A new sensitive portable plethysmograph

A new portable plethysmograph is described which is all metal and, therefore, sturdy and free from the difficulties of deterioration—an important problem when rubber membranes are employed. A device for standardization is incorporated which makes it possible to correct for finger and toe size, thereby resulting in a completed plethysmogram which can be read directly from subject to subject and from time to time in the same subject. This eliminates calculations usually required to convert volume changes to standard units. The plethysmograph also contains a master elapse time recorder which makes it possible to record time even when the camera is off. By means of a baseline adjuster and recorder, gross or large and slow variations in volume of the part can be recorded.The completed plethysmogram is discussed and five types of spontaneous deflections in volume are considered. The plethysmogram shows the volume changes at slow and fast speeds. The former makes it possible to study all five types of spontaneous deflections in volume, while the latter makes it possible to study the configurations of the pulse wave in detail.A discussion of the methods of recording the plethysmogram, precautions and possible errors in recording, and its interpretation are given. The use of plethysmography in the study of peripheral vascular disease, psychogenic states, and states of relaxation and tension are briefly indicated. Detailed applications of the plethysmogram to normal and abnormal clinical states will be presented in the near future.This plethysmograph is a new instrument which is objective, precise, simple, and practical. It has great promise in the study of many problems in health and disease which manifest themselves by disturbances in the blood vessels, lymphatics, and intercellular and intracellular and fluid volumes of the tips of the fingers and toes. By far the greatest number of experimental and clinical applications remain unknown. As with the introduction of any new instrument which has applications in the biologic fields generally and broad use in these fields, the science is in its infancy. It is only with the patient efforts of many investigators, both in the laboratory and the clinic, that the plethysmograph and plethysmogram will develop and reach a state of adequate evaluation and proper usage.     

Almanac 2012: Congenital heart disease. The national society journals present selected research that has driven recent advances in clinical cardiology

This Almanac highlights recent papers on congenital heart disease in the major cardiac journals. Over 100 articles are cited. Subheadings are used to group relevant papers and allow readers to focus on their areas of interest, but are not meant to be comprehensive for all aspects of congenital cardiac disease.     

Architectural plan for the heart: early patterning and delineation of the chambers and the nodes

During folding of the embryo, lateroanterior visceral mesoderm forms the embryonic tubular heart at the midline, just ventral to the foregut. In mice, this nascent tube contains the future left ventricle and atrioventricular canal. Mesenchymal cells subsequently recruited to the cardiac lineage at the intake and the outflow of the tube will form the atria and the right ventricle and outflow tract, respectively. Shortly after its emergence, the embryonic heart tube starts to loop, and the first signs of left ventricular chamber differentiation become visible on the outer curvature of the middle portion of the tube. Subsequently, the right ventricle differentiates cranially, and the atria caudally, while the inflow tract, atrioventricular canal, inner curvatures, and outflow tract form recognizable components flanking the chambers. The latter, nonchamber regions in turn provide signals for the formation of the cushion mesenchyme, are involved in remodeling of the heart, and form the nodes of the conduction system. This review discusses how the patterning of the heart tube relates to the localized differentiation of atrial and ventricular chambers, why some parts of the heart do not form chambers, and how this relates to the formation of the conduction system.     

Episodic Migraine With and Without Aura: Key Differences and Implications for Pathophysiology,Management, and Assessing Risks

Purpose of Review

To review the pathophysiologic, epidemiologic, and clinical evidence for similarities and differences between migraine with and without aura.

Recent Findings

The ICHD-3 has recently refined the diagnostic criteria for aura to include positive symptomatology, which better differentiates aura from TIA. Although substantial evidence supports cortical spreading depression as the cause of visual aura, the role (if any) of CSD in headache pain is not well understood. Recent imaging evidence suggests a possible hypothalamic origin for a headache attack, but further research is needed. Migraine with aura is associated with a modest increase in the risk of ischemic stroke. The etiology for this association remains unclear. There is a paucity of evidence regarding treatments specifically aimed at the migraine with aura subtype, or whether migraine with vs without aura responds to treatment differently. Migraine with typical aura is therefore often treated similarly to migraine without aura. Lamotrigine, daily aspirin, and flunarizine have evidence for efficacy in prevention of migraine with aura, and magnesium, ketamine, furosemide, and single-pulse transcranial magnetic stimulation have evidence for use as acute treatments. Although triptans have traditionally been contraindicated in hemiplegic migraine and migraine with brainstem aura, this prohibition is being reconsidered in the face of evidence suggesting that use may be safe.

Summary

The debate as to whether migraine with and without aura are different entities is ongoing. In an era of sophisticated imaging, genetic advancement, and ongoing clinical trials, efforts to answer this question are likely to yield important and clinically meaningful results.

     

T-type Ca2+ current contribution to Ca2+-induced Ca2+ release in developing myocardium

In normal adult-ventricular myocardium, Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR) is activated via Ca2+ entry through L-type Ca2+ channels. However, embryonic-ventricular myocytes have a prominent T-type Ca2+ current (ICa,T). In this study, the contribution of ICa,T to CICR was determined in chick-ventricular development. Electrically stimulated Ca2+ transients were examined in myocytes loaded with fura-2 and Ca2+ currents with perforated patch-clamp. The results show that the magnitudes of the Ca2+ transient, L-type Ca2+ current (ICa,L) and ICa,T, decline with development with the majority of the decline of transients and ICa,L occurring between embryonic day (ED) 5 and 11. Compared to controls, the magnitude of the Ca2+ transient in the presence of nifedipine was reduced by 41% at ED5, 77% at ED11, and 78% at ED15. These results demonstrated that the overall contribution of ICa,T to the transient was greatest at ED5, while ICa,L was predominate at ED11 and 15. This indicated a decline in the contribution of ICa,T to the Ca2+ transient with development. Nifedipine plus caffeine was added to deplete the SR of Ca2+ and eliminate the occurrence of CICR due to ICa,T. Under these conditions, the transients were further reduced at all three developmental ages, which indicated that a portion of the Ca2+ transients present after just nifedipine addition was due to CICR stimulated by ICa,T. These results indicate that Ca2+ entry via T-type channels plays a significant role in excitation-contraction coupling in the developing heart that includes stimulation of CICR.