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Adult left lobe (LL) living donor liver transplantation (LDLT) has not generally been recognized as a feasible procedure because of the problem of graft size. The objectives of this study were to assess the feasibility and short‐ and long‐term results of adult LL LDLT in comparison with right lobe (RL) LDLT. Data on 200 consecutive LL LDLTs, including five retransplants, were retrospectively compared with those of 112 RL LDLTs, in terms of survival, complications and donor morbidity. The mean graft weight to standard volume ratio of LL grafts was 38.7% whereas that of RL grafts was 47.6% (p < 0.0001). The 1‐, 5‐ and 10‐year patient survival rates of LL LDLT were 85.6%, 77.9% and 69.5%, respectively, which were comparable to those of RL LDLT (89.8%, 71.3% and 70.7%, respectively). The incidence of small‐for‐size syndrome was higher in LL LDLT (19.5%) than in RL LDLT (7.1%) (p < 0.01). The overall donor morbidity rates were comparable between LL (36.0%) and RL (34.8%), whereas postoperative liver function tests and hospital stay were significantly better (p < 0.0001) in LL donors. In conclusion, adult LL LDLT has comparable outcomes to that of RL LDLT. LL LDLT is viable and is the first choice in adult LDLT.

Adult left lobe (LL) living donor liver transplantation (LDLT) has not generally been recognized as a feasible procedure because of the problem of graft size. The objectives of this study were to assess the feasibility and short- and long-term results of adult LL LDLT in comparison with right lobe (RL) LDLT. Data on 200 consecutive LL LDLTs, including five retransplants, were retrospectively compared with those of 112 RL LDLTs, in terms of survival, complications and donor morbidity. The mean graft weight to standard volume ratio of LL grafts was 38.7% whereas that of RL grafts was 47.6% (p < 0.0001). The 1-, 5- and 10-year patient survival rates of LL LDLT were 85.6%, 77.9% and 69.5%, respectively, which were comparable to those of RL LDLT (89.8%, 71.3% and 70.7%, respectively). The incidence of small-for-size syndrome was higher in LL LDLT (19.5%) than in RL LDLT (7.1%) (p < 0.01). The overall donor morbidity rates were comparable between LL (36.0%) and RL (34.8%), whereas postoperative liver function tests and hospital stay were significantly better (p < 0.0001) in LL donors. In conclusion, adult LL LDLT has comparable outcomes to that of RL LDLT. LL LDLT is viable and is the first choice in adult LDLT.

Small residual liver volume after massive hepatectomy or partial liver transplantation is a major cause of subsequent liver dysfunction. We hypothesize that the abrupt regenerative response of small remnant liver is responsible for subsequent deleterious outcome. To slow down the regenerative speed, NS-398 (ERK12 inhibitor) or PD98059 (selective MEK inhibitor) was administered after 70 or 90 partial hepatectomy (PH). The effects of regenerative speed on liver morphology, portal pressure and survival were assessed. In the 70 PH model, NS-398 treatment suppressed the abrupt replicative response of hepatocytes during the early phase of regeneration, although liver volume on day 7 was not significantly different from that of the control group. Immunohistochemical analysis for CD31 (for sinusoids) and AGp110 (for bile canaliculi) revealed that lobular architectural disturbance was alleviated by NS-398 treatment. In the 90 PH model, administration of NS-398 or PD98059, but not hepatocyte growth factor, significantly enhanced survival. The abrupt regenerative response of small remnant liver is suggested to be responsible for intensive lobular derangement and subsequent liver dysfunction. The suppression of MEKERK signaling pathway during the early phase after hepatectomy makes the regenerative response linear, and improves the prognosis for animals bearing a small remnant liver.

Small residual liver volume after massive hepatectomy or partial liver transplantation is a major cause of subsequent liver dysfunction. We hypothesize that the abrupt regenerative response of small remnant liver is responsible for subsequent deleterious outcome. To slow down the regenerative speed, NS‐398 (ERK1/2 inhibitor) or PD98059 (selective MEK inhibitor) was administered after 70% or 90% partial hepatectomy (PH). The effects of regenerative speed on liver morphology, portal pressure and survival were assessed. In the 70% PH model, NS‐398 treatment suppressed the abrupt replicative response of hepatocytes during the early phase of regeneration, although liver volume on day 7 was not significantly different from that of the control group. Immunohistochemical analysis for CD31 (for sinusoids) and AGp110 (for bile canaliculi) revealed that lobular architectural disturbance was alleviated by NS‐398 treatment. In the 90% PH model, administration of NS‐398 or PD98059, but not hepatocyte growth factor, significantly enhanced survival. The abrupt regenerative response of small remnant liver is suggested to be responsible for intensive lobular derangement and subsequent liver dysfunction. The suppression of MEK/ERK signaling pathway during the early phase after hepatectomy makes the regenerative response linear, and improves the prognosis for animals bearing a small remnant liver.

Abstract: To elucidate the origin of the shrinking anisotropy of wood during the drying process, as well as to begin to gain an understanding of the interaction between the moisture and the cell wall components, the shrinking process of a single wood fiber regarding water desorption was simulated by using an analytical model which was developed in the previous report (Part 1). Resulting data were compared with the experimental ones in this paper. The following conclusions were obtained: (1) The matrix substance, as a skeleton in the secondary wall, tends to shrink isotropically. However, the cellulose microfibrils, as a rigid framework of the cell wall, almost did not shrink at all due to the water desorption. As result, wood shrinks anisotropically during a drying process. The microfibril angle in the S2 layer is one of the most important factors related to the degree of shrinking anisotropy of the wood while drying. (2) According to the simulation, the expansive strain caused in the matrix skeleton by the water sorption increases by 15% (= 150,000 micro-strains) from the oven-dried condition to the green condition. Based on this value, the moisture content at the fiber saturation point is calculated to be about 35%, which is close to the experimentally obtained one. These results give quantitative evidences that the hygroexpansion of the wood cell wall is controlled by the mechanism of the reinforced matrix hypothesis.

The changes of viscosity, optical reflection and electrical resistivity of blood due to flow are dependent on the orientation and deformation of red cells. From electrical point of view, it can be assumed that blood is suspension of small insulating particles (red cells) in conductive fluid (plasma) when the frequency of supplied voltage is lower than several hundreds KHz. When blood flows, red cells deform and orient in flow direction. Therefore, flowing blood shows anisotropic electrical and optical properties. In steady flow, blood resistivity longitudinal to flow decrease with flow rate, and transverse one increases. Blood flow in living body is not steady but pulsatile. We measured both longitudinal and transverse resistivity changes, optical reflection change and viscosity change of sinusoidally flowing blood in a rectangular conduit. The results are 1) during one period of sinusoidal flow the longitudinal resistivity change is opposite to that of transverse one, 2) the waveform of reflection light change is similar to that of resistance change, and 3) minimum points of both longitudinal resistivity and viscosity changes do not appear at the moment when flow is zero but are delayed. When the amplitude of sinusoidal flow is small and oscillation frequency is high, the phase difference between the zero crossing period of flow and the period of minimum change in resistivity, increases up to 90°. Viscosity of blood decreases with increase of amplitude and frequency of sinusoidal flow.

We propose a new type of gauge in two-dimensional quantum gravity. We investigate pure gravity in this gauge, and find that the system reduces to quantum mechanics of loop length l. Furthermore, we rederive the c= 0 string field theory which was discovered recently. In particular, the pregeometric form of the Hamiltonian is naturally reproduced.

A four-channeled aortic dissection is quite rare, which is a highly life-threatening situation predisposing to aortic rupture. We report a successful management of a four-channeled aortic dissection and an aortic rupture in a 59-year-old woman with Marfan's syndrome 11 years after an initial Bentall procedure for DeBakey type I dissection. The total arch and the descending thoracic aorta were replaced under deep hypothermia and circulatory arrest.

Summary It has been reported that left ventricular end-systolic volume decreases during arteriovenous shunt and increases during subclavian artery-left atrium shunt at a constant end-systolic pressure. The mechanism of the opposing changes in end-systolic volume during the two types of shunt is not clear. One possible cause is that left ventricular pump function with enhanced right ventricular ejection differs from that without enhancement. To investigate this hypothesis, we studied the two types of shunt (Aorto-femoral vein shunt, AoFV; aorto-left atrium shunt, AoLA) with matched reduction of systemic vascular resistance in open-chest dogs with β-blockade. Both right and left ventricular volumes and shortenings were assessed from short-axis views by two-dimensional (2D)-echocardiogram. Left ventricular end-systolic short-axis area decreased from 76 ± 3 to 62 ± 3% in AoFV shunt (p < 0.05), but tended to increase in AoLA shunt (76 ± 4 in control state vs 81 ± 5% in AoLA, NS) in spite of a similar reduction in left ventricular end-systolic pressure. There was no difference in left ventricular shortening, but significant differences were observed in right ventricular shortening (50 ± 8 in AoFV vs 24 ± 7% in AoLA, p < 0.05) and right ventricular short-axis area at end-diastole (142 ± 6 in AoFV vs 96 ± 3% in AoLA, p < 0.01), and at end-systole (92 ± 8 in AoFV vs 73 ± 7% in AoLA, p < 0.05) between the two types of shunt. We conclude that the different changes in left ventricular end-systolic short-axis area found in the two shunts are not caused by the different left ventricular shortenings, but by the different right ventricular mechanical actions. These findings suggest that left ventricular pumping action in the high output state changes, depending on whether it is accompanied by augmented ejection of the right ventricle or not.

Clostridium perfringens type A strains which differed in alpha-toxin (phospholipase C [PLC]) productivity were inoculated intraperitoneally or intravenously into mice, and then their 50% mouse lethal doses (LD50) were determined. Strain NCTC 8237 produced ninefold higher PLC activity than strain 13. The mean LD50 for the former was 1 log unit lower than that for the latter. Two isogenic strains were constructed from strain 13: strain 13(pJIR418 alpha) (pJIR418 alpha contains the plc gene), which produced ninefold higher PLC activity than strain 13; and strain 13 PLC-, which showed no PLC productivity at all because of transformation-mediated gene disruption. The mean LD50 for strain 13(pJIR418 alpha) was 1 log unit lower than those for strain 13 PLC- and strain 13. These results indicate that PLC functions as a virulence-determining factor when it is produced in a sufficient amount. Such a difference in LD50 was also observed between Bacillus subtilis with and without the cloned plc gene. Inoculation of B. subtilis PLC+ intravenously into mice caused marked thrombocytopenia and leukocytosis. Mice inoculated with B. subtilis at 2 LD50 died because of circulatory collapse. Histological examination revealed that intravascular coagulation and vascular congestion occurred most prominently in the lungs. These results suggest that PLC plays a key role in the systemic intoxication of clostridial myonecrosis, probably by affecting the functions of platelets and phagocytes.

The effects of a novel dihydrothienopyridine Ca antagonist S-(+)-methyl-4,7-dihydro-3-isobutyl-6-methyl-4-(3-nitrophenyl)-thieno [2,3-b]pyridine-5-carboxylate (S-312-d), on the amount of amino acid release during cerebral ischemia and delayed neuronal death in the hippocampal CA1 region of stroke-prone spontaneously hypertensive rats were studied and compared with those of nimodipine. The released amino acids were measured by high-performance liquid chromatography after microdialysis. Cerebral ischemia was produced by occlusion of the bilateral common carotid arteries for 20 min. Intraduodenal administration of 0.3 mg/kg of S-312-d at 60 min before the carotid occlusion significantly decreased the ischemic release of glutamate and taurine, but did not influence their basal release. However, nimodipine did not inhibit the ischemic glutamate release even at a dose of 10 mg/kg. Similar peripheral hemodynamic effects were observed before and during bilateral carotid occlusion in groups treated with S-312-d or nimodipine. During the carotid occlusion, almost no cerebral blood flow was observed in either group. Therefore, the inhibitory effect of S-312-d on ischemic amino acid release probably arises from its potent direct action on neuronal cells. The neuronal cell densities of the CA1 subfield at 7 days after 20-min bilateral carotid occlusion significantly decreased in the vehicle-control group compared with the sham-operated group. Intraperitoneal administration of 0.1 mg/kg of S-312-d at 60 min before ischemia prevented the decrease of neuronal cell density compared with the vehicle control. These results show that S-312-d can offer marked neuronal protective effects against ischemic injury.

Recovery from destruction by sodium deoxycholate (DOC) was studied with the receptor membrane of the blowfly, Phormia regina. The recovery can be divided into two processes, colchicine dependent and colchicine independent. The colchicine-dependent process was completely depressed by pretreatment with colchicine at 5 mM for 2 min (partially at 0.1 mM for 10 min), but the colchicine-independent one persisted. Vinblastine also caused depression but lumicolchicine did not. Records of responses obtained from the DOC-treated sugar receptor showed long response latencies that gradually became indistinct with recovery. Colchicine also affected this change in response latency after the DOC treatment. These results suggest that the colchicine-dependent recovery process is related to microtubules in the distal process of the receptor cell. The recovery time course and the change in response latency could be quantitatively explained by the simple assumptions that DOC underwent desorption from the receptor membrane (colchicine-independent recovery process) and that regeneration of the disrupted distal process of the receptor cell accompanied recovery in the number of available receptor sites (colchicine-dependent recovery process).

Electron micrographs of sections of the labellar chemosensilla of the blowfly, Phormia regina, showed that treatment with sodium deoxycholate (DOC; 7.2 mM for 2 min) destroyed the distal processes of the receptors from up to 10 microns from the tip of the sensillum, but these processes regenerated almost completely within 0.5 h. However, when DOC treatment was preceded by colchicine treatment (25 mM for 2 min), greater than 10 h was required for complete regeneration. Sugar receptor responses supported these findings and disclosed a more detailed time course of regeneration after DOC treatment: without colchicine pretreatment, the destroyed distal process completely regenerated in 0.3-1.0 h, but with pretreatment, regeneration began at 3 h and reached the chemosensillar tip at 8 h at the earliest. Hardly any depression of the response was observed for 8 h after treatment with colchicine alone, but a transient depression was detected at 12 h. Based on these results, the role of microtubules in the maintenance of the receptor membrane is discussed.

Three patients of ischemic heart disease associated with protein C deficiency are reported. Although delayed diagnosis of protein C deficiency resulted in the failure of repeated interventions, coronary artery bypass grafting performed after making the correct diagnosis has led to satisfactory mid-term results under strict anticoagulation therapy. The level of protein C should be measured more frequently in the field of ischemic heart disease and earlier diagnosis of its deficiency should be made, because measurement of protein C does not cost much.

AbstractNo abstract available.

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