[The changing epidemiology of tick-borne encephalitis: epidemic surveillance and disease prevention challenges].

The increasing number of cases of tick-borne encephalitis (TBE) reported in recent years in Europe and, more recently, in Poland is a consequence of factors related to climate and environmental change leading to increasing tick populations and human behavior favoring exposure. In Poland, there is considerable regional variation in the incidence of TBE, resulting, among other factors, from underreporting of all cases and limited access to laboratory diagnostics. The consequence is low public awareness of the disease and insufficient use of vaccination as optimal prevention.

Activation of limbal epithelial proliferation is partly controlled by the ACE2-LCN2 pathway.

In response to corneal injury, an activation of corneal epithelial stem cells and their direct progeny the early transit amplifying (eTA) cells to rapidly proliferate is critical for proper re-epithelialization. Thus, it is important to understand how such stem/eTA cell activation is regulated. Angiotensin-converting enzyme 2 (ACE2) is predominantly expressed in the stem/eTA-enriched limbal epithelium but its role in the limbal epithelium was unclear.

Altered kidney distribution and loss of ACE2 into the urine in acute kidney injury.

There are diverse pathophysiological mechanisms involved in acute kidney injury (AKI). Among them, overactivity of the renin-angiotensin system (RAS) has been described. Angiotensin-converting enzyme 2 (ACE2) is a tissue RAS enzyme expressed in the apical border of proximal tubules.