Cholinergic neuromodulation, a candidate mechanism for aspects of attention, is complex and is not well understood. Because structure constrains function, quantitative anatomy is an invaluable tool for reducing such a challenging problem. Our goal was to determine the extent to which m1 and m2 muscarinic acetylcholine receptors (mAChRs) are expressed by inhibitory vs. excitatory neurons in the early visual cortex. To this end, V1 and V2 of macaque monkeys were immunofluorescently labelled for gamma-aminobutyric acid (GABA) and either m1 or m2 mAChRs. Among the GABA-immunoreactive (ir) neurons, 61% in V1 and 63% in V2 were m1 AChR-ir, whereas 28% in V1 and 43% in V2 were m2 AChR-ir. In V1, both mAChRs were expressed by fewer than 10% of excitatory neurons. However, in V2, the population of mAChR-ir excitatory neurons was at least double that observed in V1. We also examined m1 and m2 AChR immunoreactivity in layers 2 and 3 of area V1 under the electron microscope and found evidence that GABAergic neurons localize mAChRs to the soma, whereas glutamatergic neurons expressed mAChRs more strongly in dendrites. Axon and terminal labelling was generally weak. These data represent the first quantitative anatomical study of m1 and m2 AChR expression in the cortex of any species. In addition, the increased expression in excitatory neurons across the V1/V2 border may provide a neural basis for the observation that attentional effects gain strength up through the visual pathway from area V1 through V2 to V4 and beyond.
Background Atrial fibrillation is common among patients with cardiovascular disease and is a frequent complication of the acute coronary syndrome. Data are needed on recent trends in the magnitude, clinical features, treatment, and prognostic impact of pre-existing and new-onset atrial fibrillation in patients hospitalized with an acute coronary syndrome. Methods The study population consisted of 59,032 patients hospitalized with an acute coronary syndrome at 113 sites in the Global Registry of Acute Coronary Events Study between 2000 and 2007. Results 4,494 participants (7.6%) with acute coronary syndrome reported a history of atrial fibrillation and 3,112 (5.3%) developed new-onset atrial fibrillation during their hospitalization. Rates of new-onset atrial fibrillation (5.5% to 4.5%) and pre-existing atrial fibrillation (7.4% to 6.7%) declined during the study. Pre-existing atrial fibrillation was associated with older age and greater cardiovascular disease burden, whereas new-onset atrial fibrillation was closely related to the severity of the index acute coronary syndrome. Patients with atrial fibrillation were less likely than patients without atrial fibrillation to receive evidence-based therapies and were more likely to develop in-hospital complications, including heart failure. Overall hospital death rates in patients with new-onset and pre-existing atrial fibrillation were 14.5% and 8.9%, respectively, compared to 1.2% in those without atrial fibrillation. Short-term death rates in atrial fibrillation patients declined over the study period. Conclusions Despite a reduction in the rates of, and mortality from, atrial fibrillation, this arrhythmia exerts a significant adverse effect on survival among patients hospitalized with an acute coronary syndrome. Opportunities exist to improve the identification and treatment of acute coronary syndrome patients with, or at risk for, atrial fibrillation to reduce the incidence and resultant complications of this dysrhythmia.
Introduction: In the United States, 3% of adults are affected by carotid artery disease, and the prevalence is higher in patients with concomitant renal insufficiency. Ischemic events are also more common in patients with renal insufficiency and significantly contribute to morbidity and mortality. Despite the prevalence of carotid artery disease in individuals with renal insufficiency, only a few studies have examined the rate of carotid disease progression in this high risk group, and the mechanisms underlying disease progression are largely unknown. Hypothesis: Patients with any stage of renal insufficiency will have an accelerated rate of carotid artery atherosclerotic progression compared to patients with normal renal function. Methods: Retrospective chart review was performed on 171 consecutive patients referred to Cooper University Hospital for non invasive evaluation of carotid artery disease. Severity of carotid artery disease was evaluated with carotid doppler, and each patient had at least two carotid doppler studies performed at least 6 months apart. The sample was divided into 2 groups - [Group 1] GFR > 60 and [Group 2] GFR <60. Demographics, comorbidities, medications, serum creatinine, MDRD GFR and ultrasound analysis (proximal peak systolic velocity (PSV), and proximal end diastolic velocity (EDV)) were recorded. The average change in the PSV between studies for the 2 groups were calculated and compared. None of the patients in the sample were on dialysis. Results: Preliminary results revealed carotid artery disease regression in both groups; however, patients with any stage of renal insufficiency had less carotid artery disease regression compared to patients with normal renal function. Conclusions: Renal insufficiency negatively impacts the rate of carotid artery disease regression in patients with carotid artery disease. These results suggest that patients with renal insufficiency may require more aggressive follow-up and/or earlier invasive interventions of carotid artery disease. Current monitoring and treatment standards should be improved to adequately address the needs of this high risk subgroup.
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