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Polysaccharides have key biological functions and can be harnessed for therapeutic roles, such as the anticoagulant heparin. Their complexity—e.g., >100 monosaccharides with variety in linkage and branching structure—significantly complicates analysis compared to other biopolymers such as DNA and proteins. More, and improved, analysis tools have been called for, and here we demonstrate that solid-state silicon nitride nanopore sensors and tuned sensing conditions can be used to reliably detect native polysaccharides and enzymatic digestion products, differentiate between different polysaccharides in straightforward assays, provide new experimental insights into nanopore electrokinetics, and uncover polysaccharide properties. We show that nanopore sensing allows us to easily differentiate between a clinical heparin sample and one spiked with the contaminant that caused deaths in 2008 when its presence went undetected by conventional assays. The work reported here lays a foundation to further explore polysaccharide characterization and develop assays using thin-film solid-state nanopore sensors., The complexity of polysaccharides significantly complicates their analysis in comparison to other biopolymers. Here, the authors demonstrate that solid-state silicon nitride nanopore sensors can be used to reliably detect native polysaccharides and to perform a simple quality assurance assay on a polysaccharide therapeutic, heparin.

To evaluate the effects of cigarette smoking on some of the circulatory and ventilatory responses to exercise, a group of young male subjects, 18 smokers and 14 nonsmokers, was studied. Exercise consisted of a standard 5-min bicycle ergometer test that achieved a mean O2 uptake of 1.44 liters/ min in the 5th min of exercise. There was no difference between smokers and nonsmokers in the O2 uptake achieved during subsequent maximal exercise. Pulmonary function studies performed on the two groups revealed normal results for each group. There was an oxygen debt accumulation among smokers that was significantly greater ( P < 0.001) and this debt represented a greater per cent of the total O2 uptake. The heart rate at rest and 3 min after exercise in smokers was significantly faster ( P < 0.02). These differences do not appear to be related to ventilatory factors and may, therefore, be due to either circulatory or metabolic differences in the two groups. Submitted on August 17, 1962

1. 1. Fourteen infusions of potassium phosphate to 12 digitalized individuals with persistent ventricular ectopic rhythms resulted in a transient depression of the ectopic focus in 12 experiments. In one there was no effect and in another the ventricular premature beats increased in number during the infusion. In 4 additional patients the ventricular ectopic beats first appeared during or after the infusion. 2. 2. Depression of A-V conduction with resultant slowing of the ventricular rate was observed during 11 of the 18 infusions. 3. 3. The parallel depression of A-V conduction and the ectopic ventricular foci suggests that the effect of potassium is one of myocardial depression. Furthermore, the short-lived beneficial effect of potassium suggests that the mechanism may be due to a transient elevation of the extracellular level of the cation.

A case of atrial parasystole is reported. The parasystolic rhythm was intermittent in character and began each time with an atrial premature beat exhibiting a constant relation to the preceding sinus beat.

A case of dissociation within the A-V node with wandering of the upper nodal pacemaker and “double” nodal tachycardia is reported.

Excerpt The Family Nurse Practitioner Program at the Indiana University Schools of Medicine and Nursing is one of seven new programs designed to train registered nurses to assume greater responsibi...

Differences have been found in the cardiopulmonary responses to exercise between young male cigarette somkers and nonsmokers. The present study was undertaken in an attempt to determine the cause of such differences. Since smokers carry a chronically elevated carboxyhemoglobin level (>4%), carbon monoxide was inhaled by nonsmokers to raise their carboxyhemoglobin level to the range seen in a control group of smokers. This maneuver caused the development in nonsmokers of an increased oxygen debt with exercise and a reduced pulmonary diffusing capacity at rest. The changes after carbon monoxide inhalation were similar to those found when comparing smokers to nonsmokers. The pathogenesis of these changes are unknown, but support carbon monoxide as a possible etiologic factor accounting for the less efficient exercise and poorer pulmonary function performance of smokers compared to nonsmokers.