Many microbial pathogens and toxins recognize animal cells via cell surface sialic acids (Sias) that are ␣2-3-or ␣2-8-linked to the underlying glycan chain. Human influenza A/B viruses are unusual in preferring ␣2-6-linked Sias, undergoing a switch from ␣2-3 linkage preference during adaptation from animals to humans. This correlates with the expression of ␣2-6-linked Sias on ciliated human airway epithelial target cells and of ␣2-3-linked Sias on secreted soluble airway mucins, which are unable to inhibit virus binding. Given several known differences in Sia biology between humans and apes, we asked whether this pattern of airway epithelial Sia linkages is also human-specific. Indeed, we show that since the last common ancestor with apes, humans underwent a concerted bidirectional switch in ␣2-6-linked Sia expression between airway epithelial cell surfaces and secreted mucins. This can explain why the chimpanzee appears relatively resistant to experimental infection with human Influenza viruses. Other tissues showed additional examples of human-specific increases or decreases in ␣2-6-linked Sia expression and only one example of a change specific to certain great apes. Furthermore, while human and great ape leukocytes both express ␣2-6-linked Sias, only human erythrocytes have markedly up-regulated expression. These cell type-specific changes in ␣2-6-Sia expression during human evolution represent another example of a human-specific change in Sia biology. Because the data set involves multiple great apes, we can also conclude that Sia linkage expression patterns can be conserved during millions of years of evolution within some vertebrate taxa while undergoing sudden major changes in other closely related ones.

Heart disease is common in both humans and chimpanzees, manifesting typically as sudden cardiac arrest or progressive heart failure. Surprisingly, although chimpanzees are our closest evolutionary relatives, the major cause of heart disease is different in the two species. Histopathology data of affected chimpanzee hearts from two primate centers, and analysis of literature indicate that sudden death in chimpanzees (and in gorillas and orangutans) is commonly associated with diffuse interstitial myocardial fibrosis of unknown cause. In contrast, most human heart disease results from coronary artery atherosclerosis, which occludes myocardial blood supply, causing ischemic damage. The typical myocardial infarction of humans due to coronary artery thrombosis is rare in these apes, despite their human-like coronary-risk-prone blood lipid profiles. Instead, chimpanzee ‘heart attacks’ are likely due to arrythmias triggered by myocardial fibrosis. Why do humans not often suffer from the fibrotic heart disease so common in our closest evolutionary cousins? Conversely, why do chimpanzees not have the kind of heart disease so common in humans? The answers could be of value to medical care, as well as to understanding human evolution. A preliminary attempt is made to explore possibilities at the histological level, with a focus on glycosylation changes.

Key Clinical MessageThe presence of Internal Jugular Valves can pose a diagnostic and procedural challenge during ultrasound‐guided cannulation. After ruling out dissection, thrombus, or ultrasound artifacts, it can still be accessed and successfully cannulated with appropriate precautions including use of Live ultrasound, positioning, use of soft‐tipped catheters, and minimizing duration of catheter placement.

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