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Non-heat-treated Al–Mg-based die casting alloys have been developed for the structural parts of automobiles. In previous studies, alloy compositions with at least 1.0%Si have been proposed to reduce the hot tearing susceptibility (HTS). On the other hand, the increase in the Si content reduces the ductility. For some automotive body structures, Al–Mg alloy die castings with Si content exceeding 1.0% should not have the required ductility. This study aims to develop an Al–Mg alloy with both high ductility and low HTSby investigating the following three characteristics of an Al–4.5Mg–1.0Mn alloy with 0.2%Si added: (1) additional elements to reduce the HTS, (2) the associated mechanical properties (requirements for the automotive company: 0.2% proof stress ≥ 140 MPa and fracture elongation ≥ 15%), and (3) the mechanism of decreasing the HTS. It was revealed that the co-addition of 0.025%Sr, 0.08%Ti, and 0.016%B reduced the HTSwhen the hydrogen content of the melt was 0.5–1.0 mL/100 g Al. Furthermore, the 0.2% proof stress and fracture elongation of a lower link arm produced via HPDC with the above composition were found to achieve the requirements. It was also indicated that the mechanism of decrease in the HTSby the Sr addition should result from the decrease in the thermal tensile load due to the formation of hydrogen porosity at a lower solid fraction than that without Sr. It is suggested that when 0.025%Sr, 0.08%Ti, and 0.016%B are added to the Al–4.5Mg–1.0Mn–0.2Si alloy, non-heat-treated automotive structural parts with both high ductility and low HTSwill be obtained by high-pressure die casting.

We examined prospectively which of the four blood pressure (BP) components (systolic BP [SBP], diastolic BP [DBP], pulse pressure [PP], and mean arterial pressure [MAP]) was best in predicting the risk of proteinuria.

Human plasma contains two actin-binding proteins, plasma gelsolin and vitamin D-binding protein. These proteins are considered to play an important role in the disposition of actin derived from injured tissue. To evaluate this actin-scavenger system, gelsolin concentrations were measured in serial plasma samples obtained from patients with acute liver injury using an enzyme-linked immunosorbent assay. Plasma gelsolin levels in 43 healthy persons were 226 ± 52 μg/mL. They were markedly reduced to 80 ± 40 μg/mL in 14 patients with an early stage of acute hepatitis and returned to normal levels of 232 ± 38 μg/mL as the disease resolved. Moreover, they showed a significant negative correlation with serum aminotransferase and bilirubin levels. In 7 patients with hepatocellular carcinoma, plasma gelsolin levels rapidly decreased from 182 ± 42 to 87 ± 41 μg/mL after transcatheter arterial embolization therapy. Because plasma gelsolin is not a hepatic protein, the decreased levels are considered to depend exclusively on the extent of actin leakage from the injured liver.

Abstract: In the brains of W/Wvmutant mice that have no mast cells, the histidine decarboxylase (HDC) level is as high as in the brain of congenic normal mice (+/+), but the histamine content is 53% of that of +/+ mice. The effects of a‐fluoromethylhistidine (α‐FMH) on the HDC activity and histamine content of the brain of W/Wrand +/+ mice were examined. In both strains, 30 min after i.p. injection of α‐FMH the HDC activity of the brain had decreased to 10% of that in untreated mice. The histamine content decreased more gradually, and after 6 h about half of the control level remained in +/+ mice, whereas histamine had disappeared almost completely in W/Wvmice. It is concluded that the portion of the histamine content that was depleted by HDC inhibitor in a short time is derived from non‐mast cells, probably neural cells. The half‐life of histamine in the brain of W/Wvmice was estimated from the time‐dependent decrease in the histamine content of the brain after administration of a‐FMH: 48 min in the forebrain, 103 min in the midbrain, and 66 min in the hindbrain.