Interactive effects of 5-HTTLPR genotype and rearing environment on affective attitude towards own infant in Japanese mothers.

Maternal positive attitude towards one's own infant is the cornerstone of effective parenting. Previous research has revealed an influence of both genetic and environmental factors on maternal parenting behavior, but little is known of the potential gene-environment interaction in shaping a mother's affective attitude. To address this gap, we investigated the effect of a mother's childhood rearing environment and a serotonin transporter gene polymorphism (5-HTTLPR) on affective attitude towards her infant. Our analyses found an interactive effect between rearing environment and 5-HTTLPR genotype on maternal attitude. Specifically, a poor rearing environment (characterized by low maternal care and high paternal overprotection) decreased positive attitude towards one's own infant in mothers with homozygous short allele genotype. In contrast, this detrimental effect was almost eliminated in long allele carriers. Altogether, our results indicate that the 5-HTTLPR gene moderates the influence of experienced rearing environment on maternal parental behavior in a manner consistent with the notion that the short 5-HTTLPR allele amplifies environmental influence.

[Anesthetic management of awake off-pump coronary artery bypass grafting (ACAB) with remifentanil and thoracic epidural anesthesia].

Two patients with total occlusion of the right internal carotid artery, were anesthetized for ACAB with remifentanil and thoracic epidural anesthesia. Case 1: A 71-year-old man with hypertension and diabetes mellitus underwent single-vessel ACAB under IV remifentanil analgesia, the dose of which was adjusted to 0.04-0.05 microg x kg(-1) x min(-1), along with an epidural infusion of 10 ml x hr(-1) of a mixture of 2% lidocaine and 2.5 microg x ml(-1) of fentanyl, the PaCO2 being maintained at 52-55 mmHg. When the patient felt pain, the remifentanil dose was elevated to 0.08 microg x kg(-1) x min(-1) and PaCO2 increased to 60 mmHg. Case 2: A 66-year-old man with rheumatoid arthritis underwent ACAB for two grafts. An intraaortic balloon pump (IABP) was inserted preoperatively. The anesthetic method used was the same as in case 1, except for an additional right femoral block to provide anesthesia for extraction of the saphenous vein. Remifentanil was infused at 0.05 microg x kg(-1) x min(-1) and PaCO2 maintained at 49-53 mmHg. In response to the patient's pain and movement, the remifentanil dose was increased to 0.07-0.10 microg x kg(-1) x min(-1) and PaCO2 to 60 mmHg.

[Heparin resistance associated with elevated factor VIII].

An 84-year-old female patient was scheduled to undergo AVR, CABG, and Maze procedure. She had a history of hypertension, cerebral infarction, and branch retinal vein occlusion. Warfarin was administered preoperatively. Before the cardiopulmonary bypass (CPB), heparin 5,000 units was administered. Activated coagulation times (ACTs) before and after CPB were 123 sec and 157 sec, respectively. Additional heparin of 5,000 units extended ACT to 221 seconds, which was not enough for the CPB. Heparin 10,000 units was added, and ACT was 157 sec. AntithrombinIII (ATIII) and platelet counts were 75% and 270,000 mm(-3), respectively. ATIII 1,500 units was administered. ACT and ATIII became 133 sec and 123%, respectively. Because heparin resistance did not respond to ATIII, the operative method was changed to off-pump CABG. A postoperative examination revealed high factor VIII activity of 263%. Other results were as follows: protein C antigen, 40%; protein S antigen, 65%; factor VII, 50%; platelet factor 4, 12%; heparin cofactor II, 104%; von Willebrand factor antigen, 181%; heparin-PF4-IgG antibody, negative; factor VIII inhibitor, negative. The low values of protein C, protein S, and factor VII may have been caused by warfarin. Other values were normal, except for the von Willebrand factor antigen.

Heavy ion irradiation inhibits in vitro angiogenesis even at sublethal dose.

Angiogenesis is essential for tumor growth and metastasis. Because endothelial cells are genetically stable, they rarely acquire resistance to anticancer modalities, and could, thus, be a suitable target for radiation therapy. Heavy ion radiation therapy has attracted attention as an effective modality for cancer therapy because of its highly lethal effects, but the effects of heavy ion irradiation on in vitro cell function associated with angiogenesis have not been reported. Our study found that in vitro angiogenesis was inhibited by high linear energy transfer carbon ion irradiation even at sublethal dose (0.1 Gy). ECV304 and HUVEC human umbilical vascular endothelial cells were irradiated with 290 MeV carbon ion beams of approximately 110 keV/ micro m or 4 MV X-ray of approximately 1 keV/ micro m. Their adhesiveness and migration to vitronectin or osteopontin were inhibited, and capillary-like tube structures in three-dimensional culture were destroyed after carbon ion irradiation concomitant with the inhibition of matrix metalloproteinase-2 activity, down-regulation of alphaVbeta3 integrin, which is one of the adhesion molecules, slight up-regulation of membrane type1- matrix metalloproteinase, and significant up-regulation of tissue inhibitor of metalloproteinase-2. On the other hand, sublethal X-ray irradiation promoted migration of endothelial cells, and the capillary-like tube structure in three-dimensional culture progressed even after 16 Gy irradiation. These results provide an implication that heavy ion beam therapy could be superior to conventional photon beam therapy in preventive effects on in vitro angiogenesis even at sublethal dose, and might inhibit angiogenesis in vivo.