Examples of pathophysiological

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How shall the search for pathophysiological substrates proceed methodologically?
Taking clinical similarities as a criterion to infer relationships among common pathophysiological substrates is rather promising.
Total dissociation between "state- and trait markers" with regard to their respective pathophysiological substrates subsequently cannot be excluded.
Both hypo- or hyper-excretion are made to stand for the same thing, an unidentified pathophysiological process.
Endophenotypes are quantitative traits (pathophysiological markers) that share a substantial genetic component with the clinical disorder.
Such data are usually acquired under conditions that do not mimic the physiological (or pathophysiological) environment.
Ideally, these high-risk samples would be followed through time to identify which pathophysiological processes are associated with the switch from trait vulnerabilities to overt illness.
Aging homeostasis cal problems relating to temperature, electrolytes and water depend on understanding physiological control and correcting pathophysiological mechanisms.
Studies from different models produce contrasting findings, resulting in divergent conclusions regarding the pathophysiological basis of absence seizures.
Additional experiments are warranted to investigate the significance of these pathophysiological mechanisms in vivo.
The data are discussed and deductions regarding plausible pathophysiological mechanisms involved in psychotic symptoms, are made.
Today there is growing knowledge about the underlying pathophysiological and psychological mechanisms.
To clarify these issues must be considered an important task which might contribute substantially to a better understanding of the pathophysiological mechanisms in psychiatric disorders.
Nevertheless, there is a specific pathophysiological correlate of fever that remains absent in patients with the same disease, but without fever.
In a medical data collection, for example, unobservable intermediate pathophysiological states are typically not recorded.
Consequently, insulin abnormalities may disrupt normal memory functioning and promote pathophysiological processes observed in patients with neurodegenerative disorders.
Such an entity almost certainly exists and is most probably on the basis of the latter pathophysiological mechanism.
Whatever the aetiology, pathophysiological mechanisms inferring the formation of calcifications are unclear.
The available pathophysiological knowledge on the endogenous mechanisms at work is qualitative but highly incomplete whereas the exogenous factors can be completely and quantitatively known.

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