Structural Changes in Titin and Nebulin Filaments Specific to Calcium Ions at 0.1 mM: Factors of Meat Tenderization During Postmortem Aging

ABSTRACT Postmortem structural changes in titin and nebulin filaments were investigated by incubating isolated myofibrils in a solution containing 0.1 mM calcium ions and various concentrations of a protease inhibitor. The inhibition curves showed 2 abnormal steps with increases in the concentration of leupeptin or calpastatin domain I. While the amounts of unchanged titin and nebulin were constant in the 1st step, the 2nd occurred at higher protease inhibitor concentrations. These facts indicated that excess amounts of leupeptin and calpastatin domain I caused deterioration in titin and nebulin properties, thus interfering with the binding of calcium ions. We concluded that the severance of titin and nebulin filaments in the 1st step were induced by calcium ions at 0.1 mM.     

Catalytic decomposition of HCFC22 (CHClF2)

The catalytic decomposition of CHClF₂ was studied over various acidic metal oxides in a fixed-bed reactor. The Cr₂O₃ZrO₂ exhibited the highest activity. The presence of water vapor in the reaction system suppresses the transformation of oxides to fluorides, progresses the formation of CO₂, and it improves the catalysts life.     

A 0.1-μm delta-doped MOSFET fabricated with post-low-energyimplanting selective epitaxy

A simple fabrication technology for delta-doped MOSFETs, named post-low-energy implanting selective epitaxy (PLISE) is presented. The PLISE technology needs no additional photo-lithography mask, deposition step or etching step even for CMOS devices. The only additional step is growing undoped epitaxial channel layers by UHV-CVD after the channel implantation. With this technology, delta-doped NMOSFETs with 0.1-μm gate length were successfully fabricated. By optimizing the epi-layer thickness and the channel doping level, short-channel effects are suppressed enough to achieve 0.1-μm gate length. Moreover, the junction capacitance at zero bias is reduced by 50%     

The cause of the uneven carbonization process in wet coal charging in coke oven chamber

In the case of the wet coal charging process in coke oven chamber, it is known that the coking process is uneven and a local carbonization delay occurs. The reason was investigated through a laboratory-scale experiment and a quantitative estimation. A partial carbonization test in a test coke oven replicated the uneven plastic layer and local carbonization delay. It was revealed that most of the gas generated in the uncarbonized coal layer results from the evaporation of condensed water and that steam can break through the plastic layer in a test coke oven. Moreover, the order estimation implied that steam that generates in the uncarbonized coal layer and breaks through the plastic layer has sufficient heat capacity to cool the heating wall and delay the carbonization. It was also shown that the steam pressure peak measured in a commercial coke oven is much lower than the estimated steam pressure in this study assuming steam not breaking through the plastic layer. The above-mentioned results and quantitative investigation strongly support the ‘steam breaking through the plastic layer’ theory proposed by Dr. Rohde that an uneven carbonization process is caused by vaporized coal moisture breaking through the plastic layer at definite, unforeseeable points, which results in cooling of the wall by the steam flow.     

Elevated serum lipoprotein (a) levels associated with ulcerative colitis in a young Japanese patient

Thromboembolism has been shown to play a role in the pathogenesis of inflammatory bowel disease (IBD). A possibility exists that lipoprotein (a) [Lp(a)], a newly-discovered prothrombotic factor, also participates in the development of at least some cases of IBD. Marked elevation of serum Lp(a) levels was observed in a young patient with ulcerative colitis. A biopsy specimen of the rectal mucosa showed findings compatible with ulcerative colitis, as well as small vessel thrombus occurring within the muscularis mucosa in the rectum. Serum Lp(a) levels were markedly elevated on admission (71 mg/dl), with a gradual decrease to 46 mg/dl on discharge. Moreover, serum Lp(a) levels decreased in parallel with clinical improvement. In the quiescent clinical stage, no small vessel thrombus was observed in the mucosa on follow-up colonoscopy. The association between IBD and hyper-Lp(a)-emia would be presumable but it has been, to our knowledge, previously unreported. The case reported here would be the first young patient, suggesting the presence of hyper-Lp(a)-emia and small vessel thrombus formation occurring in association with the development of ulcerative colitis.