Prognostic Value of Antithrombin Activity Levels in the Early Phase of Intensive Care: A 2-Center Retrospective Cohort Study.

To investigate the relationship between antithrombin (AT) activity level and prognosis in patients requiring intensive care. Patients whose AT activity was measured within 24 h of intensive care unit (ICU) admission were enrolled for analysis. The primary endpoint was mortality at discharge. Prognostic accuracy was examined using receiver operating characteristic (ROC) curves and cox hazard regression analysis. Patients were divided into 6 groups based on predicted mortality, and a χ2 independence test was performed on the prognostic value of AT activity for each predicted mortality; P < .05 was considered significant. A total of 281 cases were analyzed. AT activity was associated with mortality at discharge (AT% [interquartile range, IQR]): survivor group, 69 (56-86) versus nonsurvivor group, 56 (44-73), P = .0003). We found an increasing risk for mortality in both the lowest level of AT activity (<50%; hazard ratio [HR] 2.43, 95% confidence interval [CI] 1.20-4.89, P = .01) and the middle-low level of AT activity (≥ 50% and < 70%; HR 2.06, 95% CI 1.06-4.02, P = .03), compared with the normal AT activity level (≥ 70%). ROC curve analysis showed that the prediction accuracy of AT was an area under the curve (AUC) of 0.66 (cutoff 58%, sensitivity 61.4%, specificity 68.2%, P = .0003). AT activity was significantly prognostic in the group with 20% to 50% predicted mortality (AUC 0.74, sensitivity: 24.0%-55.5%, specificity: 83.3%-93.0%). An early decrease in AT activity level in ICU patients may be a predictor of mortality at discharge.

Intracellular calcium ion dynamics involved in long-term potentiation in hippocampal CA1 neurons in mice lacking the IP3 type 1 receptor.

In the present study, mice lacking the type 1 inositol-1,4,5-trisphosphate receptor (IP(3)R) were used to study the role of type 1 IP(3)Rs in the induction of long-term potentiation (LTP) in hippocampal CA1 neurons. The magnitude of the LTP induced by high frequency stimulation (HFS) consisting of 20 pulses at 30Hz in mice lacking type 1 IP(3)Rs was significantly larger than that in wild-type mice in terms of the field excitatory postsynaptic potential and population spike. By measuring changes in the intracellular Ca(2+) concentration ([Ca(2+)](i)) in CA1 pyramidal neurons using fluorometry, we found that the decay time of the transient increase in the [Ca(2+)](i) evoked by the HFS in mutant mice was significantly longer than that in wild-type mice, whereas the [Ca(2+)](i) at rest and the magnitude of the [Ca(2+)](i) increases caused by the HFS were no different from those in wild-type mice. In slices from the mutant mice, paired-pulse stimulation (PPS) delivered at an interval of 10ms resulted in significantly weaker paired-pulse inhibition (PPI) than in wild-type mice, suggesting that lack of type 1 IP(3)Rs reduces the PPI induced by PPS in the CA1 region. These results indicate that a lack of type 1 IP(3)Rs causes a slower decay of the transient [Ca(2+)](i) in CA1 pyramidal neurons and attenuates the activity of inhibitory interneurons, resulting in enhancement of LTP induction.

[Cerebral infarction associated with esophagectomy: a report of a case].

We report a case of cerebral infarction developed either during or immediately after an operation. A 71-year-old man with esophageal cancer and a history of hypertension and asymptomatic cerebral infarction underwent right thoracolaparotomy for a subtotal esophagectomy. Anesthesia was maintained with a combination of 2% sevoflurane in oxygen and epidural analgesia using 2% mepivacaine. The operation was uneventful and the patient was transferred to ICU with the tracheal tube in place. On removal of the tracheal tube the next day the patient was unable to speak and his grip power of the right hand was weak. On CT a cerebral infarction was found in the left frontal lobe. A left carotid echogram showed a 90% constriction. The occlusion of the middle cerebral artery by an embolus detached from the constricted origin of the carotid artery was thought a most probable cause of the cerebral infarction. The presence of a carotid constriction must be explored preoperatively in aged patients scheduled to undergo extensive manipulations in the neck