Case: A 40-year-old woman. Clinical diagnosis: Autistic disorder with mild mental retardation. Case report: The patient underwent pancreaticoduodenectomy for the treatment of her pancreatic cancer. We held several conferences with individuals from different medical fields and examined the influence of the patient's autistic disorder on the perioperative conditions. The senior author, a clinical psychologist, conducted repeated individual, acceptive, and sympathetic interviews with the patient and her family and maintained supportive relationships with them as an honorary family member. Thus, the clinical psychologist helped reduce the patient's anxiety about the medical treatment. Conclusion: The participation of a clinical psychologist in the medical conferences enabled the medical staff to understand the complications involved and provide mental support to the patient and her family. Palliat Care Res 2010; 5(2): 323-326

Renal damage caused by hemolysis during cardiopulmonary bypass (CPB) was investigated, and the preventive effects of haptoglobin in regard to this condition was also evaluated. Nineteen patients who underwent open heart surgery were divided into two groups: a control group (n=11) and a haptoglobin group (n=8). In the control group, the level of plasma-free hemoglobin increased significantly after CPB (p<0.01), and this level was strongly correlated with renal tubular leaking enzymes: NAG (r=0.76) and γ-GTP (r=0.81), in the Intensive Care Unit or on the first day after surgery. On the contrary, in the haptoglobin group, in which 4, 000 units of haptoglobin was added in the priming solution of CPB, no increased level of plasma free hemoglobin was observed. Furthermore, leak age of renal tubular enzymes were statistically less (p<0.05). It was concluded that free hemoglobin was a cause of renal damage during CPB and the damage was preventable by the administration of haptoglobin.

Objective To assess the effect of D-JNKI1, an inhibitor of c-Jun N-terminal kinase (JNK), on delayed neuronal death (DND) in a gerbil model of transient global cerebral ischemia, so as to further study the roles of JNK activation in mediating neuronal cell death in brain ischemia. Methods Fifty-five Mongolian gerbils were randomly divided into 11 groups. Animals (n=35) assigned into 7 groups (n=5 per group) were subjected to 5-min occlusion of bilateral common carotid arteries (BCCAO);among the 7 groups, different doses of D-JNKI1 (0.00012, 0.0012, 0.012, 0.12, 1.2 μmol/L in 2 μL PBS,n=5 each) were administered stereotaxically into right lateral ventricles 3 h after reperfusion; the control group (n=5) received 2 μL PBS; and another group (n=5) received 1.2 μmol/L of D-JNKI1 in 0.5 mL PBS intraperitoneally. Sham-operated animals (n=5) only received the exposure of bilateral common carotid arteries without occlusion. Three groups (n=5 in each) were pretreated with D-JNKI1 (0.00012,0.0012 μmol/L in 2 μL PBS) or only 2 μL PBS 30 min before 2-min BCCAO, and subjected to 5-min BCCAO 48 h after the first ischemic insult. All animals were sacrificed 4 d after 5-min BCCAO and prepared for frozen section and Nissl staining. Results The treatment with D-JNKI 3 h after 5-min ischemia was neuroprotective with a maximum effect at a dose of 0.0012 μmol/L. Pretreatment with D-JNKI augmented ischemic tolerance induced by 2-min ischemia. Conclusion D-JNKI1 has a potential neuroprotective effect on DND in CA1 of hippocampus in gerbils with global cerebral ischemia-reperfusion injury.