Admission to ICU represented a clinical condition of PCP as a later event that may be regarded as being critically and potentially fatally ill. In the current study, patients with PCP presented with nonspecific symptoms such as fever, cough, dyspnea, chest pain, and SB-268262 pneumothorax. The use of four or more clinical manifestations and albumin #30 g/L as predictive factors could enable clinicians to recognize the risk of PCP earlier and avoid further deterioration in the patient��s condition. This study has a number of limitations. First, it is a retrospective analysis of a small population. Retrospective studies may be less reliable in terms of the data collected, particularly physical examination data. A prospective study which includes more cases is necessary. Second, it only includes confirmed PCP patients. Some patients would not be enrolled into this study if they were too severe to confirm the diagnosis. Third, the follow up after hospital discharge was for 90 days, which does not allow an accurate prediction of long-term mortality. Previous studies have demonstrated that the A 887826 prefrontal cortex plays an important role in working memory, emotional memory, attention regulation, and behavioral inhibition. In addition, it has been shown that NMDA receptor is crucial for the function of prefrontal cortex. For example, antagonists of NMDA receptor impaired prefrontal cortex-dependent working memory. The NMDA receptors are heteromeric complexes consisting of NR1 subunit, various NR2 subunits, and NR3 subunits. The formation of functional NMDA receptors requires a combination of NR1 and at least one of NR2 subunits. Among the four subunits, NR2A and NR2B subunits are predominantly expressed in adult forebrain regions including the hippocampus and cortex. Although the roles of NR2A and NR2B subunits in hippocampal synaptic plasticity have been extensively investigated, their roles in the prefrontal cortical plasticity are not well characterized. So far, only Zhao MG et al reported that NR2A or NR2B subunit antagonists blocked LTD and LTP in prefrontal cortex, indicating that the down-regulation of NR2B subunit function led to an attenuation of NMDAR- mediated LTP and LTD in prefrontal cortex.