High sensitivity C-reactive protein (hsCRP) has been evaluated as a biomarker in stroke and relevant pathological diseases. While its predictive values in several pathological phenotypes have been confirmed, controversy exists among different studies. This review summarizes reports of the predictive values of hsCRP for the diagnosis, etiology, prognosis and mortality of stroke diseases. The current literature suggests that CRP expression is influenced by multiple factors, such as polymorphisms, the genomic backgrounds and gender. However, few reported studies analyzed data based on all these multiple factors. Future studies should focus on comprehensive analysis based on multiple factors.

Severe reduction in the β‐cell number (collectively known as the β‐cell mass) contributes to the development of both type 1 and type 2 diabetes. Recent pharmacological studies have suggested that increased pancreatic β‐cell proliferation could be due to specific inhibition of adenosine kinase (ADK). However, genetic evidence for the function of pancreatic β‐cell ADK under physiological conditions or in a pathological context is still lacking. In this study, we crossed mice carrying LoxP‐flanked Adk gene with Ins2‐Cre mice to acquire pancreatic β ‐cell ADK deficiency (Ins2‐Cre ± Adk fl/fl ) mice. Our results revealed that Ins2‐Cre +/‐ Adk fl/fl mice showed improved glucose metabolism and β‐cell mass in younger mice, but showed normal activity in adult mice. Moreover, Ins2‐Cre ± Adk fl/fl mice were more resistant to streptozotocin (STZ) induced hyperglycaemia and pancreatic β‐cell damage in adult mice. In conclusion, we found that ADK negatively regulates β‐cell replication in young mice as well as under pathological conditions, such as STZ induced pancreatic β‐cell damage. Our study provided genetic evidence that specific inhibition of pancreatic β‐cell ADK has potential for anti‐diabetic therapy.