and promote a cytokine environment that is likely to be graft protective. However, further work is needed to clarify if MSCs can function in the setting of immune suppression and discern how they may effect T-cell effector functions and influence homeostatic expansion. SUMMARY: MSCs exhibit the potential to regulate the T-cell-driven processes that underlie disease pathology in AIT, but further study may be required to maximize their therapeutic efficacy.

Prevention of contrast-induced nephropathy in STEMI patients undergoing primary percutaneous coronary intervention: a systematic review.

OBJECTIVE: To evaluate the current prophylactic strategies against CIN in patients with STEMI treated by primary percutaneous coronary intervention. BACKGROUND: Contrast-induced nephropathy (CIN) is the third leading course of acute renal failure and a recognized complication to cardiac catheterization. CIN is associated with increased risk of cardiac adverse events and mortality, and recent studies point at the risk of developing a transient or persistent renal dysfunction. Patients with ST-elevation myocardial infarction treated by primary percutaneous coronary intervention have a markedly increased risk of developing CIN. At present no strategy is universally accepted in the prevention of CIN in the acute setting of primary percutaneous coronary intervention. METHOD: We performed a systematic search in Pubmed and EMBASE and ended up including nine randomised clinical trials; six studies of N-acetylcysteine, one study of early and late hydration regimens, one study of recombinant human brain natriuretic peptide and one study comparing a low-osmolar contrast agent with an iso-osmolar contrast agent. RESULTS: Recombinant human brain natriuretic peptide and the regimens of hydration significantly reduced the incidence of CIN and administration of N-acetylcysteine in one of the six studies significantly reduced the occurrence of CIN. The iso-osmolar contrast agent was not proven to be superior to the low-osmolar contrast agent in terms of preventing CIN. CONCLUSION: Preliminary studies are promising but further studies are needed before any prevention strategy against CIN can be recommended in routine care of patients undergoing primary percutaneous coronary intervention for STEMI.

[Closed-chest porcine model is superior in intervention studies of ischaemia reperfusion injury]. / Closed-chest-grisemodellen er overlegen ved interventionsstudier af iskæmireperfusionsskade.

Ischaemia reperfusion injury affects the patients' clinical outcomes. An animal model is therefore required in order to test pharmacological interventions and improve the current treatment of acute myocardial infarction (AMI). This review focuses on the endovascular closed-chest porcine model of ischaemia and reperfusion. In contrast to the open-chest porcine model the closed-chest model closely mimics the clinical situation of an AMI and makes it possible to extrapolate the results directly to humans. The model is well suited for future interventional studies.

Measurements of T(1) -relaxation in ex vivo prostate tissue at 132 µT.

The proton T(1) was measured at 132 µT in ex vivo prostate tissue specimens from radical prostatectomies of 35 patients with prostate cancer. Each patient provided two specimens. The NMR and MRI measurements involved proton repolarization, a field of typically 150 mT and detection of the 5.6-kHz signal with a superconducting quantum interference device. Values of T(1) varied from 41 to 86 ms. Subsequently, the percentages of tissue types were determined histologically. The theoretical image contrast is quantified for each case by δ = [1 - T(1) (more cancer)/T(1) (less cancer)]. A linear fit of δ versus difference in percentage cancer yields T(1) (100% cancer)/T(1) (0% cancer) = 0.70 ± 0.05 with correlation coefficient R(2) = 0.30. Two-dimensional T(1) maps for four specimens demonstrate variation within a single specimen. These results suggest that MR images with T(1) contrast established at ultra-low fields may discriminate prostate cancer from normal prostate tissue in vivo without a contrast agent.